Assessment of dysarthria with Frenchay dysarthria assessment (FDA-2) in patients with Duchenne muscular dystrophy.

PURPOSE: The purpose of this study was to test the psychometric properties of the Japanese version of Frenchay Dysarthria Assessment (FDA-2) and to use this tool to describe the features of speech in patients with Duchenne muscular dystrophy (DMD). MATERIALS AND METHODS: The Japanese version of FDA-2 was culturally adapted, and reliability and validity were examined in 22 and 50 patients, respectively. The Japanese version of FDA-2 was administered to 51 patients with DMD. Multiple regression analysis was performed to identify factors related to FDA-2 scores. RESULTS: Inter-/intra-rater reliabilities (ICCs) and internal consistency (Cronbach's α) for total scores were 0.76, 0.97, and 0.94 respectively. For construct validity, two-way ANOVA showed a significant interaction between the disorders and FDA-2 sections (p < 0.05). In DMD patients, the item of tongue at rest was most severely affected, reflecting tongue hypertrophy. Multiple regression analysis identified age, swallowing status, and ventilator use as significantly related. CONCLUSIONS: The results showed that the Japanese version of FDA-2 has satisfactory reliability and validity. The present study demonstrated the features of dysarthria and related factors in patients with DMD.Implications for rehabilitationIn Duchenne muscular dystrophy (DMD), an absent or defective dystrophin protein causes progressive weakness of respiratory and oropharyngeal muscles, both of which are crucial contributors to speech production.This study shows that the Japanese version of FDA-2 has satisfactory reliability and validity compared to original version.The Japanese version of FDA-2 characterizes dysarthria in patients with DMD in this cohort.

Secondary Chiari malformation due to enlarged spinal arachnoid villi-like structure: illustrative case.

BACKGROUND: Secondary Chiari malformation can be caused by various disorders associated with cerebrospinal fluid (CSF) leakage at the spinal level. In this report, the authors describe a rare case of secondary Chiari malformation caused by excessive CSF absorption through the enlarged spinal arachnoid villi-like structure. OBSERVATIONS: A 20-year-old woman presented with progressive severe headache and posterior neck pain. Magnetic resonance imaging showed tonsillar herniation and decreased subarachnoid space around the spinal cord. A hypointense signal area was observed in the ventral spinal canal on a T2-weighted image. An axial image revealed multiple small, arachnoid cyst-like structures at the right T1 nerve root sleeve. Direct surgery revealed that the cyst-like structures were continuous with the arachnoid membrane and protruded into the abnormally large epidural venous sinus. The cyst-like structures were resected, and the dural sleeve was repaired using fascia. The patient showed good improvement of symptoms after surgery. LESSONS: Excessive CSF absorption through the enlarged spinal arachnoid villi-like structure can cause secondary Chiari malformation. Neurosurgeons should be aware of this unusual mechanism of CSF leakage. Simple posterior fossa decompression will be ineffective or even harmful.

Pathophysiology and surgical treatment of spinal adhesive arachnoid pathology: patient series.

BACKGROUND: Spinal adhesive arachnoid pathology is a rare cause of myelopathy. Because of rarity and variability, mechanisms of myelopathy are unknown. The authors retrospectively analyzed patients to understand pathophysiology and provide implications for surgical treatment. OBSERVATIONS: Nineteen consecutive patients were studied. Thirteen patients had a secondary pathology due to etiological disorders such as spinal surgery or hemorrhagic events. They received arachnoid lysis (4 patients), syringo-subarachnoid (S-S) shunt (8 patients) with or without lysis, or anterior decompression. Three of them developed motor deterioration after lysis, and 6 patients needed further 8 surgeries. Another 6 patients had idiopathic pathology showing dorsal arachnoid cyst formation at the thoracic level that was surgically resected. With mean follow-up of 44.3 months, only 4 patients with the secondary pathology showed improved neurological grade, whereas all patients with idiopathic pathology showed improvement. LESSONS: The idiopathic pathology was the localized dorsal arachnoid adhesion that responded to surgical treatment. The secondary pathology produced disturbed venous circulation of the spinal cord by extensive adhesions. Lysis of the thickened fibrous membrane with preservation of thin arachnoid over the spinal veins may provide safe decompression. S-S shunt was effective if the syrinx extended to the level of normal subarachnoid space.

