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עמוד בית
Fri, 05.12.25

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November 2006
D. Soffer
 Cerebral amyloid angiopathy is characterized by deposition of amyloid in the walls of leptomeninged and cerebral blood vessels. Its most common form, sporadic CAA[1] that results from deposition of β-amyloid peptide, which is the subject of this short review, is present in virtually all cases of Alzheimer diseases and is also common among non-demented subjects where its prevalence increases with age. Stroke due to massive cerebral lobar hemorrhage is the main clinical presentation of CAA, but transient neurologic symptoms due to microhemorrhages may also occur. CAA is also a risk factor for cerebral infarction and there is increasing evidence that CAA contributes to cognitive impairment in the elderly, usually in association with white matter abnormalities on imaging. Although the definitive diagnosis of CAA is neuropathologic, reliable diagnosis can be reached clinically, based on the occurrence of strictly lobar hemorrhages, particularly in the cortico-subcortical area when using gradient-echo or T2*-weighted magnetic resonance imaging. Experimental studies have shown that the origin of the vascular amyloid is neuronal, and age-related degenerative changes in the vessel walls prevent its clearance from the brain along perivascular spaces and promote Aβ[2] aggregation and CAA formation. The entrapped Aβ aggregetes are toxic to various vascular wall components, including smooth muscle cells, pericytes and endothelial cells, leading to their eventual destruction and predisposition of the vessel wall to rupture and hemorrhage. However, more research is necessary to decipher the mechanism of CAA formation and its relation to cognitive decline in the elderly.







[1] CAA = cerebral amyloid angiopathy

[2] Aβ = β-amyloid peptide


R. Segal, A. Furmanov and F. Umansky
 Background: The recent occurrence of a spontaneous intracerebral hemorrhage in Israel’s Prime Minister placed the scrutiny of local and international media on neurosurgeons as they made therapeutic decisions. In the ensuing public debate, it was suggested that extraordinary measures (surgical treatment) were undertaken only because of the celebrity of the patient.

Objectives: To evaluate the criteria used to select surgical versus medical management for SICH.

Methods: We retrospectively reviewed the files of 149 consecutive patients admitted with SICH[1] from January 2004 through January 2006 to our medical center. Their mean age was 66 (range 3–92 years), and 62% were male. SICH localization was lobar in 50% of patients, thalamus in 23%, basal ganglia in 15%, cerebellum in 13%, intraventricular in 6%, and pontine in 1%. Mean admission Glasgow Coma Score was 9 (range 3–15). Risk factors included hypertension in (74%), diabetes mellitus (34%), smoking (14%) and amyloid angiopathy (4%). Fifty percent of patients were on anticoagulant/antiplatelet therapy, including enoxaparin (3%), warfarin (7%), warfarin and aspirin (9%), or aspirin alone (34%).      

Results: Craniotomy was performed in 30% of patients, and ventriculostomy alone in 3%. Rebleed occurred in 9% of patients. Six months after the treatment 36% of operated patients were independent, 42% dependent, and 13% had died. At 6 months, 37% of non-operated patients were independent, 15% dependent, and 47% had died.

Conclusions: One-third of the SICH patients, notably those who were experiencing ongoing neurologic deterioration and had accessible hemorrhage, underwent craniotomy. The results are good, considering the inherent mortality and morbidity of SICH.


 





[1] SICH = spontaneous intracerebral hemorrhage


September 2006
A. Riskin, Y. Shiff and R. Shamir

Premature very low birth weight (< 1500 g) infants are one of the largest groups receiving parenteral nutrition. PN[1] should be optimized to answer their large nutritional requirements and suit their metabolic status, but should also be validated pharmaceutically. PN can be provided as a standard, usually commercial, formulation, representing the average needs of a large group of patients. Alternatively, an individualized PN compound adapted to the patient's needs can be prescribed and prepared, usually on a daily basis. The main advantage of individually prescribed PN is that it is tailored to suit a specific patient, thereby assuring the best possible nutrition and biochemical control. Batch-produced standardized PN bags can be readily available as ward stocks in neonatal intensive care units, enabling initiation of early PN immediately after the delivery of a premature infant. Moreover, standard PN solutions incorporate expert nutritional knowledge and support. A combination of standardized PN bags, prepared under strict standardization criteria, for most neonates, with a small number of specifically tailored individualized PN formulations for those in need for them, could reduce pharmacy workload and costs, and increase safety, while maintaining the desired clinical flexibility. For those in need of the individualized PN formulations, a computerized ordering system can save time, decrease prescription and compounding errors, and improve quality of nutritional care.






