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Anterior Choroidal Artery

Teritory Infarcts
• The anterior choroidal artery optic tract
crus cerebri lateral dan lateral geniculated
body choroid plexus di bagian inferior horn
of the lateral ventricle.
• Mensuplai optic tract, temporal genu of the
optic radiation,hippocampus, the tail of the
caudate nucleus, dan amygdaloid body.
Anterior Choroidal Artery ( AChA )
• ANATOMI
• The AChA originates from the posterior wall of
the ICA between the origin of posterior
communicating artery (PCOM), which is 2-5
mm proximally and the internal carotid
termination, which is 2-5 mm distal to the
AChA. It measures ~1 mm in diameter.
• The AChA is located lateral to the optic tract, it
then curves medially to its inferomedial
surface, to curve again laterally to run along
the lateral aspect of the optic tract and
circumvents the cerebral peduncles to reach
the lateral geniculate body. It traverses in the
posterolateral direction above the uncus to
enter the choroidal fissure.
Segment :
• cisternal segment: extends from its origin
until the choroidal fissure; measures ~2.5 cm
(range 1.5-3.5 cm) in length
• intraventricular segment: after entering the
choroidal fissure
• Vascular territory
• cisternal segment
– optic tract
– lateral geniculate nucleus and lateral aspect of the
thalamus
– posterior limb of the internal capsule
– lateral aspect of the midbrain
• intraventricular segment
– choroid plexus of the anterior part of the temporal
horns of the lateral ventricles
Variant anatomy
• occasionally it may originate from
– intracerebral carotid bifurcation
– middle cerebral artery
– posterior communicating artery
• duplication of AChA is reported in ~5% of
cases
• hyperplastic AChA in which AChA supplies the
area usually associated with PCA
Anterior Choroidal Artery ( AChA )
Carotid artery 
• optic chiasm
• optic tract
• internal capsule
• lateral geniculate body
• globus pallidus
• tail of the caudate nucleus
• hippocampus
• amygdala
• substantia nigra red nucleus
• crus cerebri
AChA Syndrom
Trias
• Contra lateral hemiplegia (posterior limb of
the internal capsule )
• Contra lateral hemi hypoesthesia (ventral
postero lateral nucleus of the thalamus )
• Homonymous hemianopsia (lateral geniculate
body)
AChA Syndrom
Gangguan neuropsikologik
• Hemineglect in right sided infarcts
• Mild afasia in left sided infarct ( jarang )
• Acute pseudobulbar mutism ( bilateral lesion )
• Amnesia
• Pseudobulbar palsy ( Bilateral or unilateral
infarct
Etiologi AChA Infarcts
• Smaller lesions : small-vessel disease with
chronic hypertension being the single most
important risk factor
• Large AChA infarcts : embolic source
• Carotid artery stenosis
• Younger age groups, male and diabetic
Terapi
• Penanganan penyebab infarct : small vessel
oclusion, emboli, dan etiologi lain
A man 68 years of age was admitted to our hospital on April 3, 2006, because of
progressive weakness on the right side and dysarthria. On March 30, 2006, the patient
had begun to feel weakness of the right upper and lower limbs. Neurologic examination
revealed a right central-type facial palsy, right upper limb weakness (Grade 1), and right
lower limb weakness (Grade 3). His past history showed vascular risk factors such as
hypertension, hyperlipidemia, smoking, and diabetes. The results of laboratory studies
were normal. Electrocardiography showed sinus tachycardia. Carotid ultrasonography
showed mild atherosclerotic changes common carotid arteries, carotid bifurcations, and
internal carotid arteries on both sides. Brain computed tomography (CT) showed
presence of infarction involving the left internal capsule region (Fig. 1). Thus an
impression of left cerebral infarction was made. Brain magnetic resonance imaging
(MRI) performed on April 4, 2006, confirmed the diagnosis of acute infarction involving
the left internal capsule region, mainly in the anterior choroidal artery (AChA) territory
(Fig. 2). Sudden loss of consciousness was noted on April 5, 2006. The Glasgow Coma
Scale (GCS) dropped to E1V1M4, and an emergent brain CT revealed subarachnoid
hemorrhage (SAH) with intraventricular hemorrhage and acute hydrocephalus (Fig. 3). A
neurosurgeon was called in for emergency consultation. The patient then underwent
emergent external ventricular drainage. The clinical condition improved after surgery
and the GCS became E3VeM5 on April 10, 2006. Carotid angiography was performed on
April 10, 2006, and it revealed a saccular-type aneurysm with pseudoaneurysm
formation in the left internal carotid artery (ICA)- posterior communicating artery
(PcomA) region (Fig. 4). The left AChA was not visualized. The patient underwent
craniotomy for clipping of the aneurysm on April 12, 2006. The operative findings
consisted of a 0.5 × 0.6 × 0.8 cm saccular-type aneurysm and a pseudoaneurysm
(1 × 1.5 × 2 cm) in the left ICA-PComA region (Fig. 5). Besides that, an occluded left
AChA was found tightly compressed by the aneurysm. The patient was kept in the
intensive care unity for postoperative care. After surgery, the GCS was still E3VeM5. The
clinical course was uneventful.
• Computed tomography of the brain showed a
hypodense area in the border zone of the left
internal capsule region; infarction was
suspected.
• Diffusion-weighted image of the brain showed
an increased signal area involving the left
internal capsule region, mainly in the anterior
choroidal artery territory; acute infarction was
suspected.
• Computed tomography of the brain showed
subarachnoid hemorrhage in the suprasellar
cistern, quadrigeminal cistern, prepontine
cistern, both cerebellopontine angle cisterns,
and left sylvian fissure. Supratentorial
hydrocephalus was also noted
• Left-carotid angiogram showed a saccular-
type aneurysm with pseudoaneurysm in the
left internal carotid artery-posterior
communicating artery region; (A) facing left;
(B) facing posterolaterally.
TERIMAKASIH