Intracranial Artery Calcium Burden Predicts Recurrent Cerebrovascular Events in Transient Ischaemic Attack Patients

Background: Patients with initial transient ischaemic attack (TIA) subsequently have a higher risk of recurrent TIA or acute ischemic stroke (AIS). The role of scoring intracranial arterial calcification (IAC) in predicting the prevalence of stroke remains unclear. We aim to evaluate if radiological CT calcium score measuring IAC burden could predict future ischemic events in a cohort of TIA patients. Methods: We studied consecutive patients from July 2014 to December 2015 who presented with first episode of TIA. All patients had noncontrasted CT or CT-angiogram of the brain on admission. CT calcium score (cm3) was quantified by measuring calcium deposition in the bilateral internal carotid arteries, middle cerebral arteries, and vertebrobasilar system. Patients were followed up for 2 years and ischemic events for either recurrent TIA or AIS were recorded. We compared patients in terms of clinical profile at presentation and CT calcium score using appropriate univariate and multivariable analyses. Results: Of 156 TIA patients studied, 22% (n = 35) had recurrent TIA or AIS within 2 years of follow-up. On univariate analyses, recurrent TIA/AIS was associated with gender (OR 0.61; 95%CI 0.40-0.95; P = .038), hypertension (mean difference 2.49; 95%CI 1.08-5.75; P = .030) and higher CT calcium score (mean difference 0.84 95%CI 0.16-1.52 P = .016). On multivariable logistic regression, a higher CT calcium score was significantly associated with recurrent TIA/AIS (adjusted OR 1.25 95%CI 1.01-1.55 P = .042). Conclusions: In TIA patients, higher IAC burden by measurement of a quantitative CT calcium score may be associated with recurrent ischemic events.     

Variability in 4-hydroperoxycyclophosphamide activity during clinical purging for autologous bone marrow transplantation

We examined the effects of varying incubation conditions on the in vitro activity of 4-hydroperoxycyclophosphamide (4HC). 4HC activity against CFU-GM and against the K562 tumor cell line decreased with increasing the RBC concentration of the incubation mixture. Increasing the concentration of nucleated bone marrow cells in the incubation mixture also decreased the 4HC activity. Evaluation of 53 consecutive patients undergoing autologous bone marrow transplantation (BMT) revealed that the incubation RBC concentration during clinical purging showed a similar effect on CFU-GM recovery. Aldehyde dehydrogenase content of RBCs and nucleated marrow cells appears to be the cause of the inhibition of 4HC activity. Although there was no difference in individual CFU-GM sensitivity to 4HC among normals, previously treated patients undergoing autologous BMT showed significant variability in CFU-GM sensitivity to 4HC. The combined effects of incubation RBC concentration and individual patient 4HC sensitivity appear to account for most of the variability in CFU-GM recovery and speed of hematologic recovery after clinical purging with 4HC.     

Medial brachial fascial compartment syndrome: anatomic basis of neuropathy after transaxillary arteriography

The authors reviewed their experience with 320 transaxillary arteriograms, as well as the English-language literature on neuropathy complicating transaxillary arteriography. Three of their patients had median and ulnar motor and sensory nerve injury, and six others had only sensory involvement. The occurrence or severity of nerve injury did not correlate well with the size or presence of an observable axillary or arm hematoma. Dissection of the axillae and arms of 25 human cadavers revealed a tough medial brachial fascial compartment (MBFC) outside a thin axillary sheath. The median and ulnar nerves were within the MBFC at an arterial puncture site just lateral to the anterior axillary fold. The radial and musculocutaneous nerves exited the MBFC more proximally. The different levels at which the major nerves of the brachial plexus exit the MBFC explain the anatomic distribution of the nerve injuries associated with compression by a hematoma after transaxillary arteriography.     

The autonomic-related cortex: pathology in Alzheimer's disease

Alzheimer's disease (AD) causes progressive deterioration of cognition and behavior. Memory dysfunction is the hallmark, but there are also changes in behavior, emotion and autonomic functions, which cannot be explained simply as a consequence of memory impairment. These observations suggest that the natural disease process of AD involves not only memory-related neural structures, but also specific neural systems related to other behaviors, emotion and autonomic functions. Since recent evidence has indicated a primary role for ventromedial frontal (VMF) cortex in such functions, we examined laminar distribution of neurofibrillary tangles and Alz 50 immunoreactive neurons in subdivisions of VMF cortex in 20 AD patients and seven age- matched controls. The densities of pathological changes were: (i) highest in the posteromedial mesocortical regions, particularly Brodmann's area 25 (A25), posterior orbitofrontal cortex (POF) and anterior insula (AI); (ii) of comparable severity between posteromedial mesocortical regions and most temporal cortices, excluding only the entorhinal cortex and temporal pole; and (iii) located predominantly in layer III and especially layer V. Further analysis demonstrated selective pathology in layer V of A25, POF and AI that would disrupt direct cortico-autonomic projections. This is the first study to detail severe AD pathology in these autonomic-related cortices, which could contribute to the behavioral changes, emotional disturbance and autonomic dysregulation that often accompany AD.      

Hepatitis C virus genotypes in a cohort of Australian blood donors and haemophiliac and liver transplant patients

The aim of the present study was to characterize hepatitis C virus (HCV) genotypes using the INNO-LiPA HCV line probe assay and direct sequencing from three different HCV-RNA-positive (serum) groups: (i) blood donors (n= 59); (ii) haemophiliacs (n= 43); and (iii) patients undergoing liver transplantation (n= 26). Of 128 HCV-RNA-positive samples, 74 (58%) were genotype 1. Of these, 41 were genotype 1a, 32 were genotype 1b and one was genotype 1 indeterminate. Of the remaining 54 samples, seven (5%) were genotype 2a, two (2%) were genotype 2b, 26 (20%) were genotype 3a, three (2%) were genotype 4a, while 16 (12.5%) were of a mixed genotype. There was no significant difference between the three groups with regard to the prevalence of any specific genotype. However, in blood donors and haemophiliac patients there was a statistically significant difference in the occurrence of genotype 3a in patients with elevated alanine aminotransferase (ALT) levels (30.3%) compared with those patients with persistently normal ALT levels (5.6%; P= 0.004; x²) Genotype 3a was also uncommon in liver transplant patients (one of 14) with ‘sporadic’ HCV infection. Genotype 4a was detected only in liver transplant patients. These patients had originated from Egypt (n= 1), Italy (n= 1) and Romania (n= 1).