Intradural lumbar radicular arteriovenous malformation mimicking perimedullary arteriovenous malformation of the conus medullaris: illustrative case.

BACKGROUND: Intradural radicular arteriovenous malformation (AVM) of the cauda equina is a rare entity of spinal AVMs. Because of the specific arterial supply of the conus medullaris and cauda equina, AVMs in this area sometimes present with confusing radiological features. OBSERVATIONS: The authors reported a rare case of intradural radicular AVM arising from the lumbar posterior root. The patient presented with urinary symptoms with multiple flow void around the conus medullaris, as shown on magnetic resonance imaging. Digital subtraction angiography demonstrated arteriovenous shunt at the left side of the conus medullaris fed by the anterior spinal artery via anastomotic channel to the posterior spinal artery and rich perimedullary drainers. There was another arteriovenous shunt at the L3 level from the left L4 radicular artery. Preoperative diagnosis was perimedullary AVM with radicular arteriovenous fistula. Direct surgery with indocyanine green angiography revealed that the actual arteriovenous shunt was located at the left L4 posterior root. The AVM was successfully treated by coagulation of feeding branches. LESSONS: Unilateral arteriovenous shunt fed by either posterior or anterior spinal artery at the conus medullaris may include AVM of the cauda equina despite abundant perimedullary venous drainage. Careful pre- and intraoperative diagnostic imaging is necessary for appropriate treatment.

[Treatment Results of Low Back and Leg Pain Considering Para-Lumbar Spine Disease and Peripheral Nerve Neuropathy].

INTRODUCTION: Here we report our treatment results of low back and leg pain(LBLP)considering para-lumbar spine disease(PLSD)and peripheral nerve neuropathy(PNN). MATERIALS AND METHODS: We enrolled 103 patients who were admitted to our institute for LBLP treatment between January and December in 2014. For the treatment, we preferentially performed intensive block therapy for PLSD. RESULT: Among 103 patients, 89 patients had PLSD. In 85 patients, we performed intensive block therapy and 82 patients experienced short-term improvement of symptoms. In 35 of these 82 patients, lumbar spine and/or PNN surgical treatment was required as the effect of block therapy was transient. Intensive block therapy was effective in 47 of 103 patients(45.6%), and the remaining patients required surgical treatment(PLSD and/or PNN:31 cases, lumbar spine:13 cases, both:8 cases). CONCLUSION: Among 103 patients with LBLP, intensive block therapy for PLSD and PNN was useful for short-term symptom improvement in 82 patients(79.6%), and for long-term symptom improvement in 47 patients(45.6%)as evaluated at the final follow-up. Surgical treatment of PLSD and/or PNN was required in 39 patients(37.9%). These results suggested that treatment of PLSD and PNN might yield good results for patients with LBLP.

Low back pain due to superior cluneal nerve entrapment: A clinicopathologic study.

INTRODUCTION: We studied the clinical and nerve pathologic features in 6 patients whose low back pain (LBP) was relieved by superior cluneal nerve (SCN) neurectomy to determine whether nerve compression was the mechanism underlying this type of LBP. METHODS: All 6 patients (7 nerves) underwent SCN neurectomy for intractable LBP. Their clinical outcomes and the pathologic features of 7 nerves were reviewed. RESULTS: All patients reported LBP relief immediately after SCN neurectomy. Pathologic study of the 7 resected nerves showed marked enlargement, decreased myelinated fiber density, an increase in thinly myelinated fibers (n = 2), perineurial thickening (n = 5), subperineurial edema (n = 4), and Renaut bodies (n = 4). At the distal end of 1 enlarged nerve, we observed a moderate reduction in the density and marked reduction in the number of large myelinated fibers. DISCUSSION: The pathologic findings and effectiveness of neurectomy suggest that, in our patients, SCN neuropathy likely elicited LBP via nerve compression. Muscle Nerve 57: 777-783, 2018.

A Diagnostic Scoring System for Sacroiliac Joint Pain Originating from the Posterior Ligament.

