Distribution of surgery for adult and pediatric brachial plexus injuries.
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\r\n\r\n\tThe book aims to include, but is not limited to, new topics in ionic liquids in the petroleum industry such as corrosion inhibitors, green demulsifiers, and so on. Moreover, an overview of natural, synthetic and modified green materials applied in different stages of the petroleum industry is encouraged. Additionaly, the book will aim to shed light on recent technologies adapted for petroleum exploration, production, transportation, and refining.
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Abdel-Raouf is a Professor of polymer science at Egyptian Petroleum Research Institute since 2012. She has supervised 14 M.Sc and Ph.D theses and published 37 research papers in international journals. She also acts as a reviewer in different journals and has attended 12 international conferences. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"4816",title:"Face Recognition",subtitle:null,isOpenForSubmission:!1,hash:"146063b5359146b7718ea86bad47c8eb",slug:"face_recognition",bookSignature:"Kresimir Delac and Mislav Grgic",coverURL:"https://cdn.intechopen.com/books/images_new/4816.jpg",editedByType:"Edited by",editors:[{id:"528",title:"Dr.",name:"Kresimir",surname:"Delac",slug:"kresimir-delac",fullName:"Kresimir Delac"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"51020",title:"Is Alzheimer's Associated Amyloid Beta an Innate Immune Protein",doi:"10.5772/63021",slug:"is-alzheimer-s-associated-amyloid-beta-an-innate-immune-protein",body:'\nAβ accumulation is believed to contribute strongly to the pathogenesis of AD, although the actual physiological function and reason for accumulation of Aβ in the brain are not known. Aβ is a fragment of the larger β amyloid precursor protein (APP) which is a transmembrane protein which can be broken down by various proteases into a variety of fragments, including extracellular and intracellular fragments and the peptide fragments Aβ1‐42 and Aβ1‐40 which are composed partly of the extracellular and partly of the transmembrane domain of APP. Aβ1‐40 is more abundant than Aβ1‐42, but Aβ1‐42 is the more amyloidogenic and neurotoxic species [1–3]. The neurotoxicity of Aβ1‐42 has been shown to depend on the ability of this peptide to form unstable oligomers (pentamers mainly), whereas the protofibrils or fibrils formed from the peptide are less neurotoxic. Recent studies are at last starting to elucidate why accumulation of Aβ, especially the 1–42 form leads to brain injury. These studies focus on the role of Aβ as a trigger of inflammation and emphasize its interaction with glial cells in the brain. A vicious cycle appears to occur in which Aβ peptides activate glial and other phagocytic cells which in turn impairs the ability of these cells to clear Aβ peptides and plaques from the brain. The reasons for production of Aβ in the brain in the first place are less clear. Recent findings that Aβ peptides function as antibacterial and antimicrobial peptides have given rise to the hypothesis that production of Aβ peptides may have evolved as part of the innate host defense system.
\nI. Evidence for a link between chronic inflammation and AD—At the outset, it is important to distinguish between early onset AD and late onset AD. Both forms of AD are strongly linked to excess accumulation of Aβ in plaques in the brain; however, the causes of Aβ accumulation may differ. In the case of early onset disease, there is a link to actual mutations in the Aβ gene or in genes involved in proteolytic processing of the precursor protein to form Aβ peptides. The most commonly used mouse model, the APP‐PS1 model, of AD is based on over‐expression of Aβ peptides in the brain in a similar manner. Late onset AD appears mainly to result from impaired clearance of Aβ peptides (rather than increased production per se) and is linked to polymorphisms of several genes as outlined below. There is strong and growing evidence for a link between chronic inflammation and the development of both forms of AD and some other dementing illnesses. We refer the reader to several recent excellent reviews for in depth consideration this topic [4–6]. A link between inflammation and AD has long been suspected in part based on clinical findings (e.g., the apparent protective effect of long‐term non‐steroidal anti‐inflammatory use against development of sporadic AD) [7, 8]. In addition, pathological studies have shown evidence of inflammation surrounding neuritic plaques in AD. Complement factors, clusters of activated microglia and cytokines has been found in and near Aβ plaques [5, 9]. These findings of inflammation were also noted as early events in the brains of patients with AD. Expression of genes associated with inflammation in brain is increased in aging, and this effect is accentuated in patients with AD [10, 11].
\nII. Microglia and monocyte/macrophages as pivotal cells in mediating clearance or inflammatory responses to Aβ peptides—Microglia are resident phagocytic cells in the brain that plays a key role in maintaining the health of neurons and responding to sterile or infectious injury. Evidence is now converging from genome‐wide association studies (GWAS), in vitro cell biologic experiments and mouse models of excess Aβ accumulation, that microglia and to an extent recruited blood monocyte macrophages, are critical in mediating either protective clearance of Aβ or damage through inflammatory activation by Aβ peptides.
\nA. GWAS studies—The first gene to show strong linkage to development of AD was the ε4 variant of apolipoprotein E (APOE). Although APOE is mainly known for its ability to regulate cholesterol and lipid transport, the APOEε4 allele is linked to accumulation of Aβ in plaques in humans and mouse models [12]. In addition, there is evidence that APOEε4 may be linked to inflammatory responses in the brain through interaction with receptors on microglia [13]. For instance, crossing APOEε4 over‐expressing mice with APP/PS1 mice results in worsening inflammatory responses to lipopolysaccharide (LPS) as compared to APP/PS1 mice over‐expressing APOEε3 [7]. Other proteins which modulate lipid metabolism, for instance surfactant protein D, have innate immune activity as well [14]. Of interest, surfactant protein D has also been linked to dementia [15]. Several other gene variants which are primarily expressed on microglia or other myeloid cells have been linked to AD. The most prominent of these is the triggering receptor expressed on myeloid cells 2 (TREM2) [6, 16–18]. This receptor mediates phagocytic activity and cytokine responses of myeloid cells and polymorphic forms of this receptor are linked to development of late onset AD with an effect size similar to APOEε4. Similar polymorphisms of the complement receptor CR‐1 and an additional myeloid cell receptor, CD33, have been linked to development of AD [19, 20]. The contributions of these and other myeloid receptors to accumulation of Aβ and neuronal injury are now being elucidated through in vivo and in vitro studies.
\nB. Cell biology and mouse model studies—There is abundant evidence that accumulation of Aβ1‐42 itself activates microglia and monocyte macrophages through binding to various receptors on these cells, either directly or through binding to other proteins (e.g., complement). A key hypothesis which brings together the various studies is that the ability of microglia to ingest Aβ1‐42, or to degrade it through proteolysis is protective, whereas production of pro‐inflammatory cytokines (e.g., TNF, IL‐1 or IL‐18) in response to Aβ1‐42 is harmful. Microglia and macrophages can have a variety of phenotypes, with two major categories being the MI and M2 phenotypes. The MI phenotype is associated with pro‐inflammatory cytokine generation as well as production of nitric oxide or superoxide radicals. In contrast, the M2 phenotype (presumably the more beneficial phenotype in the context of Aβ accumulation) is associated with enhanced phagocytosis and reduced pro‐inflammatory signaling. Given the sensitive nature of the brains and neurons, clearance of pathogens, harmful proteins, or cellular debris ideally would proceed with minimal inflammation. The beneficial or harmful effects of various myeloid receptors have been categorized according to whether they mediate either M1 or M2 like activities [5, 21].
\nMicroglial scavenger receptors—Receptors shown to promote phagocytosis and non‐inflammatory clearance of Aβ1‐42 include the scavenger receptors SR‐A or Scara‐A [22, 23]. In contrast, CD36, which is another scavenger receptor, appears to mediate pro‐inflammatory responses to Aβ1‐42 [24, 25]. Crossing of APP/PS1 with mice‐lacking SR‐A leads to greater Aβ accumulation and worsened survival, whereas crossing with mice‐lacking CD36 causes reduced brain cytokine production and Aβ accumulation and improved survival. CD33 is another receptor that is involved in uptake of Aβ peptides by microglia. CD33 is over‐expressed in microglia of humans with AD and the CD33 mutations that were found to be protective vs AD caused decreased expression of CD33 [19, 26]. Crossing of mice‐lacking CD33 with APP/PS1 mice leads to reduced Aβ peptide accumulation and plaque burden [19]. In vitro studies showed that CD33 actually reduces Aβ1‐42 uptake by microglial cells.
