Ischemic Neuropathy Research Articles

Is intimal hyperplasia a marker of neuro-ophthalmic complications of giant cell arteritis?

The ischaemic complications of giant cell arteritis (GCA) such as blindness and stroke may result from luminal narrowing of the affected arteries. This study focuses on the association between the severity of intimal proliferation on temporal artery biopsy (TAB) histology and neuro-ophthalmic complications (NOCs) of GCA. We identified 30 cases of biopsy-proven temporal arteritis. One histopathologist (blinded to the clinical details) evaluated the TAB specimens and categorized the degree of maximum stenosis due to intimal hyperplasia into four grades: grade 1 is <50% luminal occlusion due to intimal hyperplasia, grade 2 is 50-75%, grade 3 is >75% and grade 4 is complete luminal occlusion. A second histopathologist (also blinded to the clinical details) independently evaluated the TAB specimens using the same grading system. The NOCs in these patients were noted after a case record review. Of the 30 patients, 12 had NOC-10 with eye complications (complete visual loss, anterior ischaemic neuropathy, visual field defects), one patient had cerebral infarcts and one had both cerebral infarcts and vision loss. There was evidence for a statistically significant trend of NOC associated with higher intimal hyperplasia scores (P = 0.001). The scores of the histopathologists agreed for 23 (77%) patients and differed by 1 category for the remaining 7 (kappa-statistic 0.88). Our study suggests that the degree of intimal hyperplasia on TAB histology (routinely available to all hospital units) seems to be closely associated with NOCs of GCA. The study highlights the possible prognostic as well as diagnostic role of the biopsy. We feel that intimal hyperplasia noted in biopsy specimens may help us in the risk stratification of GCA patients and targeting of appropriate and novel therapies.

Acute abdominal aortic dissection: Insight from the International Registry of Acute Aortic Dissection (IRAD)

Isolated acute dissection of the abdominal aorta is an unusual event that may present with several different clinical scenarios. Because its incidence is low, the natural history is unknown. We report data from the International Registry of Acute Aortic Dissection (IRAD), the largest group of patients treated for acute aortic dissections. The aim of this study was to identify clinical characteristics, therapeutic approaches, risk factors for mortality, in-hospital outcome, and long-term results of this cohort, thus clarifying its natural history. A comprehensive analysis of 290 clinical variables on 18 patients affected by isolated acute abdominal aortic dissection (IAAAD) was performed. Among 1417 patients enrolled in the IRAD from 1996 to 2003, 532 (37.5%) had an acute type B dissection, of which 18 (1.3%) had an IAAAD. Theor mean age was 67.7 +/- 13.3 years, with a male predominance (n = 12, 67%). Aortic aneurysms pre-existed in 5 patients (28%). IAAAD was iatrogenic in 2 cases (11%). Compared with patients with type B aortic dissections, abdominal pain, mesenteric ischemia or infarction, limb ischemia, and hypotension as initial clinical signs were significantly more frequent in patients with IAAAD, whereas chest pain was more typical in patients with type B dissections. No neurologic symptoms, such as ischemic spinal cord damage or ischemic peripheral neuropathy, occurred in the IAAAD cohort. The 18 IAAAD patients were medically, surgically, or percutaneously managed in 12 (66.6%), five (27.8%), and one (5.6%) cases, respectively. The overall in-hospital mortality rate was 5.6% (n = 1). The patient who died was medically managed. No deaths were reported among patients who underwent surgery or had an endovascular procedure, irrespective of their preoperative status. A mean follow-up of 5 years (range, 1 month to 9 years) was completed for 71% (12 of 17) of the patients. Four patients (33.3%) died during the 9-year follow-up period. Overall survival was 93.3% +/- 12.6% at 1 year and 73.3% +/- 27.2% at 5 years. All patients who died during the follow-up period had in-hospital medical management (P = .04). IAAAD is a condition that may present differently compared with classic type B aortic dissections. IAAAD patients treated with surgical or endovascular procedures had a lower unadjusted in-hospital and long-term mortality rate compared with medically managed patients. On the basis of the present natural history report, continued surveillance appears mandatory. To improve the life expectancy of patients with IAAAD, aggressive surgical or endovascular management seems justified.

