Acne Scars

Int Rev Neurobiol. 2009; 87: 445-64Rochkind S, Geuna S, Shainberg APosttraumatic nerve repair and prevention of muscle atrophy represent a major challenge of restorative medicine. Considerable interest exists in the potential therapeutic value of laser phototherapy for restoring or temporarily preventing denervated muscle atrophy as well as enhancing regeneration of severely injured peripheral nerves. Low-power laser irradiation (laser phototherapy) was applied for treatment of rat denervated muscle in order to estimate biochemical transformation on cellular and tissue levels, as well as on rat sciatic nerve model after crush injury, direct or side-to-end anastomosis, and neurotube reconstruction. Nerve cells' growth and axonal sprouting were investigated in embryonic rat brain cultures. The animal outcome allowed clinical double-blind, placebo-controlled randomized study that measured the effectiveness of 780-nm laser phototherapy on patients suffering from incomplete peripheral nerve injuries for 6 months up to several years. In denervated muscles, animal study suggests that the function of denervated muscles can be partially preserved by temporary prevention of denervation-induced biochemical changes. The function of denervated muscles can be restored, not completely but to a very substantial degree, by laser treatment initiated at the earliest possible stage post injury. In peripheral nerve injury, laser phototherapy has an immediate protective effect. It maintains functional activity of the injured nerve for a long period, decreases scar tissue formation at the injury site, decreases degeneration in corresponding motor neurons of the spinal cord, and significantly increases axonal growth and myelinization. In cell cultures, laser irradiation accelerates migration, nerve cell growth, and fiber sprouting. In a pilot, clinical, double-blind, placebo-controlled randomized study in patients with incomplete long-term peripheral nerve injury, 780-nm laser irradiation can progressively improve peripheral nerve function, which leads to significant functional recovery. A 780-nm laser phototherapy temporarily preserves the function of a denervated muscle, and accelerates and enhances axonal growth and regeneration after peripheral nerve injury or reconstructive procedures. Laser activation of nerve cells, their growth, and axonal sprouting can be considered as potential treatment for neural injury. Animal and clinical studies show the promoting action of phototherapy on peripheral nerve regeneration, which makes it possible to suggest that the time for broader clinical trials has come.

Oper Orthop Traumatol. 2009 Jun; 21(2): 141-56Berger A, Hierner ROBJECTIVE: Reconstruction of powerful active elbow flexion. Reconstruction of missing muscle unit by neurovascular pedicled functional muscle transplantation. INDICATIONS: Treatment of last choice for --secondary reconstruction of active elbow flexion in case of complete lesion of the brachial plexus or musculocutaneous nerve (M0 muscle function = replacement indication), partial but incomplete lesion of the brachial plexus or musculocutaneous nerve (M1-(3) muscle function = augmentation indication); --replacement of the elbow flexor muscles in case of primary muscle loss (tumor, trauma). CONTRAINDICATIONS: Concomitant lesions of the axillary artery. No adequate donor nerve. Relative: no sensibility at all at the forearm and hand. SURGICAL TECHNIQUE: Free functional biarticular myocutaneous transplantation of gracilis muscle. A myocutaneous gracilis flap is raised at the thigh. At the upper arm the flap is fixed proximally to the coracoid process or the lateral clavicle. The distal insertion is sutured to the distal biceps tendon. Vascular anastomoses are carried out in end-to-side fashion with the brachial artery and vein. Nerval coaptation is done in end-to-end technique using the muculocutaneous nerve. POSTOPERATIVE MANAGEMENT: Complete immobilization for 6 weeks. Dorsal upper arm splint until sufficient muscle power (M(4)). Progressive increase of active range of motion for another 6 weeks. Continuation of physiotherapy for 12-18 months. Postoperative standardized compression therapy, combined with scar therapy (silicone sheet). RESULTS: Functionally useful results can be expected in 60-75% of patients, especially if there is some residual function (M1 or M2) left ("augmentation indication"). Early free functional muscle transplantation shows best results in patients with direct muscle defect, because all vascular and neuronal structures are still available, and no secondary changes such as fibrosis or joint stiffness are present yet. There are inconsistent results for patients with neurologic insufficiency (i.e., total brachial plexus palsy) or mixed neuromuscular insufficiency, such as compartment syndrome. Especially in complete brachial plexus lesion, free functional muscle transfer is often the only treatment option. Provided there is a good patient selection, satisfactory results can be achieved for elbow flexion. Whether a higher number of axons, as provided by the contralateral C7 transfer, will lead to better results is the topic of an ongoing study.

