Characteristics of platelet-rich plasma US-guided infiltrations for different nerves.
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"9165",leadTitle:null,fullTitle:"Polycystic Ovarian Syndrome",title:"Polycystic Ovarian Syndrome",subtitle:null,reviewType:"peer-reviewed",abstract:"This book includes two sections: Clinical Features, and Basic Research of Polycystic Ovary Syndrome (PCOS). 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Lembrikov is a senior lecturer at the Faculty of Electronics, Electrical and Communication Engineering of the Holon Institute of Technology (HIT), Holon, Israel. B. I. Lembrikov received his Ph.D. in Nonlinear Optics at the Technion – Israel Institute of Technology in 1996. Since then he was an invited researcher at the Haifa University, at the Max Planck Institute High Magnetic Field Laboratory at Grenoble, France, at the Technion, Haifa, Israel. Dr. B. I. Lembrikov is an author of the book \\Electrodynamics of Magnetoactive Media\\, a number of chapters in scientific books, a large number of papers in international peer reviewed journals and reports delivered at the international scientific conferences. He actively participated in a number of research projects concerning optics of nanoparticles, optical communications, UWB communications. The main research fields of interest of Dr. B. I. 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Some options to treat these damages are oral drugs, steroid injections, physical therapy or surgical interventions. Probably, nerve autografts or direct tension-free microsurgical repairs are the most common treatments aimed to enhance the intrinsic regenerative potential of injured axons. However, they do not recreate the suitable cellular and molecular microenvironment of peripheral nerve repair.
\nTo overcome this drawback, new therapeutic strategies have been developed for these conditions, using various models of nerve injuries. In vitro models of neuronal survival include cell cultures or tissue engineering advances, whereas in vivo models involve lesions in peripheral nerves of many species. These studies lead to develop new strategies based on tissue engineering approaches through molecular intervention and scaffolding, and platelet-rich plasma (PRP) represents one of these promising biological strategies. Large number of studies provides evidence for PRP application in musculoskeletal disorders and orthopedics. Applications include treatments of chondropathy, osteoarthritis, tendinopathy, muscle or ligament tear, acute and chronic soft tissue injuries, as well as enhancement of healing after bone or tissue reconstruction [1]. In addition to its positive effects on the healing of many types of tissues, recent studies reported the promising effects of PRP on nerve regeneration [2]. Indeed, several preclinical and clinical studies have proved the neuroprotective, neurogenic and neuroinflammatory properties of this therapy. Moreover, pain reduction, function improvement and nerve-muscle unit recovery have been demonstrated after applying diverse PRP formulations including liquid and scaffold form. This chapter is intended to overview the advances made on this specific field, focusing on the concept of PRP, its biological effects on nerve repair and its clinical application.
\nPRP is an autologous product with a higher platelet concentration than in blood. It consists of a pool of bioactive mediators including growth factors (GF), cytokines, microparticles and others from patient’s own blood. Currently, there are several methods and commercial devices to achieve PRP, obtaining a diversity of products including autologous conditioned plasma, platelet-enriched plasma, platelet-rich concentrate, autogenous platelet gel, platelet releasate, platelet rich in GFs and others [3]. Some parameters and characteristics such as platelet concentration, the presence of leucocytes or the fibrin architecture may vary depending on the method or device employed to obtain these refined products. The processing technique to achieve PRP mostly consists of a blood collection in the presence of an anticoagulant followed by centrifugation. This centrifugation separates the blood components with the aim of discarding substances considered as not usable such as red blood cells and concentrating the elements with therapeutic potential, for instance fibrinogen/fibrin, platelets or GF, with or without leukocytes (Figure 1). Before its administration, an activating factor such as thrombin or calcium is added to the platelet concentrate to promote platelet degranulation and exocytosis of the factors stored in the cytoplasmic granules [4].
\nPlatelet-rich plasma formulation. After withdrawing a small volume of venous blood in tubes containing anticoagulant, these are centrifuged in order to separate the blood components. The plasma fraction located just above the red blood cells is collected including or not leukocytes. PRP is activated adding thrombin or calcium to promote platelet degranulation and exocytosis of GF. This liquid formulation is used to conduct PRP injections. If after activation, the waiting time is prolonged, fibrin formation is achieved, obtaining a scaffold for applying in surgery.
