Anterior cerebral artery strokes

Stroke mechanism and clinical imaging in 100 patients. Kang SY, Kim JS. Neurology 2008;70: 2386-2393.

Findings
91 % had motor findings due to SMA/paracentral lobule involvement, 43 had apathy/abulia, due to callosal/cingulum/frontal involvement esp. bilateral. 68 patients had local athero, 10 had cardiac emboli, 6 had ICA disease. Patients with intrinsic ACA athero were more likely to have abulia and callosal involvement than those with cardiac or carotid emboli.

Anatomy: Branches of ACA: in order, orbitofrontal artery, anterior, middle and posterior internal frontal arteries, callosal marginal artery, paracentral artery, and superior parietal artery (7 branches).

30 patients were incontinent. 18 had aphasia (transcortical mixed, global, or motor). 25 had grasp reflex especially women with callosal involvement. Sensory loss was variably tested and invariably found in paretic limbs. Other findings were alien limb, lability,agitation, apraxia, amnesia, Parkinsonian, and anosognosia. Some mechanisms reported were different in studies of Western subjects. Many have impaired articulation and a soft whispering voice.
About 2/3 had callosal involvement at various levels especially the genu. Only 6 patients had subcortical involvement incl CN and PUT. Whole ACA involvement occurred only in four patients.

Motor weakness occurred including hemiparesis in 70 (in 38 leg more than arm), leg monoparesis in 18, and paraparesis in 3 patients. In 29 arm was same as leg, and in 4 arm was worse than the leg. The shoulder was more involved than the distal arm/hand. Usually the SMA was involved.

Different paper: ACA infarct caused contralateral eyelid opening apraxia (Korn et al., Arch Neurol 2004; 61-273-275. It was an occluded carotid on right with right ACA infarct and left finding. Initially brachiofacial paresis occurred, but that cleared. Alteplase was used. Authors speculated the lesion in the forceps of the callosum caused a disconnection syndrome and left lid apraxia.

Notes occlusion of the stem of the ACA prior to ACOM are well tolerated as long as the stem does not supply both sides and adequate anastomosis exists. Occlusion is usually embolic. Huebner's branch to CN head comes off and cause transcortical motor aphasia.

Differential of leg predominant weakness due to stroke-- is due to ACA only 25 %. Others include corona radiata, capsule, anterior choroidal artery stroke, perforators, brainstem, or with thalamic hemorrhage. Small strokes in premotor area can cause especially if lateral .

Superficial ACA stroke can cause syndrome of crural paresis and homolateral arm predominant ataxia. A similar syndrome can occur in the pons.