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Isolated infarction in the territory of lateral posterior choroidal arteries
  1. NAOKATSU SAEKI,
  2. KATSUNORI SHIMAZAKI,
  3. AKIRA YAMAURA
  1. Department of Neurological Surgery Chiba University School of Medicine, 1–8–1 Inohana, Chuoh-ku, Chiba-shi, Chiba Japan 260–8670
  1. Naokatsu Saeki, MD, Department of Neurological Surgery, Chiba University School of Medicine, 1–8–1 Inohana, Chuoh-ku, Chiba-shi, Chiba, Japan 260–8670. Telephone 0081 43 226 2158; fax 0081 43 226 2159.

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Lateral posterior choroid arteries (LPCAs) originate from the distal PCA trunk in the proximity of the origin of thalamogeniculate arteries or the cortical branches.1 Infarction of LPCAs, therefore, often accompany lesions of other PCA cortical branches or perforating branches.2 3 Their clinical features have often been masked by the associated and combined cortical and subcortical lesions. Accordingly the clinical features of a discrete infarction of the LPCA have been reported only a few times.2-5 This paper reports on two such patients and pertinent articles are reviewed.

(A, B, C) Patient 1. CT taken 5 days after the onset. The low density lesion was seen at the posterior part of the right caudate nucleus and dorsolateral thalamus. (D) patient 1. MRI taken a month later. T1 weighted coronal image showed that the lesion was located at the posterior part of the caudate nucleus(arrow), the thalamus (arrows), the lateral geniculate body, and the part of medial temporal lobe (arrow head). (E, F) patient 2. CT taken 3 days after the onset. Low density lesions were seen at the posterolateral thalamus (arrow) and the posterior part of the caudate nucleus (arrows).  

The first patient, a 62 year old woman with a history of untreated supraventricular arrhythmia for 10 years had sudden onset of non-pulsatile headache on the vertex. At the same time she noted blurred vision in the left visual field for a few days. The headache continued for 5 days and she visited a nearby hospital. No visual field defect was noted on confrontation. Brain CT showed a low density lesion in the posterior thalamus. As the location of the lesion was unusual, the patient was referred to our institution 3 weeks later. On admission she was free of neurological deficits including higher cortical function. The visual acuity was 12/20 on the right and 10/20 on the left. Goldman’s perimetry did not disclose any visual field defect, either. The repeated CT showed a localised low density lesion at the posterolateral thalamus extending to the area of the lateral geniculate body inferolaterally and the posterior caudate nucleus superiorly (figure A, B, and C). No other remarkable lesions were noted. Laboratory study was normal but the ECG showed atrial fibrillation. Vertebral angiography showed no obstructive or stenotic change in the posterior cerebral arteries. LPCAs were demonstrated on both sides. Brain MRI demonstrated a lesion of abnormal intensity at the posterolateral thalamus, the posterior part of caudate nucleus, and the lateral geniculate body (figure D) She was medicated with 200 mg/day ticlopidine and remained free of stroke for the next 4 years.

The second patient, a 72 year old woman with an 8 year history of hypertension noted right sided homonymous type hemianopia for a few minutes on waking up in the morning. At the same time she felt transient bilateral hand dysaesthesia. She had no headache or dizzy sensation. When she arrived at the hospital 2 hours later, she was free of neurological deficits including visual field on confrontation. Three hours later CT showed no abnormality. Results from Goldman’s perimetery were normal. Three days later repeated CT showed a newly appearing low density lesion at the left posterior thalamus, the lateral geniculate body, and the tail of the caudate nucleus (figure E, F) The superconductive MRI with T1 and T2 weighted images a month later and the CT scan 2 months later showed no abnormality. Cerebral angiography was not carried out. She was medicated with 200 mg/day ticlopidine and 300 mg/day pentxifyline and has been well for the past 2 years.

We reported two cases of infarction at the posterolateral thalamus, the lateral geniculate body, and the posterior part of the caudate nucleus.

The territory supplied by the LPCA was defined after microanatomical studies on the vasculalisation of the thalamus and previously reported CT or MRI templates.1-3 6 This territory comprises the choroid plexus of the lateral ventricle, the pulvinar, the posterior part of the dorsolateral nucleus, the lateral geniculate body, and the posterior part of the caudate nucleus. In some studies the hippocampus and the mesial temporal lobe were included as well.1 5 6Based on those microsurgical and microangiographical studies, we determined that our patients had an isolated infarction in the territory of the LPCA.

Reports on patients with discrete LPCA infarction are few.2-5 The main symptom has been related to visual field defect. It is commonly quadrantanopia or hemianopia. Characteristic visual field defects of LPCA occlusion have been described as homonymous horizontal sectoranopia or wedge shaped homonymous hemianopia.4 5 These authors stated that, with and without evidence of CT, these unusual visual field defects were due to ischaemia at the lateral geniculate body, and dual blood supply from the LPCA of PCA and anterior choroid artery of the ICA may explain this unusual visual field defect. Neau and Bogousslavisky have also stated that, although it occurs infrequently, its is specific to the lesion atthe lateral geniculate body.5 The other signs were hemisensory disturbance, to a lesser extent neuropsychological dysfunctions such as aphasia, hemineglect, and memory disturbance, and more rarely hemiparesis.2-5

In our patients the symptoms were mild and transient. The first patient had blurred vision on the left side for 5 days and in the second patient, the visual field defect lasted for a few minutes, although CT or MRI disclosed the corresponding lesions of the LPCA occlusion.

The LPCAs mainly originate from the ambient segment of the PCA trunk or its cortical branches. The number of twigs averaged 4.0 (range 1–9).1 When two or more branches are present, anterior branches penetrate the choroid fissure to supply the choroid plexus of the inferior horn of the lateral ventricle. Posterior branches supply the choroid plexus in the trigone of the lateral ventricle and far anteriorly in the third ventricle. They also supply the pulvinar, medial, and lateral geniculate bodies, fornix, and midbrain tegmentum.1 6 Many anastomoses between the branches of the LPCA and anterior choroid artery are present at the anterior third of the temporal horn as are many connections between the LPCA and medial posterior choroid arteries at the level of the foramen of Monro.1

Infrequent occurrence of occlusion of the LPCA is speculated to be due to such multiple branches and rich anastomosis. The number of arteries and development of anastomosis vary. Such ample anatomical variation in the supplying territory of these arteries may explain the wide range of severity and duration of symptoms of both our patients and others reported. Our patients represent the milder form of the clinical features of infarction of the LPCA, which has not been highlighted. The LPCA occlusion may present only with such minor complaints. Because LPCA occlusion may be prodromal signs of more serious brain ischaemia,5 we need to know a wide range of the clinical symptoms related to occlusion of the LPCA.

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