Indeed, the potential effect of PRP is closely related with the release of bioactive molecules stored in alpha granules of platelets after its activation with the activating factor [5]. Platelet-derived growth factor (PDGF), transforming growth factor (TGF-β), epidermal growth factor (EGF), insulin-like growth factor (IGF-1), hepatocyte growth factor (HGF), basic fibroblasts growth factor (FGF) and vascular endothelial growth factor (VEGF) are some of the key proteins associated with the acceleration of healing process, since they modulate angiogenesis, remodel the extracellular matrix (ECM) and affect the recruitment, proliferation and differentiation of stem cells [6]. The wide variety of elements found in platelet granules act synergistically under normal physiological conditions on local cells to promote wound healing. On the other hand, plasma activation also promotes the polymerization of fibrinogen into a three-dimensional fibrin scaffold (Figure 1), maintaining the bioactive mediators trapped through fibrin heparin sulfate-binding domains [1]. This biocompatible and biodegradable scaffold provides plastic-elastic stiffness and generates GF gradients that are essential cues for cell proliferation, differentiation, migration and correct orientation in the nascent tissue [7]. When fibrinolysis begins, a gradual, sustained release of GF and other biomolecules occurs, in contrast to a bolus delivery modality. Thus, this technology provides a fibrin scaffold as a controlled drug delivery system of GF suitable for regenerative medicine [8].
\nDue to its primarily autologous origin and relatively noninvasive collection technique, the risks of injection or immune rejection associated with PRP are minimized, making this biological therapy a powerful tool for its application on diverse medical fields. Thus, this strategy has been employed as a biological adjuvant in peripheral nerve injuries and neuropathies, enhancing the sensory and motor functional nerve-muscle unit recovery [9]. In cases of nontraumatic peripheral injuries such as compression, adhesion and/or fibrotic postsurgical side effects, PRP may help diminish undesirable consequences such as denervated organ atrophy and fibrotic scars.
\nAmong therapeutic alternatives to restore damaged nerves, PRP is gaining attention, since it provides the infiltrated environment with a pool of GF inducing healing and regeneration of the tissue. Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and PDGF are some of PRP components that can improve nerve regeneration. However, a sustained delivery of several GFs is not the unique constituent of PRP effect on nerve regeneration. Indeed, in vitro and in vivo evidence suggests that the biomolecules transmitted by PRP are instrumental agents that act as key drivers of full nerve functional recovery, offering a new possibility for nerve regeneration (Figure 2).
\nEffects of PRP on nerve repair. Biomolecules and GF participate jointly and synergistically in several biological processes involved in nerve regeneration.
An important factor that plays a critical role in many functions within the nervous system including neurogenesis and neuroprotective function is BDNF. One of the most important benefits that this biomolecule offers is its ability to inhibit neuronal and glial apoptosis after traumatic injury. A work carried out by Koda et al. proved that BDNF suppressed in a dose-dependent manner anoikis of Schwann cells (SC), which are able to promote axonal regeneration and functional recovery [10]. This effect is based on the activation or transdifferentiation of SCs, a drastic modification of the phenotype of this cell type that takes place after the disruption of the regeneration unit by the noxious agent. Macrophages will collaborate with the activated SCs clearing the myelin and other tissue debris. Moreover, these SCs come into direct contact with resident fibroblasts accumulated in large numbers at the site of injury, influencing SC migration and transdifferentiation. In another work, Wang et al. found that mesenchymal stem cells (MSCs) transfected with Ad-BDNF enhance the expression of BDNF, recovering brain damage. They suggest that BDNF-MSCs have a potential protective effect against neuron death by apoptosis [11]. In another study, Zurita et al. enriched PRP fibrin scaffolds with bone marrow stromal cells with BDNF, NGF and retinoic acid, enhancing cell survival and differentiation into the neural phenotype [12]. Another GF related with neuronal and Schwann cell survival is IGF-1. This factor acts as neurotrophic factor for sensory, motor and sympathetic neurons to promote growth cone motility and prevent apoptosis [13]. It has also been proved that neurons express PDGF receptors, and the function related with this GF on nerve injury also involves the survival for Schwann cells with trophic activity on neurons [14]. Other substances such as NGF, FGF, VEGF and TGF-β presented in PRP have shown to exert an antiapoptotic and neuroprotective effect on diverse cell types such as MSCs, neurons, Schwann cells and human neural stem cells [15].
