Rotational chair (ROTO) instead of electronystagmography (ENG) as the primary vestibular test.

OBJECTIVES: To compare the sensitivity of rotational chair (ROTO) versus electronystagmography (ENG) in peripheral vestibular pathology. METHODS: Retrospective chart review. RESULTS: One thousand consecutive patients undergoing evaluation for dizziness and imbalance at a tertiary care referral balance center were reviewed. ROTO was the primary vestibular study used in all patients with ENG used as a confirmatory test at the discretion of the treating physician. A subgroup of 478 patients underwent both ROTO and ENG. Among the patients diagnosed with peripheral vestibulopathy, sensitivity for peripheral vestibulopathy was 71% for ROTO and 31% for ENG. However, specificity was 54% for ROTO and 86% for ENG. CONCLUSIONS: We conclude that in this retrospective cohort with the authors' clinical diagnoses, ROTO is a more sensitive diagnostic study of peripheral vestibular pathology. The higher sensitivity of ROTO and the higher specificity of ENG may support the use of ROTO as the primary vestibular study and ENG as a supplemental vestibular study. Prospective analysis with distinct diagnostic criteria and defined inclusion criteria are necessary before these results can be widely extrapolated.     

Progressive myoclonic ataxia with intrathecal immune activation in six patients

In six patients with slowly progressive sporadic cerebellar ataxia and cortical multifocal action myoclonus, cerebrospinal fluid (CSF) IgG index was persistently very high (1.2–6.7) and numerous oligoclonal bands were detected. Progressive cognitive impairment and MRI cerebellar and cerebral atrophy were observed. No serum antibodies were found. Various degenerative, metabolic, inflammatory and systemic diseases were excluded. The cerebellum may be the main target of a degenerative or immune process and releases antigens that, enhancing a compartmentalised (auto)immune response, as suggested by the persistent intrathecal activation, could lead to further cerebellar damage. As the frequency of CSF oligoclonal banding in myoclonic ataxia is unknown, our patients’ disease might represent a hitherto unreported entity or a subset of progressive myoclonic ataxia.

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Sommario Descriviamo sei pazienti con atassia cerebellare sporadica e mioclono corticale d’azione multifocale, nel cui liquor i valori dell’indice IgG si mantenevano persistentemente elevati ed erano presenti numerose bande oligoclonali. I pazienti manifestavano un progressivo declino cognitivo e la RM mostrava atrofia cerebellare e cerebrale. In assenza di anticorpi identificabili non era possibile formulare una diagnosi di malattia nota. Suggeriamo che il cervelletto possa essere il principale bersaglio di un processo degenerativo o immuno-mediato e che gli antigeni liberati inducano la produzione di anticorpi che ulteriormente provocano danno cerebrale. Poiché non è nota la frequenza delle bande oligoclonali nel liquor di pazienti con atassia mioclonica, non sappiamo se la malattia qui descritta sia una entità nuova o un sottogruppo delle atassie miocloniche.

     

Percutaneous repair of aortic aneurysms: a prospective study of suture-mediated closure devices.

PURPOSE: To evaluate prospectively the safety and efficacy of totally percutaneous placement of abdominal and thoracic aortic endografts using the Prostar XL suture-mediated closure system. METHODS: From January 2002 to January 2005, we attempted to insert percutaneously all bifurcated abdominal aortic and thoracic endografts. Consecutive patients (25 men, four women), with mean age 74.9 years (range 44-84), underwent endovascular repair for 20 abdominal aortic aneurysms (AAA) and nine thoracic aortic aneurysms (repeat operation in one case). Endografts used included 21 Zenith (Cook), eight Talent (Medtronic), one AneuRx (Medtronic). For the technique, two Prostar XL 8F were used to close 22-24F access sites and one Prostar XL 10F to close 16F access sites. RESULTS: Procedural success was achieved in 21/29 (72.4%) patients and in 39/47 access sites (83%). Closure of 22-24F access sites with tandem 8F Prostar devices was successful in 23/29 (79.3%) cases. Closure of 16F access sites with 10F Prostar device was successful in 16/18 (88.8%) cases. There were seven peri-procedural failures requiring surgery to repair the femoral artery in three cases. Four access complications healed without intervention. Overall 25/29 (86.2%) patients had complete percutaneous repair. No late complications were detected during follow-up (median 17.5 months). CONCLUSIONS: Percutaneous treatment of patients with AAA and thoracic aneurysms is feasible in most cases, with a very low risk of access-related complication, providing that the operator has sufficient practical experience of this technique.     

