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Crossed cheiro-oral syndrome (CCOS) is characterized by crossed sensory disturbance confined to the unilateral perioral area and contralateral hand/finger(s). Although a few classical crossed sensory syndromes accurately predict brainstem or spinal involvement, the clinical significance of CCOS remains unclear. In this study, we analyzed the etiology, localization and outcome of CCOS patients. The results showed that ischemic stroke is the exclusive cause of CCOS. The location of responsible stroke is pertinent to the middle or upper level of the lateral medulla oblongata medial to the lateral sulcus. The vascular supply is from the vertebral artery or the posterior inferior cerebellar artery. Half of the CCOS patients progressed to Wallenberg's syndrome and complicated with disabled daily living. However, no patient died during the follow-up period. A larger size and dorsal extension of the infarction correlated with neurological deterioration. Therefore, CCOS is an independent clinical sign of medullary involvement. It strongly predicts involvement at the lateral medulla oblongata, especially the ischemic stroke, and neurological deterioration. A rapid evaluation of the infarction location and vascular status is suggested in cases of CCOS., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Cheiro-pedal syndrome (CPS) is an incomplete pure sensory disorder confined strictly to simultaneous hand/finger and ipsilateral foot/toe symptoms. However, its clinical significance and pathogenesis are unclear. We present nine patients with typical CPS, and review another seven previously reported patients. Ischemic stroke is the leading cause of CPS in these 16 patients. In 13 patients, the lesions responsible were distributed widely in the brain from the corona radiata to the medulla oblongata whereas in three patients the lesions were found in the cervical spinal cord or peripheral nerves. All patients had a favorable outcome. The close proximity of the cheiral and pedal sensory fibers in the pons, thalamus, internal capsule and the caudal thalamocortical projection increases the vulnerability for CPS. Therefore, the underlying cause of CPS should be investigated rapidly despite it causing only minor symptoms. The pathogenesis of CPS may consist of several interacting factors including preconditioned neuronal damage and proximity of the acral sensory fibers., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Pure motor hemiparesis is a vascular syndrome that is occasionally mimicked by central or spinal pathologies. However, metabolic neuromuscular disorders have not been reported to mimic this condition. We present a 52-year-old male patient with hypokalemic paralysis who presented with the early symptoms of acute-onset pure motor hemiparesis. Neurological examinations revealed right-sided weakness without bulbar, extraocular, or respiratory involvement. Ischemic stroke was initially diagnosed on the basis of the acute-onset unilateral motor deficit and the patient's history of hypertension, stroke, and previous cerebral infarctions. The right hemiparesis and weakness of the left limbs worsened on the day after admission. The patient's weakness rapidly reversed after correction of hypokalemia, and a diagnosis of hypokalemic paralysis was finally established. This unusual hemineurological presentation should alert medical personnel to the possibility of reversible metabolic neuromuscular disorders, thereby avoiding delayed diagnosis., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

We encountered three patients with hypokalemic paralysis following a convulsion in the early stages of alcohol abstinence. The transtubular potassium gradient was less than 2.0, suggesting intracellular potassium shift. Hypokalaemic paralysis may result from retention of intracellular cationic potassium bound by anionic phosphorylated compounds, precipitated by an acceleration of the (Na+)-(K+) pump in alcohol withdrawal and convulsions. These findings warn of the lethal hypokalemia that may occur after convulsions, particularly soon after alcohol abstinence associated with moderate withdrawal symptoms.

Chondrosarcoma is a malignant disease of cartilage. Systemic embolisation usually arises from cancerous invasion of pulmonary vessels or the left atrium but cerebral embolisation or ischaemia is rarely recognised. We report a man with left leg amputation for tibial myxoid chondrosarcoma who suffered multiple cerebral embolisms one year later. Cerebral angiography and aortogram did not reveal luminal stenosis and a cardiac survey was normal. Lupus anticoagulant (LAC) and a prolonged activated partial thromboplastin time were detected. A molecular mimicry between prothrombin and paracrine hormones may have accounted for his LAC. A procoagulant autoantibody reacting against metastatic cancer cells may contribute to cancerous thrombosis, such as in chondrosarcoma.

There are many reports in the literature concerning nocturnal bruxism, however, diurnal (non-sleep)/nocturnal bruxism is rarely mentioned. We report three patients with diurnal/nocturnal bruxism. They differed from the usual features of nocturnal bruxism in hypoperfusion of the left frontal lobe, a poor response to l-dopa or bromocriptine therapy and a favourable response to metoclopramide. Hypersensitive presynaptic dopamine receptors may be the underlying pathology responsible for this type of bruxism. Regional differences in dopamine receptor pharmacology may explain the perplexing relationship of bruxism to both hyper- and hypo-dopaminergic states.