\nAnti-inflammatory action of PRP is associated with an inhibition of nuclear transcription factor-kB (NF-kB) pathway, which was observed after culturing astrocytes with PRP supernatants [16]. Some of the GFs such as HGF, IGF-1, PDGF and TGF-β delivered in a sustained way after PRP infiltrations are closely related with these effects [15]. TGF-β also affects cellular behavior, the neurite outgrowth and glial scar formation [17]. Outcomes from an in vivo study further suggested that TGF-β coordinated with adipose-derived MSCs enhanced nerve regeneration affecting the host’s immune response and reducing inflammation [15].
\nPRP injections have been associated with a decrease of proinflammatory substances such as nitric oxide, cyclooxygenase and tumor necrosis factor expressed in the brain [16]. In addition, PRP is able to block Ab-induced upregulation of proinflammatory cytokine production, and this capacity was correlated with a prevention of the decrease in several synaptic proteins.
\nAmong the substances that PRP contains, VEGF is one of the most angiogenic factors. It stimulates proliferation and migration of endothelial cells, formation of new blood vessels and enhances vascular permeability. This action is conducted by transmembrane receptors found in neural tissue, especially on growth cones of sprouting axons and Schwann cells [18]. VEGF can act as a neurotrophic factor by promoting Schwann cell proliferation and neurite outgrowth and enhance nerve survival [19]. However, despite the evidence that PRP promotes angiogenesis in tendon, muscle and bone and the crucial role that blood vessels play as trackers of the axonal growth cones across the injury site, there is lack of studies assessing angiogenesis in nerve repair. Borselli et al. showed that an injectable scaffold loaded with VEGF and IGF-1 accelerated regeneration of damaged neuromuscular junction innervation together with an enhancement of angiogenesis in an ischemic limb rodent model [20]. Another study demonstrated that vein graft filled with PRP provides an earlier and more prominent neoangiogenesis than sciatic nerve gaps treated with nerve autograft alone [21]. The fibrin obtained after PRP activation provides a permissive and robust 3D matrix for angiogenesis. In fact, autologous fibrin matrix is the best tailored transient scaffold for tissue regeneration where complex morphogenetic processes for tissue regeneration take place, including angiogenesis, cell migration and proliferation [22].
\nSchwann cells provide bioactive substrates for axonal migration and they release neurotrophic factors able to regulate axonal outgrowth. An optimal proliferation and viability may affect the rapid regeneration of injured peripheral nerves. PRP might allow the sprouting of growth cones since they promote survival, proliferation and differentiation of Schwann cells. In that sense, Zheng et al. showed a dose-dependent effect of PRP on the proliferation, migration and neurotrophic function in rat Schwann cells cultured with PRP [23]. The significant role played by GF within the PRP has also been highlighted in a rat brain-spinal cord cocultured system, where the addition of PRP supernatant promoted an increase in the size and number of axons. This positive effect was significantly suppressed by the addition of antibodies against IGF-1 and VEGF [24].
\nSolid form of PRP also demonstrated its positive effect on both axonal myelination and its density enhancement. Ye et al. fabricated tissue-engineered nerves based on poly (lactic-co-glycolic acid) conduit using PRP gel for suspension of Schwann cell–like cells. PRP group presented superior functionality in both nerve conduction velocity and compound muscle action potential. They suggest that PRP gel plays a dual role: first, the fibrin network as matrix for regenerative cell incorporation, and second, biomolecules that improve the biological environment stimulating the regenerative processes of nerve fibers [25]. Indeed, the PRP bioactive proteins initiate and control the healing cascade of nerve fibers. Increasing the concentration of these bioactive proteins such as TGF-β, PDGF and IGF-1 could accelerate healing of the regenerating nerve fibers [26]. Other studies realized in rabbits after implantation of PRP together with Schwann cells [27] reported beneficial effects on axonal counts, myelination and electrophysiological parameters. Cho et al. observed considerably increased expression of neurotrophic factors such as BDNF, NGF, FGF and Glial cell–derived neurotrophic factor (GDNF) after PRP injection in guinea pigs with facial nerve transection, suggesting that PRP and MSCs act as a source of neurotrophic factors. They also could prove an enhancement of axon counts and myelination in the groups treated with PRP [27]. An inside-out vein autograft filled with PRP was used to bridge a 10-mm-long sciatic nerve defect in rats [21]. The axon diameter, the number of myelinated axons and myelin sheath were significantly superior when vein autograph was filled with PRP. In another rat model, they used platelet-rich fibrin (PRF) as a filler of silicon nerve guidance. Animals treated with PRP improved functional recovery and showed a superior sciatic functional index compared to nontreated animals [28].
