METHODS: From August 2020 to December 2021, 4 rete MCA anomalies were identified at Shuang Ho hospital. Clinical information, perfusion magnetic resonance (MR) imaging, and angiographic images were collected. Detailed angioarchitecture, including types of arterial feeders and extent of rete involvement, were analyzed based on three-dimensional volume-rendering reconstruction images obtained from the catheter-based angiographies.
RESULTS: Despite their variable clinical presentations (two hemorrhage, one ischemia, and one asymptomatic), all cases shared common angiographic findings as follows: (1) the internal carotid artery did not connect directly to the rete, (2) the anterior choroidal artery (AChA) was the artery constantly supplying the rete and (3) there was a watershed zone shift toward MCA territory. The perfusion MR cerebral blood flow map was symmetric in all studied cases.
CONCLUSION: The AChA is an artery constantly supplying the rete, which suggests that the angioarchitectural features associated with this anomaly may be the result of both congenital and acquired compensatory processes. Cerebral perfusion remains preserved at the lesion side, despite angiographic evidence of watershed zone shift. These findings will be important for making better clinical judgments about this condition.
Case presentation: We report 2 cases of hypertension with secondary hyperaldosteronism associated with accessory renal arteries. Both patients presented with hypokalemia and further investigations revealed hyperaldosteronism with unsuppressed renin levels. Imaging studies showed the presence of accessory renal artery.
Conclusion: Accessory renal arteries are a potential cause renovascular hypertension which can be detected via CT angiography or magnetic resonance angiography. Hormonal evaluation should be undertaken to determine whether its presence contributes to hypertension in the patient as targeted treatment such as aldosterone antagonist can be initiated. Surgical intervention or renal denervation may be considered in resistant cases.
METHODS: From March 2010 until June 2015, 16 patients with HOCM underwent surgical correction of obstruction. The mean age was 51 years old (range, 32-72 years). All were symptomatic being New York Heart Association (NYHA) class 3 (n = 4) or 4 (n = 12). All had systolic anterior motion at echocardiogram with severe mitral regurgitation (MR). Intraventricular gradient preoperatively was 73.5 mmHg (range, 50-120 mmHg). All patients underwent a double-stage procedure: first septal resection through (i) the aortic valve and (ii) the detached anterior leaflet (AL) of the mitral valve and at second, mitral valve repair by (i) reducing PL height (leaflet resection or artificial neochordae) (ii) increasing AL height with pericardial patch.
RESULTS: There was no in-hospital or late death. All patients were Class 1 NYHA at latest follow-up. Control echocardiography showed no MR, mean rest intraventricular gradient was 15 mmHg (range, 9-18 mmHg).
CONCLUSIONS: Our good mid-term results support the concept that HOCM is not only a septal disease and that the mitral valve pathology is a key component that should be addressed. For most patients, the ideal surgical treatment should consist in a two-step procedure. It is even necessary to be studied whether treating the mitral valve alone could not suffice.
PURPOSE: The aim of this study was to report a case of OTR with contralateral internuclear ophthalmoplegia (INO) and fifth and seventh cranial nerve palsies.
CASE REPORT: A 51-year-old gentleman with underlying diabetes mellitus presented with sudden onset of diplopia for 3 days. On examination, his visual acuity was 20/30 bilaterally without a relative afferent pupillary defect. He had a right OTR consisting of a right head tilt, a skew deviation with a left eye hypertropia, and bilateral ocular torsion (right excyclotorsion and left incyclotorsion) with nystagmus. He also had a left adduction deficit and right abduction nystagmus consistent with a left INO. Ocular examination revealed evidence of proliferative diabetic retinopathy bilaterally. Two days after the initial presentation, the patient developed left seventh and fifth cranial nerve palsies. MRI showed left pontine infarction and multiple chronic lacunar infarctions. There was an incidental finding of a vascular loop compression on cisternal portions of the left trigeminal, facial, and vestibulocochlear nerves. Antiplatelet treatment was started on top of a better diabetic control. The diplopia was gradually resolved with improved clinical signs. In this case, the left pontine infarction had likely affected the terminal decussated part of the vestibulocochlear nerve from the right VOR pathway, medial longitudinal fasciculus, and cranial nerve nuclei in the left pons.
CONCLUSIONS: The OTR can be ipsilateral to the lesion if the lesion is before the decussation of the VOR pathway in the pons, or it can be contralateral to the lesion if the lesion is after the decussation. In case of an OTR that is associated with contralateral INO and other contralateral cranial nerves palsy, a pathology in the pons that is contralateral to the OTR should be considered. Neuroimaging study can hence be targeted to identify the possible cause.