Appropriate management of asymptomatic carotid stenosis.

With modern intensive medical therapy, the annual risk of ipsilateral stroke in patients with asymptomatic carotid stenosis (ACS) is now down to ∼0.5%. Despite this, there is a widespread practice of routine intervention in ACS with carotid endarterectomy (CEA) and stenting (CAS). This is being justified on the basis of much higher risks with medical therapy in trials conducted decades ago, compared with lower risks of intervention in recent trials with no medical arm. Such extrapolations are invalid. Although recent trials have shown that after subtracting periprocedural risks the outcomes with CEA and CAS are now comparable to medical therapy, the periprocedural risks still far outweigh the risks with medical therapy. In the asymptomatic carotid trial (ACT) 1 trial, the 30-day risk of stroke or death was 2.9% with CAS and 1.7% with CEA. In the CREST trial, the 30-day risk of stroke or death among asymptomatic patients was 2.5% for stenting and 1.4% for endarterectomy. Thus, intensive medical therapy is much safer than either CAS or CEA. The only patients with ACS who should receive intervention are those who can be identified as being at high risk. The best validated method is transcranial Doppler embolus detection. Other approaches in development for identifying vulnerable plaques include intraplaque haemorrhage on MRI, ulceration and plaque lucency on ultrasound, and plaque inflammation on positron emission tomography/CT. Intensive medical therapy for ACS includes smoking cessation, a Mediterranean diet, effective blood pressure control, antiplatelet therapy, intensive lipid-lowering therapy and treatment with B vitamins (with methylcobalamin instead of cyanocobalamin), particularly in patients with metabolic B12 deficiency. A new strategy called 'treating arteries instead of risk factors', based on measurement of carotid plaque volume, is promising but requires validation in randomised trials.

[Neurophysiologic studies of POEMS syndrome and its related diseases].

OBJECTIVE: To explore the electrophysiological characteristics of polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes (POEMS) syndrome and its related diseases. METHODS: The electrophysiological characteristics were analyzed retrospectively from June 2000 to June 2013 in patients with POEMS syndrome, monoclonal gammopathy of undetermined significance (MGUS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Electromyography and nerve conduction examinations of median, ulnar, tibial, peroneal and sural nerves were performed. RESULTS: In patients with POEMS syndrome, the amplitude of compound muscle action potential (CMAP) of tibial and peroneal nerves was lower than that of median and ulnar nerves ((1.02 ± 0.23) vs (2.12 ± 0.30) mV, (P < 0.05) ); compared with patients with CIDP, the amplitude of CMAP for POEMS patients was lower ((2.12 ± 0.30) vs (3.94 ± 0.52) mV, (1.02 ± 0.23) vs (3.65 ± 0.57) mV) (P < 0.05) while terminal latency indices (TLI) was higher ((0.41 ± 0.13) vs (0.22 ± 0.01), (0.45 ± 0.16) vs (0.24 ± 0.13) ) (P < 0.05) and the occurring rate of conduction block (CB) and temporal dispersion (TD) was lower (P < 0.05). Compared with MGUS patients, the amplitude of CMAP for POEMS patients was lower ((2.12 ± 0.30) vs (3.81 ± 0.83) mV, (1.02 ± 0.23) vs (3.82 ± 0.63) mV) (P < 0.05) ; sensory conduction velocity of POEMS patients was faster ((33 ± 5) vs (20 ± 3) m/s, (28 ± 4) vs (18 ± 3) m/s)(P < 0.05)). CONCLUSION: Nerve conduction studies of POEMS syndrome implicate both axonal loss and demyelination.Uniform demyelination is more predominant in nerve trunk rather than distal nerve terminals. CB and TD occur less frequently and axonal loss is length-dependent.

[Radiological imaging in evaluation of etiologies for cerebral infarction after non-cardiac surgeries].

OBJECTIVE: To investigate the pathogenesis of cerebral infarction after non-cardiac surgeries according to imaging. METHODS: Retrospective analyses of clinical and imaging data of 17 patients with postoperative cerebral infarction (average 68 years old, total incidence 0.049%) from departments of orthopedics and general surgery were conducted during 52 months. RESULTS: Cerebral infarction occurred 39.1 hours after operation on average. Among the 17 patients, eight were detected with disturbance of consciousness, ten with hemiplegia, six with speech disorder and two with unilateral sensory disturbance. Six (35.3%) had blood lipids tests. Five (29.4%) had neck vascular ultrasound and one had intracranial magnetic resonance angiography (MRA). When discharged, one patient was declared death and ten had impaired neurological function in various degrees. Among six patients with previous stroke, one (16.7%) received neurological consultation before surgery. According to the image manifestation, ten cases were territory circulation infarcts, four centrum ovale infarcts and three watershed infarcts. CONCLUSIONS: This study suggests that total incidence of cerebral infarction after non-cardiac surgeries is lower than previously reported and there is greater involvement of atherosclerosis. Patients' conditions should be closely observed within at least four days after surgeries. Preoperative assessment should be strengthened in order to avoid occurrence of postoperative cerebral infarction.