Retrobulbar hemodynamics in normal tension glaucoma compared to anterior ischemic optic neuropathy

Abstract Purpose: To compare flow velocities of the retrobulbar vessels in chronic vascular neuropathy in normal tension glaucoma (NTG) to those of acute circulatory disorder of anterior ischemic neuropathy (AION). Methods: Fifty‐two patients with NTG (mean age: 66 ± 8 ys) and 50 patients with AION (mean age: 68 ± 10 ys) were included in the study. Blood flow velocities (peak systolic velocity PSV and end–diastolic velocity EDV) and resistive indices of the ophthalmic artery (OA), central retinal artery (CRA) and nasal and temporal posterior ciliary arteries were measured by means of colour Doppler imaging (CDI). Results: No differences were detected for heart rate, diastolic arterial pressure and IOP between the two groups. In AION patients systolic arterial blood pressure was significantly higher compared to the NTG group (148 ± 26 mm Hg vs. 131 ± 18 mmHg, p = 0.0004). CDI revealed significant differences of the resistive index of the OA (RI AION: 0.80 ± 0.06; NTG: 0.76 ± 0.07). In AION, PSV of CRA was significantly lower compared to NTG (AION: 7.2 ± 1.9 cm/s; NTG 8.0 ± 1.6 cm/s). Conclusions: The chronic vascular deficiency in NTG seems to be similar to that of the acute circulatory breakdown in AION. In both vascular disorders of the optic nerve only small differences of flow velocities may be detected by CDI.

Absence of bilateral vision loss from amiodarone: A randomized trial

Amiodarone's role as a cause of toxic optic neuropathy is based on case reports. Annual frequency estimates of 0.36% to 2.0%, which have been made without reference to the dose or duration of treatment, are 12 to 200 times higher than those for idiopathic nonarteritic anterior ischemic neuropathy. The object of this study was to determine the incidence, dose, and time until onset of bilateral vision loss from amiodarone as a secondary end point in an investigation of amiodarone's role in preventing sudden death. Randomized subjects received body weight-determined doses of closed-label amiodarone (n = 837) or placebo (n = 832) in a prospective double-masked manner. Closed-label amiodarone subjects were followed, unless death occurred, for a minimum of 27 months. Median follow-up in survivors was 45.5 months. The end point was removal from the study because of bilateral vision loss. No subject was removed from the study because of bilateral vision loss. Subjects receiving continuous amiodarone for 4 to >60 months at daily doses of >2.0 mg/kg (n = 696), >3.0 mg/kg (n = 559), or >4.0 mg/kg (n = 219) had maximum possible (95% confidence) annual incidences of bilateral toxic vision loss of 0.23%, 0.29%, or 0.74%, respectively. The maximum possible annual incidence rate of bilateral vision loss from amiodarone in all 837 subjects (median age 60 years) receiving a mean daily dose of 3.7 mg/kg (300 mg) was 0.13%. At the doses commonly used clinically, bilateral vision loss from amiodarone toxic optic neuropathy occurs infrequently, if at all.

Lower limb paralysis from ischaemic neuropathy of the lumbosacral plexus following aorto-iliac procedures

Neurological injuries following aorto-iliac procedures are rare, unpredictable and cause significant morbidity. We report four cases of lower limb paralysis following aorto-iliac procedures, in which two patients suffered internal iliac occlusion and discuss potential aetiological factors. Four male patients, age ranging between 56 and 77 years, underwent aorto-iliac procedures. Three patients underwent repair of infra-renal abdominal aortic aneurysm (2 open and 1 endovascular repair) and one patient had percutaneous angioplasty of the internal iliac artery. All patients developed a unilateral lower limb paralysis early post procedure. Neurophysiological studies were performed in three patients and confirmed the injury to the lumbosacral plexus in two cases. MRI scan performed in two patients did not show any abnormality. In two of the cases, occlusion of one internal iliac artery was implicated as the cause of lumbo-sacral plexopathy: one with the coverage of the internal artery origin with the stent, the other due to thrombotic occlusion of common and internal iliac in arteries after an elective open repair of abdominal aortic aneurysm with a bifurcated graft. Follow up ranged between 2 and 4 months. Only one patient recovered completely; the other three were left with permanent disability. Ischaemic neuropathy following aorto-iliac intervention, whether open or endovascular, remains a rare, unpredictable and devastating complication. When it occurs it is likely to result in permanent neurological disability. It is important to note that it may be related to internal iliac artery thrombosis.