Objective: Sacroiliac joint (SIJ) pain originating from the posterior ligament manifests in not only the buttocks but also the groin and lower extremities and thus may be difficult to discern from pain secondary to other lumbar disorders. We aimed to develop a simple clinical diagnostic tool to help physicians distinguish between patients with SIJ pain originating from the posterior ligament and those with lumbar disc herniation (LDH) or lumbar spinal canal stenosis (LSS). Design: Prospective case-control study. Patients and Methods: We evaluated 62 patients with SIJ pain originating from the posterior ligament and 59 patients with LDH and LSS. Pain areas, pain increasing positions, provocation test, and tenderness points were investigated. A scoring system based on multivariate logistic regression equations using the investigated items was developed. Results: Two pain areas (the posterosuperior iliac spine (PSIS) detected by the one-finger test and groin), pain while sitting on a chair, provocation test, and two tenderness points (PSIS and the sacrotuberous ligament) had high odds ratios (range, 25.87­1.40) and were used as factors in the scoring system. An integer score derived from the regression coefficient and clinical experience was assigned to each identified risk factor. The sum of the risk score for each patient ranged from 0­9. This scoring system had a sensitivity of 90.3% and a specificity of 86.4% for a positivity cutoff point of 4. Conclusion: The scoring system can help distinguish between patients with SIJ pain originating from the posterior ligament and those with LDH and LSS.

Treatment of low back pain elicited by superior cluneal nerve entrapment neuropathy after lumbar fusion surgery.

OBJECT: Low back pain (LBP) attributable to fusion failure, implant failure, infection, malalignment, or adjacent segment disease may persist after lumbar fusion surgery (LFS). Superior cluneal nerve (SCN) entrapment neuropathy (SCNEN) is a clinical entity that can produce LBP. We report that SCNEN treatment improved LBP in patients who had undergone LFS. METHODS: Between April 2012 and August 2015, we treated 8 patients (4 men and 4 women ranging in age from 38 to 88 years; mean age, 69 years) with SCNEN for their LBP after LFS. Our criteria for the diagnosis of SCNEN included a trigger point over the posterior iliac crest 7 cm from the midline and numbness and radiating pain in the SCN area upon compression of the trigger point. Symptom relief was obtained in more than 75% of patients within 2 h of inducing a local nerve block at the trigger point in the buttocks. The mean postoperative follow-up period was 28 months (range, 9-54 months). RESULTS: LBP was unilateral in 3 and bilateral in 5 patients. The senior author (T.I.) operated all patients for SCNEN under local anesthesia because they reported recurrence of pain after the analgesic effect of repeat injections wore off. This led to a significant improvement of their LBP. CONCLUSIONS: SCNEN should be considered in patients reporting LBP after LFS. Treatment of SCNEN may be a useful option in patients with failed back surgery syndrome after LFS.

Long-term Outcome of Surgical Treatment for Superior Cluneal Nerve Entrapment Neuropathy.

STUDY DESIGN: Prospective observational cohort study. OBJECTIVE: The objective of this study was to present the long-term surgical outcomes of operative treatment for superior cluneal nerve (SCN) entrapment neuropathy (SCNEN) and to analyze the causes of poor results and further treatment required. SUMMARY OF BACKGROUND DATA: There are a few reports of the outcomes of surgical treatment for SCNEN, and most studies describe results for operations conducted under general anesthesia with short follow-up periods. METHODS: Surgery was performed for SCNEN in 52 consecutive patients on 79 sides, excluding patients who had undergone previous surgery on the lumbar spine. Entrapment was unilateral in 25 patients and bilateral in 27. The mean postoperative follow-up period was 41.3 months (range, 29-58 months). All patients had received conservative treatment without improvements, and operations were performed under local anesthesia. RESULTS: Twenty-three cases (44%) involved only low-back pain (LBP), and 31 cases (60%) involved LBP associated with leg numbness or pain. The mean number of SCN branches decompressed in the operative field at the first operation was 1.4 (range, 1-4 branches). There were no local or systemic complications during or after the operation. All patients reported symptom improvement, but LBP caused by SCNEN recurrence was reported for 10 sides (13%) in seven patients who subsequently underwent repeat surgery. In the second surgery, the number of additionally treated SCN branches was 2.0 (range, 1-5). Additional surgeries were performed in two cases for lumbar disorders. All patients showed significant improvement at the last follow-up visit (P < 0.05), including those who developed recurrence. CONCLUSION: Long-term outcomes of surgical treatment for SCNEN were satisfactory. For prevention of recurrence, as many SCN branches as possible should be decompressed in the operation field during the first operation. LEVEL OF EVIDENCE: 4.