[Hyperdense middle cerebral artery sign among patients with severe ischemic attack on ultra-early phase].

OBJECTIVE: To detect the frequency of hyperdense middle cerebral artery sign (HMCAS) among patients with severe ischemic attack (baseline NIHSS score ≥ 10) in the middle cerebral artery (MCA) territory within 3 hours after onset and compare the baseline characteristics and 90-day outcomes between the HMCAS (+) and HMCAS (-) groups. METHODS: A total of 43 patients were evaluated with baseline clinical characteristics, laboratory tests and brain CT/MRI. Follow-up evaluation at the end of 90 days included the modified Rankin Scale (mRS), the Bathel Index (BI) and death. RESULTS: Ten out of forty-three (23.3%) patients were HMCAS (+).The 24-hour NIHSSS of HMCAS (+) group was significantly higher than that of HMCAS (-) group (20.2 ± 5.4 vs. 14.8 ± 7.2, P= 0.037). The follow-up scanning confirmed that all HMCAS (+) patients had larger MCA territory infarction and the ratio of large MCA territory infarction was significantly higher than that of HMCAS (-) group (100% vs. 39.1%, P = 0.001). There were no significant differences in age, gender, risk factors, time intervals, laboratory tests, 90-day functional outcomes between the two groups. CONCLUSION: The HMCAS (+) patients had notable deterioration 24 hours after onset and had more severe MCA infarction. HMCAS detected by non-enhanced CT at admission should be considered as an alarming sign among patients with severe neurological deficit of MCA territory infarction.

Preliminary investigation of effect of granulocyte colony stimulating factor on amyotrophic lateral sclerosis.

We investigated the safety and efficacy of the granulocyte colony stimulating factor (G-CSF) in 13 patients with amyotrophic lateral sclerosis (ALS). Five-day administration of 2 microg/kg once a day was followed by a six-month observation period. The primary and secondary endpoints were the changes of ALS functional rating scale (ALSFRS) and the compound muscle action potential (CMAP) amplitude, respectively. We found that the declines of ALSFRS and CMAP amplitude after G-CSF administration were significantly less than those measured prior to the treatment. The results suggest G-CSF is safe in ALS patients, and may affect the rate of motor decline.

[Comparison of multiple point stimulation and incremental stimulation in patients with amyotrophic lateral sclerosis].

OBJECTIVE: To compare two common techniques for motor unit number estimation (MUNE), multiple point stimulation and incremental stimulation to determine which is preferable in patients with amyotrophic lateral sclerosis (ALS). METHODS: Surface recorded motor unit action potentials of median nerve or thenar muscle were measured in 60 ALS patients and 60 controls. The maximal baseline to negative peak compound muscle action potential (CMAP) amplitude was recorded. For multiple point stimulation, the stimuli sites included the skin of wrist, 6 cm above the wrist, elbow and 6 cm above the elbow. Individual motor unit responses were obtained by moving the stimulating electrode and isolating threshold responses with distinct morphologies. Then, with finely graded stimulus intensity at one point, 3 steps in a CMAP were investigated. 10 - 12 different single motor unit action potentials (SMUPs) were recorded. For incremental stimulation, stimulus intensity was slowly increased from subthreshold levels until a small all-or-none response was evoked. The intensity was slowly increased until the response increased in a quantal fashion. This process was repeated for a total of 10 increments. Individual motor unit amplitudes were obtained by subtracting amplitudes of each response from that of prior response. Both techniques were performed twice, electrodes changed and results averaged. RESULTS: For controls, MUNE was 228 +/- 30 for multiple point stimulation and 198 +/- 26 for incremental stimulation. Test-retest correlation coefficients and coefficients of variation for mean of two MUNE were 0.88 - 0.91 and 13.20% - 15.24% for multiple point stimulation, 0.86 and 13.30% - 15.65% for incremental stimulation. For ALS patients, MUNE was 64 +/- 6 and 59 +/- 7 respectively. CONCLUSION: Both MUNE methods are similarly reproducible and are equally effective at documenting progression of a lower motor neuron disorder in ALS patients.

VEGF C2578A polymorphism does not contribute to amyotrophic lateral sclerosis susceptibility in sporadic Chinese patients.

A linkage and association of the VEGF (vascular endothelial growth factor) C2578A polymorphism and amyotrophic lateral sclerosis (ALS) has been found in some studies. We analysed the C2578A polymorphism in sporadic ALS patients from a Chinese population. The polymorphism was analysed in 115 patients and 200 healthy individuals by amplifying across position 2705 to 2494 of the promoter region of the VEGF gene. It was found that the frequency of the allele A was 24% in ALS patients and 28% in healthy individuals (p = 0.264). Comparing the background of this polymorphism in healthy individuals between Chinese and Caucasians, significant decreases were found in the frequencies of the A/A genotype and allele A (p(s)<0.001). We concluded that VEGF C2578A polymorphism did not confer a susceptibility to sporadic Chinese ALS patients, which was in disagreement with that reported previously in Caucasian populations and might be ascribed to the different genetic background between Chinese and Caucasians.