\nThe acceleration of axonal growth can prevent muscle atrophy, since it reduces the time to establish a connection between the sprouting axon and target muscle [29]. PRP applications induce an earlier axonal regeneration and functional recovery, which also can have a consequence reducing the target muscle atrophy. In the work carried out by Sánchez et al., they could observe this positive effect since nerves repaired with intraneural infiltrations of PRP were associated with lower muscle atrophy and an earlier electrophysiological recovery [30]. In some peripheral nerve injuries such as carpal tunnel syndrome or fibrotic postsurgical side effects, the main pathological agent is compression, adhesion and/or fibrosis. The use of PRP may additionally avoid or at least diminish denervated organ atrophy and undesirable fibrotic scars, thereby accelerating the functional recovery of the nerve-muscle unit, due to its antifibrotic effects [24, 31]. Intramuscular injection of PRP 24 hours after the induction of limb ischemia in mice mitigated fibrosis and muscle atrophy [32]. These results are in agreement with the reduction of atrophy in denervated muscle reported when muscle was infiltrated with cells [33], effects suggested to be mediated by IGF-1 [34].
\nAlthough the biological effects described previously mean a promising therapeutic tool, the success to achieve optimal clinical results lies in several factors such as PRP preparation, dosage and application protocols.
\nPhysicians face a large number of systems to obtain PRP and therefore different types of final products. These depend on variables such as platelet concentration, the presence or absence of leukocytes and the exogenous activation of PRP. Although there is still no consensus on which is the best product to use in orthopedic pathologies, according to preclinical research and our experience, we suggest choosing a product with specific characteristics.
\nAn excessive number of platelets could not only suppress the therapeutic action of PRP but also inhibit the tissue repair process. PRP with excess platelet concentration had negative influence over cellular responses such as proliferation, viability or differentiation [35]. Thus, it seems that a concentration of platelet slightly higher than blood is suitable to achieve an optimal response. The presence of leukocytes in PRP products is more controversial. While in tissues like cartilage the scale tips in favor of the PRP without leukocytes, in other applications, it is not clear. The presence of leukocytes fosters the nuclear NF-κB p65 protein expression, which is key in the activation of cellular inflammation, and oddly enough, it is inhibited by PRP [36]. Finally, and although platelets within PRP can be activated endogenously by tissue collagen, we recommend the previous activation in an exogenous way, which is carried out by adding calcium to PRP. As calcium was chelated during blood extraction to avoid coagulation, we restore the levels of it in PRP preventing hypocalcemia in nerve environment during infiltration. The activation triggers the formation of a fibrin 3D liquid scaffold that spreads over the tissue, delivering GF in a control manner. After activation, PRP must be injected immediately during the following 10 minutes. Without activating, it can be stored for 3–4 hours without losing its efficacy. PRP can be applied also as a fibrin scaffold for using in surgery. This scaffold is obtained in the same way as the liquid formulation, except that after its activation, the waiting time before its use is prolonged until the formation of the fibrin scaffold (Figure 1). Despite these recommendations, it is in the hands of the professional who applies PRP to choose the best suitable type, and following the manufacturer’s protocol is advisable to obtain an optimal product.