\nTriggering receptor expressed on myeloid cells 2 (TREM2)—TREM2 has a more complex role in that it can mediate either phagocytic clearance or pro‐inflammatory cytokine responses by myeloid cells [6]. Like CD33, it is highly expressed in microglia and monocytes in the brain. In particular, it is highly expressed in microglia surrounding amyloid plaques in APP/PS1 mice [16]. In one study using this mouse model, deletion of TREM2 reduced inflammatory pathology in the brain [27]. In contrast, in another study, over‐expression of TREM2 in these mice improved pathology [28]. The GWAS studies suggest that polymorphisms associated with decreased TREM2 production increase risk of development of AD or other neuro‐degenerative diseases [16]. Based on this, it has been postulated that loss of TREM2 impairs non‐inflammatory phagocytic clearance of Aβ peptides or of damaged neurons. TREM2 is well described as a phagocytic receptor for bacteria. Further studies will be needed to understand the complex role of TREM2 in AD. Of interest, two recent studies provide potential links between the contributions of APOEε4 and TREM2 to inflammation in AD. APOE was shown to bind to wild‐type (but not mutant) TREM2 [29] and the APOEε4 variant has distinctive effects (as compared to other APOE subtypes) in modulating microglial prostaglandin production and TREM2 expression [30].
\nComplement and complement receptors—The complement receptor CR‐1 also appears to have a complex role in AD [20]. CR‐1 is the receptor for complement factors C3b and C4b. Aβ can activate the complement cascade and bind to C3b. This in turn leads to binding of Aβ peptides to CR‐1. CR‐1 is expressed on myeloid cells and erythrocytes. In the case of erythrocytes, it serves to mediate clearance of complement bound proteins or organisms from the circulation. There is some evidence that this may promote clearance of Aβ outside the brain [31]. CR‐1 also mediates phagocytosis of complement bound proteins and pathogens by phagocytes. Aβ can activate the complement system via the alternative pathway. This could conceivably lead to increased inflammation in the brain. However, it has been found that C3 deficiency or inhibition of complement worsens Aβ accumulation and neurodegeneration in mice [32]. These finding suggest that the complement activation may overall be beneficial vs AD. A possible explanation for the role of CR‐1 is that the polymorphism most tightly linked to increased risk for AD (CR1‐S) has an increased C3b/C4b binding site and that CR‐1 actually acts to inhibit further activation of the complement cascade after binding to C3b/C4b [20].
\nToll like receptors—Toll‐like receptors (TLRs) and the associated adaptor protein also have been found to mediate phagocyte activation by Aβ [24, 33–37]. Once again the exact role of TLRs in AD pathology is unclear. A simplistic hypothesis would assume that TLR activation should worsen AD pathology; however, there is also evidence that the reverse may be true [33, 38]. Of interest, IL‐10 which is predominantly an anti‐inflammatory cytokine has been found to have adverse effects in AD mouse models [39].
\nInflammasomes—Another important line of evidence relates to the role of nucleotide‐binding domain leucine‐rich repeat containing 3 (NLRP3) inflammasomes in AD [4, 40, 41]. Inflammasomes are multi‐molecular complexes in phagocytic cells which mediate production of the pro‐inflammatory cytokines IL‐1 and IL‐18 through the action of caspase 1 and induction of an inflammatory form of cell death called pyroptosis [42, 43]. Inflammasomes are involved in phagocyte mediated host defense against various pathogens. In the case of bacteria, the inflammasomes are activated by pathogen‐associated molecular patterns (or PAMPs), like LPS. Increasingly, however, inflammasomes have been implicated in various inflammatory states triggered by self molecules termed damage‐associated molecular patterns or DAMPs. NLRP3 inflammasomes activation has been linked to inflammatory bowel diseases, celiac disease, gout, multiple sclerosis, and type II diabetes mellitus. It appears that NLRP3 inflammasomes also mediate chronic inflammatory responses to Aβ peptides. NLRP3 inflammasomes are one subtype among a variety of inflammasomes. Figure 1 illustrates the potential mechanism of assembly and activation of NLRP3 inflammasomes by Aβ peptides. Aβ peptides appear to act as a DAMP. As noted, two signals are required for activation, both of which could be triggered by Aβ peptides. The NLRP3 inflammasome complex consists of oligomeric assemblies of the NLRP3 protein, the apoptosis‐associated speck‐like protein containing a caspase activation and recruitment domain (ASC) protein and caspase 1. Crossing of mice‐lacking caspase 1 or NLRP3 with APP/PS1 mice results in increased clearance of Aβ peptides and plaques, reduced neurodegeneration and a skewing of microglia to the M2 phenotype. Pro‐inflammatory signaling in response to Aβ peptides mediated through inflammasomes appears to lead to a vicious cycle in which microglia acquire and M1 phenotype and cause increasing injury and decreased Aβ clearance [21].
\nChemokines—Chemokines and their receptors also appear to modulate Aβ‐related pathology. The chemokine CXCL10 is expressed at high levels in AD brain. Deletion or inhibition of the receptor for this and other CXCL chemokines (CXCR3) increased microglial uptake of Aβ in vitro and in vivo [44]. Deletion of CXCR1 had a similar effect [45]. These findings imply that these chemokines worsen the inflammatory effects which lead to increased injury or impaired clearance of Aβ. An active area of investigation as well is the role of recruited monocyte macrophages to AD pathology or Aβ clearance. Deletion of the monocyte receptor CCR2 in mice reduces monocyte recruitment and increases amyloid pathology in APP/PS1 mice [46], indicating that these cells play a role in clearance. Similarly CCR5 deletion increased Aβ deposition and neurological loss [47]. Other cytokines, like IL‐12, are linked to exacerbation of AD as is activation of oxidant production by microglia [48–50].
\nC. Epidemiological studies—Life‐style or other factors which are known to increase AD incidence also may mediate their effects through chronic inflammation. Examples include obesity, lack of exercise, peri‐odontitis, or diabetes [5]. Overall these studies lend strong support to the hypothesis that the innate immune system, and specifically, resident or recruited phagocytic cells play a pivotal role in determining the balance between protective Aβ clearance or damaging Aβ peptide‐induced inflammation.
\nMicroglial NLRP3 inflammasome activation by Aβ oligomers—the NLRP3 inflammasome can be activated by various PAMPs or DAMPS. Aβ oligomers can be considered as a DAMP which leads to NLRP3 activation in microglia. To induce NLRP3 activation, there needs to be at least two signals. The first signal causes increased production of the NLRP3 protein, and the second signal induces assembly of the multimolecular inflammasome complex. Other proteins involved in this complex include ASC and caspase 1. Activation of caspase 1 results in cleavage of pro‐IL‐1β and pro‐IL‐18 to form active IL‐1β and IL‐18. An additional effect of inflammasome activation is induction of a form of cell death caused pyroptosis. The result is a significant induction of local inflammation but also impairment of microglial phagocytosis, reducing further clearance of Aβ. The exact triggers of signal 1 and 2 are have not been fully elucidated. Since Aβ can trigger TLR activation, it is possible that this provides signal 1. In the case of some bacteria, rupture of phagosomes appears to provide signal 2, possibly by release of cathepsin B. We speculate that this could be involved in NLRP3 inflammasome activation by Aβ. Other possible mediators of the second signal include reactive oxygen species release or activation of plasma membrane ion channels.