Selektive Immunadsorption bei neurologischen Komplikationen eines systemischen Lupus erythematodes

Vasculitis of the nervous system is a rare cause of multifocal neurologic symptoms and may involve both the central and peripheral nervous systems. Typical symptoms include headache, encephalopathy with cognitive impairment and psychotic symptoms, epileptic seizures, and peripheral neuropathies. Here we report the case of a 71-year-old female presenting with Raynaud's syndrome and paresthesia of the feet. Several weeks later she was admitted to our hospital with a status epilepticus and complex partial seizures. On admission she had mild aphasia, distal paresis of the arms without sensory deficits, and disorientation with hallucinations. Cerebral MRI revealed small, multifocal infarctions in several arterial territories. Multiple cerebral artery stenoses were detected by ultrasound. Examination of the CSF was unremarkable. Serologic tests for autoimmune disorders detected Ro antibodies compatible with systemic lupus erythematosus or Sjögren's syndrome. A sural nerve biopsy revealed ischemic axonal neuropathy. During administration of i.v. methylprednisolone, the symptom progression stopped but dosages could not be tapered due to severe CNS symptoms (mental decline, disorientation, aphasia, hallucinations). Slow but sustained clinical improvement was achieved by immunoadsorption over 3 weeks followed by a combined high-dose immunosuppressive treatment with cyclophosphamide and prednisolone that paralleled a reduction in anti-Ro titers and normalization of cerebral blood flow velocities as detected by repeated transcranial Doppler sonography. Systemic vasculitis may present with multiple neurologic and psychiatric symptoms due to involvement of the central and peripheral nervous systems. After excluding systemic infection, immunosuppressive therapy should be started early. In our case a combination of high-dose methylprednisolone, immunoadsorption with elimination of Ro antibodies, and cyclophosphamide led to the patient's recovery.

Ophthalmologic Complications Associated With Prone Positioning in Spine Surgery

Visual impairment and blindness associated with general anesthesia and prone positioning in spine surgery have been increasing in incidence over the past several decades. Corneal abrasion, the most common ophthalmologic injury, is usually self-limiting. However, prolonged surgical procedures (>7 hours) associated with acute blood loss anemia, hypotension, and hypoxia may lead to posterior ischemic optic neuropathies. Direct pressure to the periorbital region of the eye can cause increased intraocular pressure and blindness as the result of central retinal artery occlusion. Hypoxia and cerebral embolism are associated with occipital cortical infarct or cortical blindness. The prognosis for visual recovery from ischemic neuropathy and retinal artery occlusion is poor. Cortical blindness usually improves to varying degrees. Effective treatment of perioperative amaurosis is lacking and usually ineffective, making prevention the cornerstone of management. To best prevent permanent ophthalmologic complications associated with prone positioning during spine surgery, orthopaedic surgeons should be aware of pathophysiology and related risks associated with spine surgery in the prone position, and initiate preventive measures and predictable treatment options.

‘Just a sharp scratch’: permanent radial, median and ulnar neuropathy following diagnostic venepuncture

An 82-year-old woman was admitted to hospital with acute left ventricular failure following a recent myocardial infarction for which she had been commenced on clopidogrel. An uneventful venepuncture in her left antecubital fossa yielded a normal full blood count and coagulation profile. Diuretics were commenced to which she responded well. Five days later she described pain, swelling and bruising of her left forearm with numbness over her thumb, index and middle fingers. Prophylactic low molecular weight heparin was discontinued and the arm elevated. Nine days later she was unable to move her left hand. Bruising extended from the shoulder to the hand with swelling distal to the antecubital fossa (Figures 1 and 2). Woody subcutaneous oedema was present around the antecubital fossa with forearm tenderness. The radial pulse was present with good capillary circulation in all fingers. Neurological examination revealed complete wrist drop, minimal finger flexion and no small muscle function of the hand. The dorsal aspect of the forearm and hand were hypersensitive, with numbness over the volar aspect of the thumb, index and middle fingers. These findings were consistent with an ischaemic neuropathy of the median, radial and ulnar nerves as a result of compartment syndrome, secondary to a compressive haematoma at the antecubital fossa following venepuncture. Surgery to relieve compartment pressures at this stage was thought to provide little chance of recovery, with the additional risk of supervening infection. Initial treatment was therefore conservative consisting of physiotherapy, vitamin B and gabapentine. An ultrasound scan confirmed the presence of a haematoma occupying the entire flexor compartment of the forearm. Nerve conduction studies revealed completely absent sensory potentials, with motor potentials 1%, 30% and 60% of normal in the radial, median and ulnar nerves respectively. This confirmed a severe subtotal axonotmesis of the radial nerve with partial axonal injury to the median and ulnar nerves. The prognosis was one of permanent major neurological deficit and despite intensive hand physiotherapy there was little functional recovery 1 year later.

