Carotid dissection causing occipital lobe infarction

Abstract

Abstract-Background: Elevated plasma total homocysteine (tHcy) is a risk factor for cardiovascular disease and is reported to be an independent risk factor for Alzheimer disease (AD) and cognitive decline. tHcy may potentiate neurotoxic and vasculopathic processes, including amyloid ␤ protein (A␤) metabolism, implicated in neurodegenerative diseases. Objective: To examine the relationship of plasma total tHcy levels with clinical, demographic, biochemical, and genetic factors in aging, mild cognitive impairment (MCI), AD, cerebral amyloid angiopathy (CAA), and Parkinson disease (PD). Methods: Plasma tHcy, folate, vitamin B 12 , creatinine, and A␤ levels were assessed in individuals evaluated in the Memory, Stroke, and Movement Disorders Units of Massachusetts General Hospital with diagnoses of AD (n ϭ 145), MCI (n ϭ 47), PD (n ϭ 93), CAA (67), hypertensive intracerebral hemorrhage (hICH) (n ϭ 25), and no dementia (n ϭ 88). Results: The tHcy levels did not differ across AD, MCI, CAA, hICH, and nondemented control subjects but were increased in the PD group (p Ͻ 0.01). The elevated levels within the PD group were due to high tHcy in individuals taking levodopa (p Ͻ 0.0001). Increasing tHcy was associated with worse cognition in the PD cases, but not the other diagnostic groups. tHcy levels positively correlated with plasma A␤ levels even after adjustments for age and creatinine (p Ͻ 0.0001). Conclusions: Mean tHcy levels increased with age but did not discriminate diagnostic groups aside from significant elevation in patients with PD taking levodopa. The positive association between tHcy and plasma A␤ levels raises the possibility that these circulating factors could interact to affect AD risk and cognition in PD.

Fetal-Type Variants of the Posterior Cerebral Artery and Concurrent Infarction in the Major Arterial Territories of the Cerebral Hemisphere

“…All things considered, the most likely mechanism of paradoxical PCA occlusion in Patient 1 is right ICA-to-PCA embolism through a patent PcomA. Although an FPCA has been implicated in nearly all cases of paradoxical PCA occlusion, 12 - 20 the PcomA is a potential conduit for cross embolization from the ICA to the PCA P2 segment or its distal branches. 12 , 21 The rarity of PcomA embolism may be due to the low ICA-PCA pressure gradient across the PcomA.…”

“…Emboli can move up the ICA, enter and occlude the FPCA or its branches, and result in a paradoxical PCA territory infarction-with [12][13][14][15] or without [16][17][18][19][20] attendant occlusion of other ICA branches. A left FPCA was clearly the reason for the left-sided paradoxical infarction in Patient 2.…”

“…Some authors refer to this anatomic variant, not as FPCA or "true fetal" PCA, but as hyperplastic AChA. 24,32,33 With a prevalence rate in the 11% to 46% range [3][4][5][6][7][8][9][10] and an established role in the pathogenesis of multi-territory or paradoxical strokes, [12][13][14][15][16][17][18][19][20][21] FPCA certainly deserves more clinical attention. FPCA should be suspected in patients with infarcts in the anterior and posterior circulation territories of one hemisphere.…”

Infarto de la arteria cerebral posterior secundario a oclusión aguda de la arteria carótida interna

“…La primera pregunta es cómo se explica que haya daño de la arteria cerebral posterior debido a una lesión carotídea. De acuerdo con la literatura, el primer reporte se tituló: "Infarto occipital con hemianopsia desde la enfermedad carotídea oclusiva" (7), los otros informes existentes son de pacientes con disección carotídea con presencia de infarto occipital (8,(17)(18)(19). La mayoría de las veces en que se compromete la arteria cerebral posterior la causa es una isquemia de la circulación posterior; sin embargo, la unión de la circulación anterior con la posterior en el polígono de Willis se da por la arteria comunicante posterior (20).…”

“…Desde luego, para que suceda un infarto occipital por compromiso de la circulación anterior se deben dar algunas variantes anatómicas: la primera es la hipoplasia del segmento P1 o segmento precomunicante de la arteria cerebral posterior ipsilateral a la carótida ocluída (17,21), en la que la arteria comunicante posterior lleva la circulación al segmento postcomunicante (P2). La segunda variante se presenta cuando la arteria cerebral posterior se origina directamente de la arteria carótida interna; esto es lo que se llama el "origen fetal" de la arteria cerebral posterior (7,8,19). Bayona H.…”