III. What is the physiological stimulus for Aβ production?—Thus far most of the studies we, we have discussed consider the downstream effects of Aβ accumulation on inflammation or cellular dysfunction. For early onset AD, and for the APP/PS1 mice, increased Aβ accumulation is the result of alterations of the Aβ protein itself or of the enzymes involved in cleavage of the precursor protein. It is unclear, however, what triggers Aβ production under normal circumstances or in late onset AD. Attempts to directly reduce Aβ levels through the use of antibodies against Aβ peptides have not been highly successful, although it is possible that use in earlier stages of the disease (prior to major cognitive impairment) may be beneficial. There is also hope that intervention to reduce inflammatory response to Aβ may be beneficial, although here again it may be necessary to act early in the course of disease since the inflammatory phenotype seems to precede clinical AD.
\nIf it was possible to determine the initial causes for Aβ accumulation in the brain, this might provide another approach to early intervention. One hypothesis is that infection initiates or sustains the process of Aβ accumulation. Excess accumulation of Aβ has been linked to Human Immunodeficiency Virus‐related dementia [51, 52], and the virus can cause Aβ accumulation in vitro as well [53, 54]. Similarly Herpes Simplex Virus (HSV) induced encephalitis, and HSV infection in vitro is associated with Aβ accumulation [55–59], again implying that viruses may be a stimulus of Aβ production or impaired clearance. These findings suggest that viruses that infect the brain could be triggers for accumulation of Aβ, perhaps as part of an aberrant or sustained innate immune response. Antibodies to Cytomegalovirus, Epstein Barr Virus, or Human Herpes Virus 6 (HHV6) have also been associated with AD [60, 61] in some studies. In contrast, another study showed no link between AD and antibodies to HHV6 [62]. A variety of studies have also linked bacterial infection, including with chlamydia to development of AD [63, 64]. Of great interest, recent studies found fungal forms and sequences in brains of AD patients but not in controls [65–67]. Of course of a causal connection between these infections and AD is far from proven.
\nIV. Aβ peptides as antimicrobial agents—An alternative hypothesis to explain Aβ peptide and ultimately plaque production is that it is part of a host defense response to infectious or traumatic injury. Aβ peptides resemble some anti‐microbial peptides or AMPs in their structure [68, 69]. Aβ peptides are similar to the porcine AMP, protegrin, in ability to form channels in membrane structures which is believed to be one of the anti‐bacterial and anti‐fungal mechanisms of AMPs. Recently, Soscia et al. demonstrated antibacterial and antifungal activity for Aβ peptides [70]. In addition, this study showed that Aβ isolated from the brain of AD patients had antimicrobial activity and that incubation of these brain‐derived samples with antibodies to Aβ ablated the antimicrobial activity. More recently, we demonstrated that Aβ peptides also have antiviral activity using influenza A virus as a model [71]. In our study and that of Soscia et al., Aβ1‐42 was found to have greater antimicrobial or antiviral activity than Aβ1‐40. We demonstrated that Aβ1‐42, but not Aβ1‐40, caused viral aggregation which appears to contribute to its antiviral effects. This implies a possible connection between the ability of Aβ1‐42 to assemble into oligomers and its antiviral activity, since this peptide has a greater propensity to form oligomers and fibrils than Aβ1‐40.
\nThe finding that Aβ peptides, especially, Aβ1‐42 act like other cationic antimicrobial peptides may also explain its ability to activate phagocytic cells. AMPs have direct antimicrobial and antiviral activities but they also trigger recruitment and activation of immune cells [34, 36, 72]. We also recently showed that Aβ1‐42 modulates responses of neutrophils and monocytes to the influenza virus [71]. Aβ1‐42 increased neutrophil uptake of influenza A virus and potentiated neutrophil respiratory burst and neutrophil extracellular trap (NET) formation in response to the virus. Aβ1‐42 also reduced inflammatory cytokine production triggered by influenza virus in monocytes. The opsonizing activity of Aβ1‐42 was again not replicated with Aβ1‐40. More recently, we found that Aβ peptides can increase neutrophil uptake of bacteria as well (unpublished data). Overall, these studies lend support to the hypothesis that Aβ peptides serve a host defense role and that chronic infectious or inflammatory stimuli may result in an aberrant prolongation of what normally would be a helpful response.
\nThere is now abundant evidence from a variety of sources that AD is characterized by a chronic inflammatory response in the brain. The key elements in this process include the ability of Aβ peptides, especially Aβ1‐42, to directly activate phagocytic cells, most notably microglia and, to a lesser extent, monocyte/macrophages. Figure 2 summarizes the microglial receptors, cytokines, and signaling mechanisms known to be linked to responses to Aβ peptides. These phagocytic cells are at the cross‐roads of innate immune responses in the brain, and they appear to play a pivotal role in determining whether the response to Aβ peptide accumulation is non‐inflammatory phagocytosis or pro‐inflammatory cytokine production. One conclusion from these studies is that inhibition of pro‐inflammatory responses early in the evolution of Aβ related pathology could be protective. For example, inhibition of inflammasome activation has been proposed as an approach to treatment. One dilemma is that there is not a simple correlation between processes normally thought of as pro‐inflammatory and reduction of neuronal injury in AD models. As prime examples, activation of the complement system or of toll‐like receptor pathways appears to be protective in some studies. In addition, the role of TREM2, while clearly important, is not as simply as initially expected. The recent findings that Aβ peptides (especially Aβ1‐42) function like other AMPs suggest that Aβ peptides may play a beneficial physiological role in vivo and may actually be part of an innate immune response to infection. If this is so then discovery of underlying infectious triggers of AD might provide a different modality of treatment.
\nMicroglial receptors and signaling pathways that are involved in response to Aβ—receptors, signaling pathways or extracellular cytokines shown to promote neuronal injury are shown in red, whereas those shown in green are protective vs neuronal injury or progression of AD like pathology. Receptors shown in as a mixture of green and red have been found to have both beneficial or adverse effects in various studies.
The field of peripheral nerve surgery has evolved significantly over the past century, with many lessons learnt [16]. The practice of peripheral nerve surgery can be both rewarding and frustrating due to prolonged recovery times and outcomes ranging from excellent to dismal, particularly for injuries involving the brachial plexus [44]. The most crucial aspect of planning surgical intervention in brachial plexus injury is selecting the timing of surgery [8]—preferably explored within 5 months after injury [8, 13]. This might be as early as 2 months for pan-plexus injuries which have demonstrated no improvement or as late as 5–6 months for distal neurotization repairs for upper plexus injuries. Generally, the armamentarium of the peripheral nerve surgeon includes (1) the initial history and examination, (2) preoperative electrophysiology, (3) preoperative rehabilitation, (4) longitudinal preoperative clinical and electrophysiological course (i.e., recovery/no recovery), (5) preoperative radiological assessment, (6) intraoperative anatomic study, (7) intraoperative electrophysiology, (8) operative procedures, and (9) postoperative rehabilitation.
\nHowever, this ideal kind of practice is obtainable mainly in the developed countries. Dedicated neurosurgical peripheral nerve surgery centers are still quite few in India and most other developing countries where majority of these patients either remain untreated or are palliated with physiotherapy as the only intervention, mainly as a result of lack of the required expertise and the necessary facilities. In this article, we looked at the pattern and trend of these problems in our practice, and present our early experience and outcomes, along with a brief review of previously documented results on similar surgical problems in the literature. Finally, we summarize the general principles and currently accepted practice guidelines required for optimal outcomes.