[1] PN = parenteral nutrition


May 2006
L.M. Shulman, Y. Manor, D. Sofer, T. Swartz and E. Mendelson

Background: Poliovirus rapidly evolves by nucleic acid substitutions and genetic recombination with other polioviruses and non-polio enteroviruses. Evolving oral poliovirus (Sabin strains) can rapidly revert to neurovirulence and undergo antigenic alterations.

Objectives: To evaluate the threat of vaccine-derived poliovirus (1–15% divergence from the respective Sabin strain) for a poliomyelitis-free population in a country with a long-standing routine vaccination program.

Methods: We characterized genetic and antigenic changes in OPV[1] strains isolated from sewage in Israel and evaluated intestinal immunity by measuring fecal excretion after OPV challenge of vaccinated children.

Results: Characterization of poliovirus from sewage revealed eight type 2 and three type 3 vaccine polioviruses that had replicated and started to evolve (vaccine that replicated and diverged by 0.5 to ≤ 1.0%) and nine highly diverged type 2 vaccine-derived polioviruses (1–15% divergence from the respective Sabin strain) with 8–14% divergence between the years 1998 and 2005. Six of the eleven VRPV[2] uniquely recombined with OPV and/or NPEV[3]. The nine VDPV[4] were epidemically related, genotypically neurovirulent, and had 10–15 amino acid substitutions in antigenic sites altering their antigenicity, but shared a single recombination. Type 2 OPV was excreted by 23% and 17% of infants challenged with OPV 3 months after partial immunization (two doses each of OPV and enhanced inactivated poliovirus) or full immunization (three doses of each) respectively, despite high humoral antibody titers.

Conclusions: Our findings, which show that OPV is excreted for a significant period by children with high humoral immunity, emphasize the long-term potential threat from VDPV in highly vaccinated populations. An adequate immunization program, combined with environmental surveillance, is necessary to prevent poliomyelitis and community transmission of poliovirus. 


 




[1] OPV = oral poliovirus

[2] VRPV = vaccine poliovirus that has replicated and started to evolve but is < 1 % but at least 0.5% diverged from the respective Sabin strain

[3] NPEV = non-polio enterovirus

[4] VDPV = vaccine-derived poliovirus 1–15% divergence from the respective Sabin strain


February 2006
R. Dabby, M. Sadeh, O. Herman, E. Berger, N. Watemberg, S. Hayek, J. Jossiphov and Y. Nevo

Background: Persistent creatine kinase elevation is occasionally encountered in subjects without any clinical manifestation of a neuromuscular disorder or any condition known to be associated with increased serum CK[1] levels. It is still unresolved whether extensive investigations and specifically a muscle biopsy should be performed in clinically normal individuals with elevated CK levels.

Objective: To study the muscle pathology of patients with asymptomatic or minimally symptomatic hyperCKemia.

Methods: The clinical and laboratory data of patients with persistent hyperCKemia and normal neurologic examination were reviewed and their muscle biopsies evaluated.

Results: The study group included 40 patients aged 7–67 years; the male to female ratio was 3:1. Nineteen patients were completely asymptomatic, 20 had mild non-specific myalgia, and 1 had muscle cramps. Electromyography was performed in 27 patients and showed myopathic changes in 7 (26%). Abnormal muscle biopsy findings (e.g., increased variation in fiber size, increased number of central nuclei and occasional degenerating fibers) were detected in 22 of the 40 patients (55%). No fat or glycogen accumulation was detected. Immunohistochemistry demonstrated abnormal dystrophin staining in 3 patients (8%), resembling the pathologic changes of Becker muscular dystrophy. No abnormal findings were detected on immunohistochemical staining for merosin, dysferlin, caveolin 3, or alpha and gamma sarcoglycans. The EMG[2] findings did not correlate with the pathologic findings.

Conclusions: Abnormal muscle biopsies were found in 55% of patients with asymptomatic or minimally symptomatic hyperCKemia. Specific diagnosis of muscular dystrophy, however, was possible in only 8% of the patients.






[1] CK = creatine kinase

[2] EMG = electromyography


S.C. Shapira

The care of the trauma victim can be divided into five to six phases, none of which can be bypassed.

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