The Relationship between Carotid Stump Pressure and Changes in Motor-Evoked Potentials in Carotid Endarterectomy Patients.

Background The threshold of ischemic tolerance has not been completely identified in human clinical studies. Distal carotid artery pressure can be easily measured through the internal shunt tube during carotid endarterectomy (CEA). To confirm the critical threshold of intracranial arterial pressure and its maximum duration, we investigated the distal internal carotid artery (ICA) pressure and motor-evoked potential (MEP) changes during ICA clamping. Material and Methods Between September 2012 and March 2014, 9 patients (10 sides) with carotid stenosis (70-99%) were surgically treated at our hospital. All CEAs were performed under general anesthesia, and we routinely used a carotid shunt with the intraoperative MEP monitors. When the MEP amplitude decreased to < 50% of the control during carotid clamping, the MEP amplitude was defined as significantly reduced. Results The MEP amplitude significantly decreased in 2 of the 10 procedures (20%) during ICA clamping. The mean distal ICA pressure varied widely, ranging from 13 to 48 mm Hg. In seven cases with a mean distal ICA pressure > 20 mm Hg, there were no significant changes in the MEP during ICA clamping. However, there were three cases with a mean distal ICA pressure < 20 mm Hg, and the MEP amplitude significantly decreased in two of those three patients from 4 to 5 minutes after clamping. Conclusions The present study provides considerable information about a higher incidence of MEP amplitude deterioration in CEA patients with a mean distal ICA pressure < 20 mm Hg during ICA clamping.

Decompression of the gluteus medius muscle as a new treatment for buttock pain: technical note.

PURPOSE: The clinical features and etiology of low back pain and buttock pain remain poorly understood. We report ten patients with buttock pain who underwent gluteus medius muscle (GMeM) decompression under local anesthesia. METHODS: Between December 2012 and November 2013 we surgically treated ten patients (four men, six women; mean age 65.1 years) for buttock pain. The affected side was unilateral in seven and bilateral in three patients (total sites, n = 13). The interval from symptom onset to treatment averaged 174 months; the mean postoperative follow-up period was 24 months. Decompression of the tight gluteal aponeurosis over the GMeM was performed under local anesthesia. Assessment of the clinical outcomes was on the numeric rating scale (NRS) for low back pain (LBP), the Japanese Orthopedic Association (JOA) score, and the Roland-Morris Disability Questionnaire (RDQ) score before and at the latest follow-up after treatment. RESULTS: There were no intraoperative surgery-related complications. The buttock pain of all patients was improved after surgery; their NRS decreased from 7.0 to 0.8 and JOA and RMDQ scores indicated significant improvement (p < 0.05). CONCLUSION: In patients with buttock pain, pain around the GMeM should be considered as a causative factor. Less invasive surgery with cutting and opening of the tight gluteal aponeurosis over the GMeM under local anesthesia yielded excellent clinical outcomes.

Repetitive Plantar Flexion Test as an Adjunct Tool for the Diagnosis of Common Peroneal Nerve Entrapment Neuropathy.