\nThe clinical and operative details of all patients who underwent peripheral nerve surgery at the neurosurgery department of Amrita Institute of Medical Sciences, Amrita University in Kochi, India over a period of 5 years from January 2010 till January 2015 were obtained from the hospital database and retrospectively reviewed. This department is a major neurosurgical referral center located in south-west of India serving both local and international patients. The senior author (AP) was responsible for the clinical and surgical management of all patients under review. The spectrum of cases ranged from nerve injuries and peripheral nerve sheath tumors to nerve entrapment syndromes. Short descriptions of the key approach and techniques which we used are briefly detailed as follows (with illustrations):
\nAll our nerve repairs involved microanastomosis with 10.0 nylon epineural sutures (1–3 per coaptation) and fibrin glue, as described in the literature [45]. Our cable graft sources included the sural nerve, medial antebrachial cutaneous nerve (MACN), and occasionally the greater auricular nerve in infants. Some of our employed techniques for the extraplexal repairs included Somsak’s selective distal neurotization of the axillary nerve with branch to long head of triceps [46], posterior approach and transfer of the spinal accessory nerve to the suprascapular nerve for shoulder abduction, Oberlin I selective transfer of ulnar nerve fascicle to the musculocutaneous nerve and Oberlin II transfer of branch to brachialis with median nerve motor fascicle for elbow flexion [34]. Our extraplexal transfer techniques also used included contralateral C7 transfer with cable grafts tunneled through the prevertebral space (in 11 patients) to the posterior division of upper trunk for axillary and radial nerve reinnervation and/or the medial cord/branches in OBPI (obstetric brachial plexus injury) for hand function, and thoracoscopically harvested full length phrenic nerve transfer to medial root of median nerve for hand prehensile function (in 4 patients) (Figure 1A–C). Donor fascicle functional integrity and recipient nerve nonfunctionality was confirmed by the presence or absence of innervated muscle contraction in response to direct monopolar nerve stimulation. Post-operative immobilization of the affected limb was maintained for 3 weeks, and thereafter patients were commenced on a rigorous rehabilitation protocol by the second author (RS) as early as possible.
\nIntraoperative pictures of a sample extraplexal neurotization repair of pan-plexus injury. (A) Full-length phrenic nerve transfer to medial root of the median nerve for prehensile hand function and coaptation of contralateral C7 (Cont. C7) to the posterior cord for axillary and radial nerve functions. (B) Sural nerve cable graft in the same pan-plexus repair to neurotize the musculocutaneous nerve (MCN) from the spinal accessory nerve (SAN) for elbow flexion. The coaptation was made in the infraclavicular space into the MCN distal to the branch to the coracobrachialis. (C) Supraclavicular coaptation of ipsilateral C4 motor root and SAN as donor sources into sural nerve cable graft neurotizing the MCN.
Under general anesthesia or regional anesthesia, the affected nerve segment was exposed, the epineurium was incised and tumor dissected in its subcapsular plane for PNSTs to ensure that non-involved fascicles remained functionally intact (Figure 2c). The entire limb was prepared and draped in order to assess all individual muscles with direct nerve stimulation as per the resection needs. Either direct NAP (nerve action potential) was recorded across the segment (2 cases) or absence of stimulation-induced target muscle twitching was ascertained before sacrificing the primary fascicle giving rise to the PNST. For malignant peripheral nerve sheath tumors (MPNSTs), an oncological wide resection at least 2–3 cm proximal and distal to the tumor, sacrificing the entire parent nerve, was done followed by functionally matched fascicular repair using sural nerve cable grafts (Figure 3). MPNSTs were often diagnosed preoperatively using FDG-PET (fluorodeoxyglucose positron emission tomography) scan to counsel and plan for nerve sacrifice and immediate repair.
\n(A–C) Excision of a benign peripheral nerve sheath tumor. The affected nerve segment was first exposed, followed by incision of the epineurium and the tumor was then dissected out complete in its subcapsular plane.
(A–D) Excision of a malignant peripheral nerve sheat tumor. Notice the extent of involvement of the affected limb. An oncological wide resection proximal and distal to the tumor was done along with excision of the involved parent nerve (C), followed by functionally matched fascicular repair using harvested cable grafts, as shown in (D).
Nerve entrapments distal to the shoulder (cubital tunnel, PIN entrapment, Guyon’s canal entrapment) were operated under regional (supraclavicular block) or local anesthesia. Previously described techniques were followed [1, 2, 21, 30] (Figure 4A and B).
\n(A, B) Guyon’s canal release. Notice the extent of the skin incision to both the wrist and palmar line (A) to ensure adequate exposure and release of the ulnar nerve and artery at the level of the canal.
Following surgery in each patient, the limb was immobilized with a splint for 2–3 weeks before commencing physiotherapy, to allow for epineural healing without tension at the anastomosis. Once the concerned limb was mobilized, our primary goals were prevention of contracture and prevention of complex regional pain syndrome (CRPS) following muscle reinnervation, by starting with passive ROM (range of motion). Once a flicker of contraction was found in the concerned muscles, we began isolating and strengthening them with gravity initially, progressing to “against gravity,” and then with resistance. Once the patient could move against gravity, it was useful to add functional tasks into the exercise programme since motor coordination is as important as strength in recovery. With this process, the patient would gradually develop “different” ways of doing old tasks to compensate for weakness of the primary effector muscle. This was achieved by utilizing the secondary effector muscles which changed the appearance of task performance.
\nIf there was little hope of recovering function at this point, then focusing on stabilizing the involved muscles above and below became more practical but if the chances of functional recovery were high, then training the concerned muscle to become activated at the correct time in the kinetic chain became more useful than just purely strengthening it. Once the reinnervation waiting period was over, one of three patterns would usually emerge: (1) the patient recovered function in the limb and used it, (2) the nerve failed to reach and innervate the muscle, or (3) the reinnervation occurred but disuse would have reduced cortical representation and then, the patient may not know “how to” use the muscle. Electrophysiology was quite useful in differentiating such cases, and modifying the rehabilitation plan at this stage taken into consideration depending on which of these patterns was the case.
\nOur measurement of functional outcomes following surgery was defined as follows based on the Medical Research Council (MRC) motor power grading system [4, 20].
No improvement in power = only flicker of movement of the affected muscle groups (or affected limb) = MRC 0–1
Slight or mild improvement in power of affected muscle groups or the involved limb = MRC 2–3
Significant improvement in power of affected muscle groups or the involved limb = MRC 4–5
The evaluations were carried out at 6 months, 1 year and 2 years after surgery at follow-up in our outpatient clinics.
\nA total of 68 surgeries were completed in 58 patients for various peripheral nerve disorders over the 5-year period. There was an average of about 13.2 surgeries per year, with an increasing frequency as the programme developed. The age of the patients ranged from 2 month to 68 years, with a sex distribution of 41 males and 17 females (ratio of 2.4:1). Overall mean time of presentation was at 18.3 months either post-injury or following onset of symptoms for non-traumatic peripheral nerve problems, with the earliest presentation being 1 day post-obstetric brachial plexus injury in a newborn at birth and the latest being 15 years in 2 patients (one with a left ulnar nerve nodule and the other with a left brachial plexus PNST respectively). The majority of the cases were for brachial plexus injuries (n = 30, 44.1%) comprising 19 adult surgeries and 11 pediatric surgeries. Among the 19 adult surgeries, there were 10 procedures for pan-brachial plexus injuries, 7 for upper brachial plexus injuries and only 2 for lower brachial plexus injuries (Table 1). Of the 11 pediatric surgeries, 9 were for obstetric brachial pan-plexus injuries (OBPI—Erb’s-Klumpke type) with one of the patients undergoing surgery twice while the remaining 2 were for road traffic accident traumatic injuries (Table 1). There were 21 excisions for peripheral nerve sheath tumors of which four were malignant, with one of these three patients requiring surgery twice (Table 2). There were 8 peripheral nerve entrapments comprising 3 posterior interosseous nerve entrapments, 3 cubital tunnel syndromes, 1 thoracic outlet syndrome and 1 Guyon’s canal entrapment syndrome. The remaining 9 surgeries included repair for 2 patients with penetrating ulnar nerve injury, 2 patients with iatrogenic nerve injuries from PNST surgeries done elsewhere (brachial plexus and common peroneal respectively), and procedures for chronic neuralgia (which included 3 DREZ-otomies, image-guided radiofrequency lesioning, open neurotomy of lateral cutaneous nerve of the right forearm and selective fascicular neurectomy of the left distal ulnar nerve). Among the benign lesions, 12 (57.1%) were benign schwannomas, while the remaining 42.9% consisted of various other lesions. Of note, 3 patients undergoing PNST using the fascicular-sparing subcapsular dissection technique noted post-op sensory deficits or paresthesias which were generally transient and none was noted to have any motor deficits.