Ischaemic monomelic neuropathy in a non-diabetic patient following creation of an upper limb arteriovenous fistula

The incidence of end-stage renal disease (ESRD) in Australia is estimated at 0.05% of the population. The majority of these patients will choose haemodialysis as the preferred form of renal replacement therapy, requiring creation of an arteriovenous fistula (AVF). The subsequent haemodynamic disturbance can lead to neurological or ischaemic problems. The reported frequency of such complications varies between 1 and 10% and is most common following proximal procedures involving the upper limb. Ischaemic neuropathy describes damage to a peripheral nerve caused by compromise of blood supply. The first description of such an injury following formation of an arteriovenous shunt was made by Bolton et al. [1], although the term ischaemic monomelic neuropathy (IMN) was coined by Wilbourn et al. [2]. He described a type of ischaemic neuropathy associated with interference of a major limb artery resulting in multiple, distal, axonal-loss mononeuropathies. The clinical features of IMN are typically sensorimotor with dysaesthetic sensory symptoms in the hand and forearm and associated weakness or paralysis of muscles in the same area [3]. The syndrome develops quickly (typically within hours) of AVF formation. There is no description of IMN precipitated by distal forearm procedure. It is distinct from steal syndrome, the most commonly recognized complication of vascular access surgery [4]. In the latter, the onset is more insidious, there are typically signs of skin and muscle infarction and other trophic changes, and the degree of ischaemia is generally more profound. IMN has been reported exclusively in patients with diabetes mellitus (DM), who often have pre-existing neuropathy and concomitant accelerated atherosclerosis. Brachiocephalic fistulae are most commonly associated with ischaemic complications; anatomically the brachial artery provides the only arterial inflow to the distal arm and in the absence of collateral blood vessels the risk of ischaemia is increased. In addition, the antecubital area is the watershed area of vasae nervorum for the three nerves supplying the upper limb [5]. We report on the first documented case in a non-diabetic individual.

Neurological Symptoms in Type A Aortic Dissections

Aortic dissection typically presents with severe chest or back pain. Neurological symptoms may occur because of occlusion of supplying vessels or general hypotension. Especially in pain-free dissections diagnosis can be difficult and delayed. The purpose of this study is to analyze the association between type A aortic dissection and neurological symptoms. Clinical records of 102 consecutive patients with aortic dissection (63% male, median age 58 years) over 7.5 years were analyzed for medical history, preoperative clinical characteristics, treatment and outcome with main emphasis on neurological symptoms. Thirty patients showed initial neurological symptoms (29%). Only two-thirds of them reported chest pain, and most patients without initial neurological symptoms experienced pain (94%). Neurological symptoms were attributable to ischemic stroke (16%), spinal cord ischemia (1%), ischemic neuropathy (11%), and hypoxic encephalopathy (2%). Other frequent symptoms were syncopes (6%) and seizures (3%). In half of the patients, neurological symptoms were transient. Postoperatively, neurological symptoms were found in 48% of all patients encompassing ischemic stroke (14%), spinal cord ischemia (4%), ischemic neuropathy (3%), hypoxic encephalopathy (8%), nerve compression (7%), and postoperative delirium (15%). Overall mortality was 23% and did not significantly differ between patients with and without initial neurological symptoms or complications. Aortic dissections might be missed in patients with neurological symptoms but without pain. Neurological findings in elderly hypertensive patients with asymmetrical pulses or cardiac murmur suggest dissection. Especially in patients considered for thrombolytic therapy in acute stroke further diagnostics is essential. Neurological symptoms are not necessarily associated with increased mortality.

Do vardenafil and tadalafil have advantages over sildenafil in the treatment of erectile dysfunction?