Oper Orthop Traumatol. 2009 Jun; 21(2): 126-40Hierner R, Berger AOBJECTIVE: Active elbow flexion is necessary for bimanual tasks. Reconstruction of powerful active elbow flexion. Reconstruction of missing muscle unit by neurovascular pedicled functional muscle transposition. INDICATIONS: Treatment of second choice (first choice bipolar latissimus dorsi transfer according to Zancolli & Mitre, transfer of the flexor/pronator muscle onto the distal humerus, or transposition of the triceps onto the biceps): --(Secondary) reconstruction of active elbow flexion in case of lesion of the brachial plexus or musculocutaneous nerve. --Replacement of the elbow flexor muscles in case of primary muscle loss (tumor, trauma). CONTRAINDICATIONS: Ongoing spontaneous or postoperative nerve regeneration. Ankylosis of the elbow joint (in case of good shoulder and hand function, one should consider arthrolysis or even total joint replacement). Insufficient power of the pectoralis major muscle (< M(4)). Lesion of the axillary artery involving the thoracoacromial artery. Relative: concomitant lesion of the latissimus dorsi and teres major muscles (loss of glenohumeral adduction [thoracohumeral pinch]. SURGICAL TECHNIQUE: Distal muscle transposition: transposition of the origin--pars abdominalis, pars sternocostalis, pars clavicularis (unipolar or bipolar, partial or complete distal transfer): --Unipolar partial pectoralis major muscle transposition according to Clark. --Bipolar partial pectoralis major muscle transposition according to Schottstaedt et al. --Bipolar complete pectoralis major muscle transposition according to Dautry et al. and Carroll & Kleinmann, respectively, possibly in combination with transfer of the pectoralis minor muscle. --Myocutaneous flap in case of concomitant skin defect at the upper arm level. Proximal tendon transfer: transposition of the tendinous insertion at the humerus of the pectoralis major muscle. POSTOPERATIVE MANAGEMENT : Immobilization for 6 weeks in a dorsal upper arm splint, a Gilchrist bandage or a thorax-arm abduction orthesis with the elbow in 90 degrees flexion and supination. Early passive motion depending on pain within the sector 90-140 degrees. Progressive increase of active range of motion after 6 weeks. Protected exercise from "out of the splint" with increasing elbow extension of 10 degrees per week. It is important, that there is still an extension lag of 30-40 degrees at 3 months after transfer, in order to protect the reinnervated muscle and avoid overstretching. Although complete elbow extension should be the aim after 1 year, most patients will keep an extension lag of 20-30 degrees. Physiotherapy must continue for 12-18 months. Postoperative standardized compression therapy, combined with scar therapy (silicone sheet). RESULTS: Meta-analysis of the literature and personal results show functional (very good and good) results in 54-86% of patients. There are only few complications.

Heart Rhythm. 2009 Aug; 6(8 Suppl): S70-6Haqqani HM, Marchlinski FEThe electrophysiologic substrate underlying the development of ventricular tachycardia (VT) in patients with prior infarction has been studied in depth. An increased understanding of its composition and role in the maintenance of reentrant VT has led to the development of substrate modification approaches to ablation of unmappable VT. The area of low bipolar voltage that corresponds to the subendocardial projection of the scar as well as specific potential targets within it have been defined. These targets are selected because they may be involved in forming, or are in close proximity to, critical diastolic isthmuses during VT. The targets include sites of good pacemaps in the border zone, corridors of relatively preserved voltage within dense scar, regions between electrically unexcitable scar, isolated potentials, very late potentials, and regions with good pacemaps which display long stimulus to QRS delays. Ablation strategies have been designed based on these targets, mostly incorporating linear lesions to transect putative isthmus sites. This review examines the role that the electrophysiologic substrate plays in the mechanism of scar-related VT and how this substrate is mapped, defined, and ablated.