\n\n | n | \nPercentage | \n
---|---|---|
Pan-brachial plexus injury (adult) | \n9 | \n30.0% | \n
Upper brachial plexus injury (adult) | \n7 | \n23.3% | \n
Lower brachial plexus injury (adult) | \n2 | \n6.67% | \n
Obstetric brachial plexus injury (OBPI) | \n10 | \n33.3% | \n
Surgically managed Non-obstetric traumatic brachial plexus injuries | \n2 | \n6.67% | \n
Total | \n30 | \n100.0% | \n
Distribution of surgery for adult and pediatric brachial plexus injuries.
\n | n | \nPercentage | \n
---|---|---|
Peripheral nerve sheath tumors | \n21 | \n55.3% | \n
Peripheral nerve entrapments | \n8 | \n21.1% | \n
Chronic neuralgia | \n5 | \n13.2% | \n
Common peroneal nerve injury | \n1 | \n2.6% | \n
Ulnar nerve injury | \n3 | \n7.9% | \n
Total | \n38 | \n100.0% | \n
Distribution of surgery for other lesions (adults and children).
As shown in Table 3, the majority of the injuries were repaired with various extraplexal neurotization transfers alone (25.8%), followed by repair with various combinations of extraplexal transfers and intraplexal neurotizations (22.6%), while 19.4% had repair with only intraplexal neurotizations. Figure 5 summaries all surgeries done over the 5 year period. Brachial plexus injury repairs and PNST excisions formed the bulk of the procedures. Outcomes at 6 month, 1 year and 2 years post-op are as summarized in Tables 4 and 5. Complications following surgery are as shown in Table 6.
\n\n | n | \nPercentage | \n
---|---|---|
Intraplexal neurotization | \n6 | \n19.4% | \n
Extraplexal neurotization/distal nerve transfers | \n8 | \n25.8% | \n
Combined intra + extraplexal neurotizations | \n7 | \n22.6% | \n
Exploration with internal/external neurolysis | \n3 | \n9.7% | \n
Microsurgical dorsal root entry zone lesioning (DREZ-otomy) | \n4 | \n12.9% | \n
Only microsurgical exploration + neurophysiological studies | \n3 | \n9.7% | \n
Total | \n30 | \n100% | \n
Breakdown of all procedures done for brachial plexus injuries.
Summary of various peripheral nerve surgeries done over the five year period under review. Brachial plexus injury repairs and PNST excisions formed the bulk of the procedures.
\n | 6 months post-op | \n1 year post-op | \n2 year post-op | \n
---|---|---|---|
N | \n19 (100%) | \n19 (100%) | \n18 (95%) | \n
No improvements in function | \n12 (63.2%) | \n3 (15.8%) | \n— | \n
Slight improvement | \n3 (15.8%) | \n7 (36.8%). | \n3 (15.8%) | \n
Significant improvement | \n2 (10.5%) | \n5 (26.3%) | \n8 (42.1%) | \n
No follow-up | \n2 (10.5%) | \n4 (21.1%) | \n7 (38.9%) | \n
Summary of outcomes for the adult brachial plexus injury repair.
\n | 6 months post-op | \n1 year post-op | \n2 years post-op | \n
---|---|---|---|
N | \n11 (100%) | \n11 (100%) | \n10 (91%) | \n
No improvements in function | \n3 (27.2%) | \n— | \n— | \n
Slight improvement | \n4 (36.4%) | \n3 (27.2%) | \n— | \n
Significant improvement | \n2 (18.2%) | \n5 (45.5%) | \n8 (72.8%) | \n
No follow-up | \n2 (18.2%) | \n3 (27.2%) | \n2 (18.2%) | \n
Summary of functional outcomes for the pediatric brachial plexus injuries.
Complication | \nn | \nPercentage (%) | \n
---|---|---|
Voice hoarseness | \n2 | \n13.3 | \n
Muscle weakness (post-PNST excision) | \n3 | \n20.0 | \n
Operative wound dehiscence | \n2 | \n13.3 | \n
Operative wound infection | \n3 | \n20.0 | \n
Severe intra-op hemorrhage | \n1 | \n6.67 | \n
Apnoeic attacks | \n1 | \n6.67 | \n
Malunion (following claviculectomy for access) | \n1 | \n6.67 | \n
Deep venous thrombosis of affected limb | \n1 | \n6.67 | \n
Post-op pleural effusion | \n1 | \n6.67 | \n
Total | \n15 | \n100.0 | \n
Post-operative complications.
Majority of the entire 58 patients were first seen at the out-patient clinic, while a few of them presented via the emergency room. Similar to observations in the literature, the more commonly affected anatomic side was the right side (58.5%) compared to 36.9% of the patients who had their problems on the left, with the remaining 4.6% who were mainly Neurofibromatosis-1 patients having bilateral PNSTs. There was a slight male preponderance of 2.4:1 in this study. Most other investigators similarly reported male predominance in their work (Table 6). From the observations as shown in the results, the majority of them were injury cases which were generally brachial plexus injuries (n = 30, 44.1%). Among the adult cases, pan-brachial plexus injuries were the commonest (n = 9; 50%), closely followed by upper brachial plexus injuries (n = 7; 38.9%) while lower brachial plexus injuries were the least (n = 2; 11.1%). Most of these presented fairly late (overall average time of presentation was 18.3 months) as a result of considerable length of time required for referral and transfer to our center following occurrence of the injury. As a result, majority of the procedures were done on elective basis instead of as emergencies. A few other factors which were probably responsible for late presentation possibly included poverty, living far away from our institution, initial visitation or consultation to other alternative healers, and sometimes delayed referral from other medical facilities. The follow-up rate at the end of the 2 year period was 95% for adults (Table 4) and 91% for the pediatric cases (Table 5) of the brachial plexus injury surgeries. The peripheral nerve sheath tumors ranked next in frequency (n = 21, 30.9%). The timing and pattern of presentation of this set of patients did not differ significantly from the nerve injury patients. Similar to the general pattern in the literature [14], the majority of the peripheral nerve tumors were benign. We had only 8 peripheral nerve entrapments while procedures for chronic neuralgia were the fewest (n = 3, 4.4%). Estimated blood loss was negligible in all surgeries except in one case of longstanding left brachial plexus PNST (Table 6). The post-operative complications noted in 22.1% of the patients post-operatively were mostly wound infection and post-PNST excision muscle weakness (Table 6).
\nAnyone would agree that timing of surgery is very crucial in the ultimate outcome. Yet, in spite of the fairly late presentation in the majority, it is clear from Tables 4 and 5 that despite the relatively small number of 58 patients in our series, there was generally a steady rise in number of those with marked improvement of functional recovery, with a simultaneous decline in the proportion of “no improvements at all” over the same period. We did more of adult brachial plexus injury repairs and became less enthusiastic about pediatric cases as our practice developed because the adult cases generally benefitted from surgical repair (Figure 6). In our personal experience with managing 196 cases of Erb’s and Erb’s plus palsies, excellent recoveries were possible in majority of cases with just a proper rehabilitation programme consisting of cerebral retraining and judicious management of co-contracture deformities.
\n(A) Examination to evaluate function at 1 year post-op for extraplexal neurotization repair in a 19 year old male patient who had right brachial plexus injury involving upper and middle trunks. Notice the quite remarkable extent of power recovered particularly with elbow flexion. (B) Examination to evaluate function at 2 years after surgery for distal intraplexal neurotization repair in another 19-year-old male patient who had injury involving only the upper trunk of his right brachial plexus. Compared with the contralateral limb, he had recovery of power to almost the same level with the pre-morbid state.