Erectile dysfunction (ED) affects up to 50% of men between the ages of 40 and 70 years of age. Sildenafil, vardenafil and tadalafil have all been shown to be similarly effective in the treatment of men with ED of vary etiologies, to have similar adverse effects profiles, and to improve quality-of-life by similar amounts. As these phosphodiesterase 5 (PDE5) inhibitors all increase the hypotensive effects of nitrates, they are not suitable for use in patients taking nitrates for the treatment of ischaemic heart disease. All three inhibitors must be used with caution in patients taking alpha(1)-adrenoceptors antagonists for benign prostatic hyperplasia. Although nonarteritic anterior ischaemic neuropathy has been reported in some users of the PDE5 inhibitors, there is no conclusive evidence that PDE5 inhibitors cause this rare effect. Tadalafil has a longer half-life than sildenafil or vardenafil, and a longer duration of action than sildenafil and vardenafil. Most preference studies have shown tadalafil to be preferred, but there are serious limitations to some of these studies. One approach to treatment is to give each patient a short- and long-acting agent, and for individuals to decide their preference.

Dialysis shunt-associated ischaemic monomelic neuropathy: neurological recovery preserving the dialysis access

Dialysis shunt-associated ischaemic monomelic neuropathy: neurological recovery preserving the dialysis access

Multiple effects of hypothermia on inflammatory response following ischemia–reperfusion injury in experimental ischemic neuropathy

Hypothermia is neuroprotective in peripheral nerve ischemia, but the mechanism(s) of neuroprotection are not well known. A major mechanism of ischemia–reperfusion (IR) injury is the inflammatory response. We therefore dissected the effects of hypothermia on inflammatory mediators in peripheral nerve ischemia of rats. Following functional and pathological evaluations for the effect of hypothermia on IR injury, we undertook immunohistochemical studies of inflammatory cells, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and nuclear factor kappa B (NF-κB) in nerve subjected to IR under defined hypothermic conditions with varying time delays (0, 1, 3, and 4 h) and depth of hypothermia (28°C, 32°C, and 35°C). Functionally and pathologically, significant hypothermic neuroprotection was confirmed in the intraischemically treated groups but not in the postischemically treated groups. In endoneurial microvessels, intraischemic hypothermia inhibited ICAM-1 upregulation but not TNF-α, NF-κB, and IL-6 expressions. We demonstrated significantly reduced granulocyte and mononuclear phagocyte infiltration into nerve with intraischemic hypothermia but not with postischemic hypothermia. Cytokine (TNF-α and IL-6) positive cells were significantly decreased in both epineurium and endoneurium with intraischemic hypothermia. Excess NF-κB expression was seen in both Schwann cell and axon under normothermia (35°C) but was inhibitable with deep hypothermia (28°C). We conclude that intraischemic hypothermia significantly attenuates the inflammatory response by its effect on multiple key mediators including cytokines, ICAM-1, and NF-κB.

P15.4 Ischemic monomelic neuropathy after vascular access procedures: Report of five cases

P15.4 Ischemic monomelic neuropathy after vascular access procedures: Report of five cases

Vision loss after spine surgery: a new hypothesis

To the Editor: As new reports concerning vision loss after spine surgery continue to be published,1,2 it is crucial to explore possible mechanisms. The incidence of vision loss after noncardiac surgery is 0.0008%,3 while it is 0.2% following spine surgery,4 with the causes usually taken to be anemia or hypotension.5 We hypothesize a possible additional mechanism: that the use of large amounts of crystalloids in such cases can lead to an accumulation of edema in the eye socket with the production of an “eye compartment syndrome”. Presumably, increased eye socket pressure in this setting can lead to ischemia of the optic nerve, especially in the posterior segment having a single blood supply derived from the ophthalmic artery.6,7 Our hypothesis is supported by the frequent observation of facial edema and chemosis in long spine cases carried out in the prone position, as well as by occasional cases of blindness after bilateral neck dissection where the internal jugular veins have been sacrificed.8 Here, the loss of vision is attributed to back pressure from the distended ophthalmic veins, leading to ischemic neuropathy. Experience suggests that prone positioning for spine surgery may play a particularly important role. We recommend that, where possible, prone patients should be positioned so that their heads are higher than the heart, and that any position that might impair venous drainage of the head be avoided. In addition, anything that might lead to direct pressure on the orbit must be carefully prevented. We believe that eye compartment syndrome as a cause of blindness should be considered in any prone spine case managed with extensive use of crystalloids and where anemia and hypotension have been excluded. We also speculate that the use of colloids for spine cases in the prone position may offer the potential to reduce eye socket edema and subsequent vision loss.