OBJECTIVE: The diagnosis of common peroneal nerve entrapment neuropathy (CPNEN) is based on clinical symptoms and nerve conduction studies. However, nerve conduction studies may not detect abnormalities. Under the hypothesis that repetitive plantar flexion that loads the peroneal nerve (PN) at the entrapment point without lumbar loading would be a useful CPNEN provocation test, we evaluated the repetitive plantar flexion (RPF) test as an adjunct diagnostic tool for CPNEN. The study design was a retrospective analysis of prospectively collected data. METHODS: Our study population consisted of 18 consecutive patients whose ipsilateral CPNEN improved significantly after PN neurolysis. Using repetitive ankle plantar flexion as a CPNEN provocation test, results were recorded as positive when it elicited numbness and/or pain in the affected area of the PN. RESULTS: The RPF test induced symptoms on all affected sides in the course of 57.4 seconds (range, 14-120 seconds). In 3 patients it induced numbness in the affected area of the PN in the normal leg. Receiver operating characteristic analysis showed that the diagnostic sensitivity and accuracy of the test were 94.4% each. The suggested cutoff point was 110 seconds and the area under the receiver operating characteristic curve was 0.97 (95% confidence interval 0.93-1.02). The positive and the negative predictive values were 89.5% and 94.1%, respectively. CONCLUSIONS: Our simple RPF test elicited the symptoms of CPNEN and our provocation test helped to identify dynamic PN entrapment neuropathy as the origin of intermittent claudication.

Association between intermittent low-back pain and superior cluneal nerve entrapment neuropathy.

OBJECT Superior cluneal nerve (SCN) entrapment neuropathy (SCNEN) is a cause of low-back pain (LBP) that can be misdiagnosed as a lumbar spine disorder. The clinical features and etiology of LBP remain poorly understood. In this study, 5 patients with intermittent LBP due to SCNEN who had previously received conservative treatment underwent surgery. The findings are reported and the etiology of LBP is discussed to determine whether it is attributable to SCNEN. METHODS Intermittent LBP is defined as a clinical condition in which pain is induced by standing or walking but is absent at rest. Between April 2012 and March 2013, 5 patients in this study who had intermittent LBP due to SCNEN underwent surgery. The patients included 3 men and 2 women, with a mean age of 66 years. The affected side was unilateral in 2 patients and bilateral in 3 (total sites, 8). The interval from symptom onset to treatment averaged 51.4 months; the mean postoperative follow-up period was 17.6 months. The clinical outcomes were assessed using the numerical rating scale (NRS) for LBP, the Japanese Orthopaedic Association (JOA) scale, and the Roland-Morris Disability Questionnaire (RDQ) preoperatively and at the last follow-up; these data were analyzed statistically. RESULTS None of the 5 patients reported LBP at rest. Intermittent LBP involving the iliac crest and buttocks was induced by standing or walking an average of 136 m. In 2 patients with unilateral involvement, LBP was improved only by SCN block. Surgeries were performed on 6 sites in 5 patients because the SCN block was only transiently effective. Patients' SCNs penetrated the orifice of the thoracolumbar fascia. SCN kinking at the orifice was exacerbated at the lumbar-extension provocation posture, and radiating pain increased upon manual intraoperative compression of the SCN in this posture. After releasing the SCN surgically, disappearance of the pain was intraoperatively confirmed by manual compression of the SCN with the patients in the lumbar-extension posture. Surgery was effective in all 5 patients, and all clinical outcome scores indicated significant improvement (p < 0.05). CONCLUSIONS To the authors' knowledge, this is the first report of patients with intermittent LBP due to SCNEN. Clinical and surgical evidence presented suggests that their LBP was exacerbated by lumbar extension and that symptom relief was obtained by SCN block or surgical release of the SCN entrapment. These results suggest that SCNEN should be considered as a causal factor in patients for whom walking elicits LBP.

Treatment of low back pain in patients with vertebral compression fractures and superior cluneal nerve entrapment neuropathies.

BACKGROUND: Superior cluneal nerve entrapment neuropathy (SCN-EN) may contribute to low back pain (LBP). However, it is often misdiagnosed as lumbar spine disorder and poorly understood. METHODS: Between April 2012 and September 2013, we treated 27 patients (3 men, 24 women; mean age 75.0 years) with LBP due to SCN-EN elicited by vertebral compression fractures. Symptoms were unilateral in 4 patients and bilateral in 23 patients. The interval between symptom onset and treatment averaged 10.8 months; the mean postoperative follow-up period was 19.0 months. The clinical outcomes were assessed utilizing the numeric rating scale (NRS) for LBP, the Japanese Orthopedic Association (JOA) score, and the Roland-Morris Disability Questionnaire (RDQ) before and after treatment (e.g., until the latest follow-up). RESULTS: LBP in 17 patients was immediately improved by SCN block only. The remaining 10 patients required surgery (involving 18 sites) as SCN blocks were only transiently effective. Operative intervention resulted in the immediate and continued improvement of their LBP. Notably, their NRS decreased from 7.4 to 1.5, their RDQ scores from 19.6 to 7.0, and their JOA scores increased from 10.7 to 20.3. CONCLUSIONS: In this series, 27 patients with LBP due to SCN-EN responded either to SCN blocks (17 patients) or surgical release of SCN entrapment (10 patients at 18 sites).