Among those patients undergoing peripheral nerve procedures for pain, the outcomes were generally poor. The patient with painful neuralgia involving lateral cutaneous nerve of forearm responded only temporarily to two RF (radiofrequency) lesioning procedures, but was relieved completely by proximal neurotomy. However, the same patient eventually later developed another painful neuralgia from the medial antebrachial cutaneous nerve being entrapped in the previous neurotomy surgery scar. The patient who had selective ulnar fasciculotomy for left common palmar digital neuralgia experienced temporary relief for just 2 weeks, followed by recurrence of the same pain. Patients who had DREZ-otomy (dorsal root entry zone lesioning) had excellent initial relief with cessation of incapacitating pain attacks, but constant background neuralgic pain persisted with lesser severity than it was preoperatively. Additionally, for the brachial plexus injury patients, in spite of our meticulous techniques, the restoration of function below the elbow following either partial root avulsion or total root avulsion was our biggest challenge. The benefit of surgery over natural history was not also clear in the cases of OBPI, even despite the fact that only pan-plexus OBPI (Erb’s-Klumpke type) were selected for surgical reinnervation. This explains why we did more of adult brachial plexus injury repairs and became less enthusiastic about pediatric repairs as the peripheral nerve programme went on.
\nFinally, among the several investigative imaging modalities required as standard pre-operative evaluation for peripheral nerve problems, one imaging modality which is emerging as a useful tool in preoperative selection and planning of peripheral nerve surgery is the MR neurogram [4, 41] but this was unavailable for investigating our patients at the time of their evaluation.
\nOne of the key aspects of the practice that can often lead to discouraging results if not properly addressed especially at the initially starting phase is how to select the right cases for surgery and get them properly managed after surgery. We realized that the ability of our efforts to manage these problems individually was limited. We constituted a multidisciplinary team comprising the neurosurgeons, neurologists, physiotherapists, orthopedician and plastic surgeon to review each patient and ensure adequate and appropriate pre-operative planning. The team met once a week and, this way, we were able to prevent the possibilities of inadequate or suboptimal clinical and electrophysiological localization/understanding of the process in each patient, know of any limitations of nerve repairs per case, plan ahead for accurate and reliable intraoperative electrophysiology as well as for reconstructive procedures at the muscle and tendon level. This arrangement also helped with meeting the need for regularized and effective rehabilitation as well as for motivation & consistent follow-up. At surgery, we utilized cable grafts as much as possible to prevention tension on our repair and made use of the operating microscope to ensure adequate microanastomosis. Interestingly, we did not have to advertise our work. There was already a strong referral pattern in our institution for other neurological/neurosurgical problems, and this was further consolidated for peripheral nerve related-problems by our multidisciplinary team. Regarding the problem of getting late referrals, we could only plan surgery based on how late the presentation was. Luckily, none of the patients in our series was too late on arrival as to benefit from only free muscle transfers. Unfortunately for most of such cases, we could not be in contact with the referring physician or health facility to ensure earlier referrals for subsequent cases.
\nTable 7 shows previous publications on surgery for various peripheral nerve problems and the documented outcomes. Reports from some of these studies highlight on a few technical factors positively influencing the results post-operatively. With respect to trauma, single coaptation repair of a donor nerve to the recipient nerve (neurotization repair) without tension is thought to be generally superior than indirect repair with a cable graft [13]. Bhatia et al., clearly demonstrated faster recovery and better functional results with direct coaptation compared to nerve graft interposition in carrying out contralateral C7 transfers while in a retrospective study on the effect of combining direct repair with nerve transfer procedures on the clinical outcomes in 74 patients by Sulaiman et al., all patients who had combination of nerve transfers with direct repair using either C5 or C6 recovered elbow flexion to Medical Research Council grade 3, compared to the same extent of recovery in only 87% of those in whom only nerve transfers were done [29, 36]. This further confirms the effectiveness of bypassing the long distance of regeneration by neurotizing the injured distal nerve stumps with more proximally located dispensable donor nerves [29]. In our experience however, though we did not do any comparative assessments like these authors, we attribute our outcomes as presented to the dedicated techniques and approach along with a strict rehabilitation program. We used combinations of cable graft techniques with direct neurotization transfers for majority of the brachial injury surgeries (Table 3) and for the functional priorities, elbow flexion and extension were generally the most important function of target we aimed to restore, closely followed by selective reinnervation of the median nerve for prehensile hand function or pincer grip.
\nAuthors and year | \nNo. of patients studied | \nMean age | \nSex distribution (M:F) | \nType of lesion/injury | \nSurgical techniques evaluated | \nKey results/outcomes | \nMaximum/mean follow-up | \n
---|---|---|---|---|---|---|---|
Guha et al. 2017 [35] | \n175 | \n45.2 years | \n96:79 | \n19 MPNSTs, 133 schwannomas, 49 neurofibromas | \nN/A | \nLess motor deficits with full resection of tumor; Increased recurrence with subtotal resections. | \n29.5 months | \n
Bhatia et al. 2017 [36] | \n22 | \n23 years for direct coaptation group; 24 years for nerve graft group | \n19:3 | \nBrachial plexus injuries | \nContralateral C7 transfer: By direct coaptation in 12 With graft interposition in 10 | \nDirect coaptation group = Grade 3 flexion in wrist + fingers in 10; Grade 2 flexion in 2 Nerve graft group = Grade 3 flexion in wrist + fingers in only 2; Grade 2 flexion in 7; total failure in 1 | \n26 months for direct coaptation group; 28.5 months for nerve graft group | \n
Sulaiman et al., 2009 [29] | \n74 | \n32 years | \n60:14 | \nBrachial plexus injuries; tumor; irradiation | \nMedial pectoral to musculocutaneous N. transfers (Group 1); Intercostal to musculocutaneous N. transfers (Group 2) | \nRecovery of elbow flexion to MRC grade 3 in all (100%) who had both nerve transfer + direct repair with C5/C6 combined, but in only 87 and 22% of those who had only nerve transfers in Group 1 and Group 2 respectively | \n3.5 years | \n
Badr et al., 2009 [4] | \n16 | \n16 months | \nN/A | \nOBPI (2 Erbs, 6 Erbs plus, 8 Erb-Klumpke palsies) | \nNeurolysis; graft repairs; nerve transfers | \nImprovement from preoperative average biceps grade of 0 to 1/5 to average postoperative biceps grade of 2.9 and average shoulder abduction grade of 2.5 | \n23.5 months | \n
Sequeira and Martins, 2009 [27] | \n10 | \n24.8 years | \n9:1 | \nComplete brachial plexus palsy | \nNerve transfers: phrenic to musculocutaneous N + spinal accessory to suprascapular N | \nRecovery to functional level in 7 (MRC Grade 3 in 5; Grade 4 in 2) No clinically significant respiratory problem in all 10 cases. | \n3.4 years | \n
Previous publications on outcomes of various surgical techniques for peripheral nerve problems.
N/A, information not available; MPNSTs, malignant peripheral nerve sheath tumors; MRC, Medical Research Council; OBPI, obstetric brachial plexus injury.
Regarding tumors, Guha et al., in managing 201 peripheral nerve sheath lesions (182 benign and 19 malignant) in 175 patients over a 17-year period, observed that subtotal resection was associated with the increased recurrence of the benign lesions and that the probability of motor function worsening postoperatively was much less in patients in whom the tumors were fully resected [35]. They also observed that the extent of resection in those who had schwannoma was greatly influenced by tumor location, with lesions located in the extremities being more likely to be fully resected than plexal tumors that were brachial, thoracic, or lumbosacral [35]. This was likely due to better anatomical accessibility [35]. They concluded by suggesting gross total resection for all benign lesions as much as possible [35]. In our own strategy however, we similarly dissected the tumor in its subcapsular plane for PNSTs to ensure that non-involved fascicles remained functionally intact but observed no recurrence of the benign lesions in any of our patients whereas oncological resection and not subcapsular dissection was our goal for the malignant ones (MPNST) in view of the life-threatening nature of the pathology, even at the cost of functional compromise.