脳卒中の外科における合併症の予防と対策 硬膜動静脈ろうの血管内治療における合併症の現状と対策

To evaluate complications and their prevention in endovascular treatment of dural arteriovenous fistulas (AVFs), we analyze the medical records of 105 patients (47 men 58 women, mean age of 64.2 years) treated with endovascular procedures from 1990 to 2003 in our clinic. Dural AVF was located at the cavernous sinus in 43 patients, transverse-sigmoid sinus in 43, and other regions in 19. There were 201 procedures, including 97 transarterial embolizations (TAE), 84 transvenous embolizations (TVE), 17 surgical TVEs, and 3 sinoplasties. Twelve complications were recorded in 10 patients (3 cavernous sinus, 5 transverse-sigmoid sinus, and 2 craniocervical junction lesions). The complications were divided into 4 categories: wrong strategy (1 case), venous thrombosis (2 cases), procedural error (7 cases), and general condition (1 case; pulmonary embolism). One of the superficial middle cerebral veins was obliterated after coiling of the cavernous sinus in 1 patient, resulting in a mild transient hemiparesis (wrong strategy). The syndrome of paradoxical worsening occurred in 1 patient with cavernous sinus dural AVF after TAE (venous thrombosis of the central retinal vein). One patient with sigmoid sinus dural AVF suffered long-lasting dizziness after TVE. Ipsilateral endolymphatic hydrops were observed and speculated to be a causative factor of the patient's dizziness (venous thrombosis of the inner ear). The procedural error included trigeminal nerve palsy due to excess coil packing (1 case in TVE), ischemic cranial neuropathy (3 cases in TAE), and migration of the embolic materials via the feeding arterial collateral network (3 cases in TAE). Morbidity and mortality were 4.8% and 1.0%, respectively. We discuss causes and preventive measures.

Ischemic nephropathy: Detection and therapeutic intervention

Although the real prevalence of ischemic nephropathy as a cause of end-stage renal disease is unknown, its incidence has increased in past years. The diagnosis of this pathology requires that a number of functional and anatomic tests be carried out. The initial approach should be to perform duplex Doppler ultrasonography which, besides providing data on the size and extent of the stenosis, enables the intrarenal resistive index to be estimated to determine the pattern of renal parenchyma injury and the expected progression if revascularized. The most frequently used morphologic techniques are magnetic resonance angiography and computer tomography angiography. In the event of ischemic neuropathy, it is necessary to perform a renal arteriography regardless of the inherent risks of contrast toxicity or atheroembolism. Various therapeutic options are reviewed, with emphasis on percutaneous transluminal renal angiography plus stent as the first indication. Even though initial reports were contradictory, several meta-analyses have concluded that better blood pressure control and renal function improvement are achieved with percutaneous transluminal renal angiography plus stent than with conventional medical therapy. Surgical revascularization is preferable in patients with severe aorto-iliac pathology and renal artery ostium complete thrombosis. The risks and benefits of these procedures must be evaluated on an individual basis.

TB or TB plus vasculitis: Occam versus Hickam – reply

Dear Editor, We reported an unusual case of Mycobacterium tuberculosis infection complicated initially by fever, palpable purpura and mononeuropathy multiplex (MNM), and later by chylothorax [1]. The relationship between the purpura-associated ischaemic neuropathy, i.e. vasculitis, and the pulmonary tuberculosis was identified by the disease course, exclusion of other aetiologies, and the response to antituberculosis drugs. In our patient, the palpable purpura developed on the lower extremities concurrently with foot drop, where an electromyographic study showed the ischaemic change with active axonopathy. This was the clinical findings of cutaneous small vessel vasculitis with peripheral nerve system involvement. Cutaneous vasculitis has many causes. It may be a manifestation of systemic vasculitis, rheumatic diseases, hypersensitivity reactions, or malignancy. In addition, numerous viral and bacterial infections have been associated with the cutaneous vasculitis, including tuberculosis [2]. We have searched for an underlying cause for the development of palpable purpura and MNM in the patient. Pulmonary tuberculosis was proven to be the cause of fever of unknown origin, and other infectious, malignant, or immunological aetiologies were excluded after extensive studies. There were no clinical or laboratory evidences of eyes, kidney, musculoskeletal system or gastrointestinal tract involvement, which were more or less observed in systemic vasculitis or rheumatic diseases. The low-dose prednisolone therapy was prescribed for MNM at nearly 1 month postadmission. It is of low possibility to miss major clinical manifestations of a systemic vasculitis or rheumatic disease. Although palpable purpura, peripheral neuropathy and pulmonary involvement were common features of certain forms of vasculitis, such as Wegener's granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis, there was little evidence to support the diagnosis in our patient. There were also a few diagnostic clues from the disease course and history to suspect Behçet's disease or Henoch-Schönlein purpura in the reported case, although these vasculitis were occasionally reported to cause chylothorax. Moreover, the results of serological tests including antineutrophil cytoplasmic antibody (ANCA) were all normal, except a mild elevated level of rheumatoid factor. Furthermore, there were no further relapses of palpable purpura, peripheral neuropathy, chylothorax or other vasculitis features after the completeness of antituberculosis therapy, even when the usage of prednisolone was discontinued. Relapses of the disease course, which were commonly seen in most systemic vasculitis, did not occur in this patient. This as a result also implied that the underlying cause of the cutaneous vasculitis was the M. tuberculosis infection. In conclusion, concurrence of MNM and chylothorax as the manifestations of pulmonary tuberculosis is a rare condition. The relationship between vasculitis and tuberculosis was indirect; however, it was reasonable to make the illation. This illation requires a longer follow up of the patient and more reported cases to support. No conflict of interest was declared.