Chronic lower extremity ischemia: a human model of ischemic tolerance.

BACKGROUND: Ischemic preconditioning (IPC) has been found in animals to have a protective effect against future ischemic injury to muscle tissue. Such injury is unavoidable during some surgical procedures. To determine whether chronic ischemia in the lower extremities would imitate IPC and reduce ischemic injury during vascular surgery, we designed a controlled clinical study. PATIENTS AND METHODS: Two groups of patients at a university-affiliated medical centre with chronic lower-extremity ischemia served as models of IPC: 6 patients awaiting femoral distal bypass (FDB) and 4 scheduled for aortobifemoral (ABF) bypass grafting for aortoiliac occlusive disease. Seven patients undergoing elective open repair of an infrarenal abdominal aortic aneurysm (AAA) were chosen as non-IPC controls. Three hematologic indicators of skeletal-muscle injury, lactate dehydrogenase (LDH), creatine kinase (CK) and myoglobin, were measured before placement of the proximal clamp, during surgical ischemia, immediately upon reperfusion, 15 minutes after and 1 hour after reperfusion, and during the first, second and third postoperative days. RESULTS: Baseline markers of skeletal-muscle injury were similar in all groups. In postreperfusion samples, concentrations of muscle-injury markers were significantly lower in the 2 PC groups than in the control group. For example, at day 2, LDH levels were increased by about 30% over baseline measures in the elective AAA (control) group, whereas levels in the FDB and ABF groups remained statistically unchanged from baseline. Myoglobin in controls had increased by 977%, but only by 160% in the FDB and 528% in the ABF groups. CK levels, in a similar trend, were 1432% higher in the control group and only 111% (FDB) and 1029% (ABF) in the study groups. Taken together, these data represent a significant level of protection. CONCLUSIONS: Patients with chronic lower-extremity ischemia suffered less severe ischemic injury after a period of acute ischemia than those with acute ischemia alone. Ischemic preconditioning is one proposed mechanism to help explain this protective effect.     

Does systemic inflammation trigger local exercise-induced oxidative stress in COPD?

Inflammatory abnormalities may be involved in the inadequate basal oxidant/antioxidant balance and local exercise-induced oxidative stress in chronic obstructive pulmonary disease (COPD) patients. The time course of oxidative stress and inflammation was investigated in 10 COPD patients and seven healthy subjects before and after local dynamic quadriceps endurance exercise at 40% of maximal strength. Venous samples were collected before, immediately after and up to 48 h after exercise. At rest, levels of an oxidant released by stimulated phagocytes, the superoxide anion, were significantly higher in patients, as were plasma levels of C-reactive protein, tumour necrosis factor-alpha and interleukin-6, inflammatory markers. An inverse relationship was found between baseline C-reactive protein levels and endurance time in patients. Six hours after exercise, superoxide anion release and levels of protein oxidation products, an index of oxidative stress, increased similarly in both groups, whereas thiobarbituric acid reactive substance levels, another index of oxidative stress, increased significantly only in patients. Plasma nonenzymatic antioxidant and inflammatory cytokine levels were unchanged by the exercise protocol. The increased baseline systemic inflammation in chronic obstructive pulmonary disease patients could be related to disturbed oxidant/antioxidant balance, and, together, these may have triggered the exercise-induced oxidative stress. The absence, however, of local exercise-induced systemic inflammation suggests that additional mechanisms explain local exercise-induced oxidative stress.