\nDetailed examination of these patients should be followed up by nerve conduction studies and radiological imaging to localize and characterize peripheral nerve lesions or associated neurologic injury [3, 5, 8, 22]. The appropriate imaging modalities for evaluation should be selected depending on the particular clinical circumstance [3, 5, 8]. Plain-film X-ray, computerized tomography myelogram (CT), magnetic resonance imaging (MRI), ultrasound (US), as well as positron emission tomography (PET) all have their various indications in the management of peripheral nerve problems [3, 40]. For instance, transverse process fractures of the cervical vertebrae on cervical spine x-rays might indicate root avulsion at the same level [3, 22] and a distal neurotization repair can be preoperatively decided upon. CT myelography can be used to define the level of nerve root injury preferably within 4 weeks of the injury [3, 22]. Ultrasound may be used in some selected situations for localizing peripheral nerve entrapment and for image guidance in percutaneous interventions [3, 10]. One imaging modality which is emerging as a useful tool in preoperative selection and planning of peripheral nerve surgery is the MR (magnetic resonance) neurogram [3, 15, 37]. Of all these modalities, MRI and CT myelogram are generally the main radiological investigations for diagnosis of problems involving the brachial plexus [3, 5, 9, 37, 40].
\nElectrodiagnostic studies are equally essential, particularly electromyography (EMG) and nerve conduction studies (NCS). For example, preservation of sensory nerve action potentials (SNAPs) in extensive brachial plexus injuries with severe motor deficits is highly indicative of preganglionic injury and root avulsion. Additionally, serial compound motor action potential (CMAP) studies at 6 week periods give the surgeon an estimate of the spontaneous recovery potential of an injury (i.e., the classical neuropraxia and axonotmesis injury versus neurotmesis patterns) [18, 25]. When the electrophysiology findings are combined with the longitudinal clinical evaluation of motor recovery, the surgeon can then better decide upon timing and extent of repair required.
\nIntra-operatively, the integrity of the donor nerve is a major determining factor for successful outcomes [13]. Single coaptation repair of a donor nerve to the recipient nerve (neurotization repair) without tension is generally considered superior to indirect repair with a cable graft, since only one microanastomosis is required [13, 45]. This is particularly important for weak donor nerves such as the spinal accessory nerve [13, 51]. According to functional priorities, elbow flexion and extension are generally the most important function to restore [19, 43]. Active shoulder control and stability is then considered next most important [50], followed by abduction, external rotation, wrist extension and scapular stabilization prioritized in that order [19]. Finally, managing each patient’s expectations is perhaps the most important part of pre-operative planning and preparation [19]. Patients must be made to understand the limits of the best possible outcome and the possibility that either no improvement at all or limited functional improvement may occur after surgery [19].
\nThe workhorse of brachial plexus repair surgery is still largely the neurotization transfers and nerve grafting [5, 6, 13, 17, 19, 23, 24, 29, 38, 42, 44, 48, 50, 51]. The muscles of the shoulder and the biceps brachii have classically been the main targets for repair of brachial plexus injuries [17, 29, 38, 48]. However, there is now more importance on equally focusing on restoring at least elbow extension for functionality and even newer attempts at selective reinnervation of the median nerve for prehensile hand function or pincer grip [33, 39, 42]. For proximal upper limb functions, the two most important distal transfers are neurotization of the suprascapular nerve with spinal accessory nerve through a posterior approach for shoulder abduction and Oberlin’s double fascicular transfer of ulnar and median nerve fascicles to the biceps and brachialis branches of the musculocutaneous nerve for elbow flexion [8, 19, 23, 24, 26, 31, 33, 38, 47]. Case series reports have demonstrated very low long term donor nerve functional impairment resulting from thoracoscopic full-length phrenic nerve harvest and transfers and contralateral C7 transfer [8, 12, 13, 19, 27, 28, 33, 43, 44]. Our experience with these two procedures was very similar. Microsurgical dorsal root entry zone lesioning (DREZ) has been used to effectively control the intractable pain that follows brachial plexus injuries, particularly for the refractory cases [7, 11].
\nFor treatment of cubital tunnel syndrome, the anterior transposition of ulnar nerve may be done in either the subcutaneous or the intramuscular plane [30]. In situ decompression of the ulnar nerve with or without medial epicondylectomy as an alternative technique has also been well described with its pros and cons [30]. For patients with Guyon’s canal syndrome, initial approach should be conservative care including immobilization, ergonomic modifications of habitual movement, and local injection of cortisone is advocated except for the refractory cases [2]. However, early motor involvement is common and one should then proceed to surgical decompression. At surgery, the skin incision should extend to both the wrist and palmar line, and the ulnar nerve and artery should be adequately freed at the level of the Guyon’s canal [2] (Figure 4A and B). Posterior interosseous nerve (PIN) entrapment creates a functionally disabling pure motor deficit. For PIN release, the nerve must first be identified proximally between brachioradialis and extensor carpi radialis longus and distally between extensor carpi radialis brevis and extensor digitalis communis at the point where it enters the supinator, and should also include adequate division of the compressive supinator fibers.
\nThe goal of surgical intervention in PNST is excision of the tumor to alleviate the symptoms caused by neural compression without incurring a sensorimotor deficit [14]. In MPNST, however, oncological resection is the goal given the life-threatening nature of the pathology, even at the cost of functional compromise. In such situations, nerve graft repair can be planned preoperatively. General, regional or local anesthesia may be used [14]. For general anesthesia, anesthetist must avoid the use of muscle relaxants since these agents would ultimately prevent the use of intraoperative stimulation and monitoring [14]. The limb should be exposed so as to monitor the distal muscle response to fascicular stimulation (Figure 3). The incision should be made over the involved portion of the nerve starting from 2 to 4 cm proximal to and extending 2 to 4 cm distal to the tumor [14]. The probability of malignant degeneration of a PNST to MPNST should be assessed preoperatively by (1) size, (2) presence and character of pain, (3) radiological criteria (MRI, PET), and (4) the presence of type 1 neurofibromatosis (which has a 20% propensity for MPNST). If suspicion of MPNST is low, a subcapsular enucleation of the tumor mass (usually schwannomatous) offers the best chance of gross total excision with relief of compressive symptoms and simultaneous functional preservation of the nerve fascicles. However, when any combination of these features indicate high suspicion of an MPNST, thorough preoperative planning and counseling should be done for nerve sacrifice to maintain oncologically complete resection and subsequent grafting repair. Oncologically speaking, the option of initial tumor biopsy for confirming the histology followed by total resection is not ideal since violation of soft tissue planes leads to a higher chance for adjacent tissue seeding of sarcomatous cells and even delayed distant recurrence. If a nerve graft was done, the limb should be immobilized with a splint for 2–3 weeks to allow for epineural healing without tension at the anastomosis [14]. Fortunately, the majority of peripheral nerve tumors are benign [14].
\nRehabilitation constitutes the remaining postoperative period until the patient achieves maximal functional and neurological recovery [49]. This can often be rather prolonged, and major depression related to extent of injury and surgery is a common factor that needs specific attention in order to improve outcomes. Once the concerned limb can be mobilized, the primary goals are prevention of contracture by passive ROM (range of motion) [41, 49]. This helps prevent complex regional pain syndrome (CRPS), and allows for a more useful limb once muscle reinnervation occurs. Within this time frame, orthotics is useful in preventing contractures at rest. This phase can extend up to 6–9 months post-operatively.
\nOnce a flicker of contraction was found in the concerned muscles, we began isolating and strengthening them with gravity initially, progressing to “against gravity,” and then with resistance. Once the patient could move against gravity, it was useful to add functional tasks into the exercise programme since motor coordination is as important as strength in recovery [41]. With this process, the patient would gradually develop “different” ways of doing old tasks to compensate for weakness of the primary effector muscle. This was achieved by utilizing the secondary effector muscles which changed the appearance of task performance. It remained with the physiotherapist to track recovery and see if these different ways were acceptable or not, followed by modification of the therapy plan as required. For example, the patient may develop “whip-like” movements to initiate shoulder abduction. If there was little hope of recovering deltoid function, then focusing on stabilizing the involved muscles above and below became more practical than utilizing electrical current to recover this muscle’s mass. If the chance of functional recovery was high, then training the concerned muscle to become activated at the correct time in the kinetic chain became more useful than just purely strengthening it. Once the reinnervation waiting period was over, one of three patterns would usually emerge: (1) the patient recovers function in the limb and uses it, (2) the nerve fails to reach and innervate the muscle, or (3) the reinnervation occurs but disuse would have reduced cortical representation and then, the patient may not know “how to” use the muscle. Electrophysiology was useful in differentiating such cases, and modifying the rehabilitation plan taken into consideration depending on which of these patterns was the case.