Does radial artery harvesting for coronary revascularization cause neurological injury in the forearm and hand?

Radial artery (RA) is now used widely as a conduit of choice in coronary artery bypass grafting. Although RA removal is considered safe in the presence of adequate collateral arterial supply, there is still a considerable suspicion on the functional status of the forearm and hand. However, a neurological dysfunction may occur owing to either surgical trauma or ischemic neuropathy. This study was aimed to investigate the functional outcome of the donor forearm nerves of the patients who underwent coronary artery bypass grafting surgery with RA conduits. A consecutive series of 50 patients who underwent coronary artery bypass graft surgery with one or two RA grafts were investigated in the study. Motor and sensory functions of donor forearm nerves were measured by ENMG studies, pre- and postoperatively at the third week and sixth month of the operation. The conduction velocities, distal latencies and amplitudes of action potentials for motor and sensorial conductions of radial, ulnar and median nerves were measured in each ENMG examination. Neurologic status of the donor forearm and hand was assessed by the same neurologist who performed a detailed neurologic physical examination and ENMG studies. Results were statistically compared using one-way ANOVA test. The incidence of any neurologic symptoms was 32% in early postoperative period. All reported neurologic complaints were associated with sensory conduction deceleration in ENMG investigations of related nerves. In postoperative assessment, median nerve sensory-motor, and ulnar nerve motor conduction records were slightly lower than the preoperative values, but no statistical difference was observed. Pre- and postoperative radial nerve motor and sensory conduction records were statistically similar (P>0.05). We advocate that removal of RA does not lead to any major neurologic hand complications in the presence of adequate collateral arterial blood supply. ENMG studies confirmed minimal conduction alterations with no statistical significance, even if neurologic symptoms were stated.

The therapeutic window of hypothermic neuroprotection in experimental ischemic neuropathy: Protection in ischemic phase and potential deterioration in later reperfusion phase

Hypothermia will neuroprotect peripheral nerve from ischemia–reperfusion (IR) injury, but the therapeutic window of hypothermic neuroprotection has not been defined. Unilateral IR injury was produced by the ligation and release of nooses tied around supplying arteries to the right sciatic–tibial nerve of the rat. Using this model, 114 rats were divided into 12 groups according to the delay (0, 1, 3, and 4 h) and the depth of hypothermia (28, 32, and 35°C). All rats were subjected to 3 h ischemia and 7 days reperfusion followed by behavioral, electrophysiological, and pathological evaluations. We demonstrated significant hypothermic neuroprotection with both deep (28°C) and mild (32°C) hypothermia initiated during ischemia (0 and 1 h delay), but not hypothermia initiated during reperfusion (3 and 4 h delay) in both behavioral and electrophysiological evaluations. In addition, the pathologically significant differences were observed between deep hypothermia (28°C) and normothermia (35°C) initiated during ischemia. We conclude that the therapeutic window of hypothermic neuroprotection is optimal during the intraischemic period and that mild and deep hypothermia provide neuroprotection. Prolonged delay of hypothermic treatment results in worsening of IR injury.