Microsurgical Decompression for Peroneal Nerve Entrapment Neuropathy.

Peroneal nerve entrapment neuropathy (PNEN) is one cause of numbness and pain in the lateral lower thigh and instep, and of motor weakness of the extensors of the toes and ankle. We report a less invasive surgical procedure performed under local anesthesia to treat PNEN and our preliminary outcomes. We treated 22 patients (33 legs), 7 men and 15 women, whose average age was 66 years. The mean postoperative follow-up period was 40 months. All patients complained of pain or paresthesia of the lateral aspect of affected lower thigh and instep; all manifested a Tinel-like sign at the entrapment point. As all had undergone unsuccessful conservative treatment, we performed microsurgical decompression under local anesthesia. Of 19 patients who had undergone lumbar spinal surgery (LSS), 9 suffered residual symptoms attributable to PNEN. While complete symptom abatement was obtained in the other 10 they later developed PNEN-induced new symptoms. Motor weakness of the extensors of the toes and ankle [manual muscle testing (MMT) 4/5] was observed preoperatively in 8 patients; it was relieved by microsurgical decompression. Based on self-assessments, all 22 patients were satisfied with the results of surgery. PNEN should be considered as a possible differential diagnosis in patients with L5 neuropathy due to lumbar degenerative disease, and as a causative factor of residual symptoms after LSS. PNEN can be successfully addressed by less-invasive surgery performed under local anesthesia.

[Clinical feathers and treatment of peroneal nerve entrapment neuropathy].

OBJECTIVE: Peroneal nerve entrapment neuropathy (PEN) is generally known as a drop foot with sensory disturbance. However, some patients experience numbness and pain in the affected area without severe paresis due to PEN. We report the clinical features and our surgical results of PEN cases. METHODS: We encountered 17 cases of PEN. The patients were 7 females and 10 males and their ages ranged from 30 to 78 years(average 56.1 years). In these cases, conservative therapy was unsuccessful;therefore, we performed surgical treatment for PEN. RESULTS: Among the 17 cases, 4 were of bilateral and 13 were of unilateral PEN. There was no severe paresis, as in drop foot;however, mild paresis (4/5, manual muscle test, MMT) was noted in 15 cases. In all cases, intermittent claudication presented, which ranged from 10 to 800 m (average 150 m). In 13 cases, radiological abnormality of the lumbar region was noted and 8 cases had a history of lumbar surgery (they had failed back surgery syndrome). In all the cases, we performed neurolysis of the peroneal nerve under local anesthesia;there was no surgical complication. After the surgery, symptoms improved, and the numerical rating of the lower limb improved from 8.6/10 to 0.8/10. Intermittent claudication also improved in all of the cases. CONCLUSIONS: We successfully treated 17 cases of PEN, which had lower limb pain without severe paresis, as in drop foot. Our results indicate that PEN should be recognized as a cause of intermittent claudication. Neurolysis for PEN under local anesthesia is less invasive and is useful for the treatment of lower limb pain.

Neurovascular bundle decompression without excessive dissection for tarsal tunnel syndrome.