\nIn spite of a growing number of good surgical alternatives currently available such as introduction of phrenic nerve transfer to medial root of median nerve for prehensile hand function, the restoration of function below the elbow following either partial root avulsion or total root avulsion presently remains the biggest challenge in brachial plexus surgery [8, 13, 25, 33, 39, 42]. Avulsion injuries from C5 to T1 have been shown to be amenable to restoration of good shoulder and elbow function, but the restoration of satisfactory distal function is still yet to be well demonstrated [8]. However, new techniques to circumvent this problem have recently been proposed [39, 42]. For the obstetric brachial plexus injuries, another particular challenge is the restoration of abduction and external rotation in the shoulder joint [18] which is largely limited due to developmental apraxia which occurs at a cerebral level.
\nRegarding investigation and preoperative planning, EMG and nerve conduction studies have their own limitations [18, 25]. EMG itself only reflects the function of the individual motor units in a nerve and not really that of the entire nerve or the cerebral retraining required to establish function [25]. Also, in severe cases with a flail anesthetic arm, the absence of SNAPs often clearly indicates damage to post-ganglionic elements but cannot exclude a mixed lesion with associated root avulsion [18].
\nFurthermore, there are currently only limited algorithms to guide the surgeon on carrying out nerve transfers [13, 52]. The choice of which transfer to utilize in each case is largely dependent on each surgeon’s philosophy, knowledge and experience as well as patient-related factors, a clear understanding of the involved anatomy of the brachial plexus in each patient, what is uninjured and still viable for nerve transfer repair, as well as available facilities and equipment [8, 13, 52]. A combination of long and variable recovery periods, variable patterns of injury, individual patient recovery factors and lack of uniformity in rehabilitation all lead to the overall lack of objective evidence-based guidelines for management. For pediatric patients, the criteria and timing of surgical intervention also still remains controversial [4]. Some have used the absence of recovery of the biceps muscle or shoulder function by 3 months of age as the indication for surgery in obstetric brachial plexus injury (OBPI), while others use 4 months or even 9 months as the time limit [4, 32]. In our personal experience with managing 196 cases of Erb’s and Erb’s plus palsies, excellent recoveries were possible in majority of cases with a proper rehabilitation programme consisting of cerebral retraining and judicious management of co-contracture deformities. Some would argue that deformities are less common with early nerve repair in OBPI, but this is yet to be proven definitively.
\nFinally, even though microsurgical repair of nerve injuries has advanced significantly over time, satisfactory functional recovery still remains a challenge [29]. The ultimate goal of a nerve repair should be a functional improvement that creates satisfaction for the patient in his or her daily activities and occupation and not simple improvement in the muscle power grading. This requires dedicated efforts in physical, psychological and vocational rehabilitation. Augmentation of the paralyzed limb using reanimative muscle or tendon transfer surgeries by the plastic surgeon often improves outcomes. Hence, a multidisciplinary team is ideal.
\nIn this chapter, we have described the pattern and trend of peripheral nerve problems in our practice, and presented our challenges and outcomes, as well as the steps we followed to organize our peripheral nerve unit, followed by a review of general guidelines and principles of care. Peripheral nerves related problems, are unfortunately only palliated in most developing countries across the world. Although our experience in surgically treating these problems is still developing and with the few limitations as presented, the final outcomes demonstrate that surgical intervention is still better than just palliative measures alone or even nothing at all. We could still manage the problems successfully with fairly good outcomes despite few setbacks such as late presentation of patients, as well as unavailability of full investigative imaging modalities required as standard pre-operative evaluation for peripheral nerve problems. We are hopeful that this brief presentation would be a useful impetus for the introduction, development and implementation of nerve surgery programmes in other developing countries around the world.
\nThe authors declare that they have no competing interests.
None.
\nThis is a brief overview of the main steps involved in publishing with IntechOpen Compacts, Monographs and Edited Books. Once you submit your proposal you will be appointed a Author Service Manager who will be your single point of contact and lead you through all the described steps below.
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\n\nPlease complete the publishing proposal form. The completed form should serve as an overview of your future Compacts, Monograph or Edited Book. Once submitted, your publishing proposal will be sent for evaluation, and a notice of acceptance or rejection will be sent within 10 to 30 working days from the date of submission.
\n\n2. SUBMIT YOUR MANUSCRIPT
\n\nAfter approval, you will proceed in submitting your full-length manuscript. 50-130 pages for compacts, 130-500 for Monographs & Edited Books.Your full-length manuscript must follow IntechOpen's Author Guidelines and comply with our publishing rules. Once the manuscript is submitted, but before it is forwarded for peer review, it will be screened for plagiarism.
\n\n3. PEER REVIEW RESULTS
\n\nExternal reviewers will evaluate your manuscript and provide you with their feedback. You may be asked to revise your draft, or parts of your draft, provide additional information and make any other necessary changes according to their comments and suggestions.
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\n\nIf the manuscript is formally accepted after peer review you will receive a formal Notice of Acceptance, and a price quote.
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\n\nWe will send you your price quote and after it has been accepted (by both the author and the publisher), both parties will sign a Statement of Work binding them to adhere to the agreed upon terms.
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\n\nIf you feel that IntechOpen Compacts, Monographs or Edited Books are the right publishing format for your work, please fill out the publishing proposal form. For any specific queries related to the publishing process, or IntechOpen Compacts, Monographs & Edited Books in general, please contact us at book.department@intechopen.com
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Focus of his research activity is drug delivery, physico-chemical characterization and biological evaluation of biopolymers micro and nanoparticles as modified drug delivery system, and colloidal drug carriers (liposomes, nanoparticles etc.).",institutionString:null,institution:{name:"Marmara University",country:{name:"Turkey"}}},{id:"61051",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"100762",title:"Prof.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"St David's Medical Center",country:{name:"United States of America"}}},{id:"107416",title:"Dr.",name:"Andrea",middleName:null,surname:"Natale",slug:"andrea-natale",fullName:"Andrea Natale",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Texas Cardiac Arrhythmia",country:{name:"United States of America"}}},{id:"64434",title:"Dr.",name:"Angkoon",middleName:null,surname:"Phinyomark",slug:"angkoon-phinyomark",fullName:"Angkoon Phinyomark",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/64434/images/2619_n.jpg",biography:"My name is Angkoon Phinyomark. I received a B.Eng. degree in Computer Engineering with First Class Honors in 2008 from Prince of Songkla University, Songkhla, Thailand, where I received a Ph.D. degree in Electrical Engineering. My research interests are primarily in the area of biomedical signal processing and classification notably EMG (electromyography signal), EOG (electrooculography signal), and EEG (electroencephalography signal), image analysis notably breast cancer analysis and optical coherence tomography, and rehabilitation engineering. I became a student member of IEEE in 2008. During October 2011-March 2012, I had worked at School of Computer Science and Electronic Engineering, University of Essex, Colchester, Essex, United Kingdom. In addition, during a B.Eng. I had been a visiting research student at Faculty of Computer Science, University of Murcia, Murcia, Spain for three months.\n\nI have published over 40 papers during 5 years in refereed journals, books, and conference proceedings in the areas of electro-physiological signals processing and classification, notably EMG and EOG signals, fractal analysis, wavelet analysis, texture analysis, feature extraction and machine learning algorithms, and assistive and rehabilitative devices. I have several computer programming language certificates, i.e. Sun Certified Programmer for the Java 2 Platform 1.4 (SCJP), Microsoft Certified Professional Developer, Web Developer (MCPD), Microsoft Certified Technology Specialist, .NET Framework 2.0 Web (MCTS). 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