Tarsal tunnel syndrome (TTS) is an entrapment neuropathy of the posterior tibial nerve and its branches in the tarsal tunnel. We present our less invasive surgical treatment of TTS in 69 patients (116 feet) and their clinical outcomes. The mean follow-up period was 64.6 months. With the patient under local anesthesia we use a microscope to perform sharp dissection of the flexor retinaculum and remove the connective tissues surrounding the posterior tibial nerve and vessels. To prevent postoperative adhesion and delayed neuropathy, decompression is performed to achieve symptom improvement without excessive dissection. Decompression is considered complete when the patient reports intraoperative symptom abatement and arterial pulsation is sufficient. The sensation of numbness and/or pain and of foreign substance adhesion was reduced in 92% and 95% of our patients, respectively. In self-assessments, 47 patients (68%) reported the treatment outcome as satisfactory, 15 (22%) as acceptable, and 7 (10%) were dissatisfied. Of 116 feet, 4 (3%) required re-operation, initial decompression was insufficient in 2 feet and further decompression was performed; in the other 2 feet improvement was achieved by decompression of the distal tarsal tunnel. Our surgical method involves neurovascular bundle decompression to obtain sufficient arterial pulsation. As we use local anesthesia, we can confirm symptom improvement intraoperatively, thereby avoiding unnecessary excessive dissection. Our method is simple, safe, and without detailed nerve dissection and it prevents postoperative adhesion.

Treatment strategy for bilateral carotid stenosis: 2 cases of carotid endarterectomy for the symptomatic side followed by carotid stenting.

Since the introduction of carotid stenting (CAS), a combined treatment for bilateral lesions using carotid endarterectomy (CEA) and CAS has been developed. However, there has been only 1 report about CEA then CAS. Herein we describe 2 patients with bilateral severe carotid stenosis who were treated by CEA for the symptomatic side and CAS for the contralateral asymptomatic side. A 71-year-old man underwent CEA for the symptomatic side. Although the patient suffered hyperperfusion syndrome after CEA, he recovered fully after 3 weeks of rehabilitation. Two months later, CAS was performed for the asymptomatic side, and he was discharged with no deficit. A 67-year-old man underwent CEA for the symptomatic side. The patient developed no postoperative neurologic deficits except for hoarseness. Four weeks later, CAS was performed for the contralateral asymptomatic side. After the procedure, however, severe hypotension occurred, and treatment by continuous injection of catecholamine was necessary to maintain systematic blood pressure. The patient was ultimately discharged with no deficit. The combined therapy of CAS for the asymptomatic side and then CEA for the symptomatic side has been recommended by several authors. However, one of the problems of this strategy is the higher incidence of postprocedural hemodynamic complications, and hypotension after CAS may be dangerous for the symptomatic hemisphere. We suggest a combined therapy using CEA for the symptomatic side and then CAS for the asymptomatic side can be 1 beneficial treatment option for patients with bilateral carotid stenosis without coronary artery disease.

The impact of atherosclerotic factors on cerebral aneurysm is location dependent: aneurysms in stroke patients and healthy controls.

Previous studies have indicated that cerebrovascular diseases (CVDs) seem to increase the occurrence of unruptured intracranial aneurysms (UIAs). However, this maybe explained by the fact that CVDs and UIAs share common risk factors, such as hypertension (HT) and smoking. To clarify the impact of atherosclerotic risk factors on cerebral aneurysmal formation, we explored the incidence of UIAs and their locations in healthy controls and patients with CVD, who frequently have atherosclerotic risk factors. This study included consecutive 283 asymptomatic healthy adults and 173 acute stroke patients, from patients diagnosed with acute cerebral hemorrhage or cerebral infarction and admitted to our hospital. The incidence, maximum diameter, and location of UIAs were evaluated, and we also investigated the following factors: age, gender, current smoking, HT, diabetes mellitus (DM), and dyslipidemia. UIAs were found in 19 of the total 456 subjects (4.2%), 11 of 283 healthy subjects (3.9%), and 8 of 173 stroke patients (4.6%). These differences are not statically significant. The incidence of middle cerebral artery (MCA) aneurysms was significantly higher in the CVD patients than in the healthy controls (P = .03), and the incidence of paraclinoid aneurysms was significantly higher in the healthy controls than in the CVD patients (P = .03). Moreover, higher incidences of HTs and CVDs in the MCA aneurysms than in the other locations of UIAs were observed. These results indicate that the impact of atherosclerotic factors on cerebral aneurysmal formation depends on their location and that there is a stronger impact on MCA aneurysms than on paraclinoid aneurysms.