\nIn order to achieve the biological effects described in Section 3, PRP must be administered in an adequate manner to reach the target tissue and cells that are key elements in nerve repair process such as Schwann cells. However, they are in the innermost compartment of the nerve, inside the fascicles that enclose the axons covered by the myelin sheaths, and getting to them is a major issue. For many years, nerve infiltration has been and still is a controversial point for physicians and medical specialists. Although a possible cause of nerve lesions during an injection is the ischemic damage due to increased pressure inside the nerve, the most likely reason is the neurotoxicity of the injected drug such as corticosteroids or local anesthetics. Several studies demonstrated that the injuries caused to the nerve after infiltrations were because of the injected drug or its dose, and not because of the physical act of infiltrating [37].
\nThe compartment of the nerve where the injection is performed is also a sensitive point to consider. Although some studies recommend avoiding intraneural injection due to high risk of nerve lesion [38], it is necessary to be more precise in this description. We must distinguish between extrafascicular and intrafascicular injection, the former being safe and without any evidence of nerve injury [39]. In contrast, some studies conclude that the main cause of neurologic injury is the intrafascicular injections [40]. Brierley et al. studied the progression of nerve lesions in some diseases like tetanus or poliomyelitis using radioactive phosphorus. He found that the phosphorus reached the blood stream, the cerebrospinal fluid and the nervous system when the needle penetrated into the fasciculus, thus being an intrafascicular injection [41]. Diffusion studies of PRP into the nerve carried out by our group showed that PRP previously stained with methylene blue was accumulated around the perineurium after intraneural but not intrafascicular injections, without reaching inside the fascicle through the perineurium [2] (Figure 3).
\nNerve infiltration. During the procedure, two injections are conducted. First, intraneural infiltration (A) reaches the intrafascicular epineurium (2) and next, the perineural infiltration (B) is performed around the nerve. 1 = epineurium; 2 = intrafascicular epineurium; 3 = perineurium; 4 = fascicle; 5 = endoneurium; 6 = axon covered by myelin.
Throughout this section, we will describe the procedures to perform US-guided infiltrations of PRP in some nerves susceptible to peripheral lesions, namely median nerve (Figure 4), ulnar nerve (Figure 5) and common peroneal nerve (Figure 6). The infiltrations of the nerves mentioned in this section share a large number of key points, which are described below. The details of each nerve are shown in Table 1.
\nMedian nerve infiltration. The median nerve is located by means of US in the area of the wrist (A). Under US control with the probe placed in long-axis, the nerve (blue) is observed above the epiphyses of the distal radius (red) and lunate bone (white) (B). The needle (green) is inserted in distal-proximal direction, and PRP is injected in an intraneural (yellow) and perineural way (asterisk) (C).
Ulnar nerve infiltration. The ulnar nerve is located by means of US in the area of the elbow (A). Under US control with the probe placed in long-axis, the nerve (blue) is observed above the epicondyle (white) (B). The needle (green) is inserted in distal-proximal direction, and PRP is injected in an intraneural (yellow) and perineural way (asterisk) (C). In this case, the injection could be conducted in proximal-distal direction if the access is difficult.
Common peroneal nerve infiltration. Two approaches are possible to infiltrate common peroneal nerve. In the first approach, the nerve (blue) is located by US above the popliteal fossa with the US transductor in the long axis (A and B). In the second approach, the nerve is located in the lateral side of the knee (D). With the probe placed in the short axis, the nerve (blue) is observed above the peroneal head (white) and close to tibialis anterior muscle (red) (E). In both cases, the needle (green) is inserted in proximal-distal direction, injecting PRP in an intraneural (yellow) and perineural way (asterisk) (C and F).
\n | Median nerve | \nUlnar nerve | \nCommon peroneal nerve | \n|
---|---|---|---|---|
Approach 1 | \nApproach 2 | \n|||
Indication | \nCompressive neuropathies such as CTS | \nCompressive neuropathies such as UTS | \nNerve lesions associated to knee injuries | \n|
Patient position | \nSitting with the arm flexed and supported on flat surface | \nSupine position | \nProne position | \nLateral position over the healthy side | \n
Limb position | \nSupination, the palm of the hand facing upward | \nPronation, with the elbow lightly flexed and on a padded support | \nExtended leg | \nLightly knee flexion and on a padded support | \n
Infiltration area | \nWrist, around the distal area of the radius | \nBehind medial epicondyle, into cubital tunnel | \nBack of the thigh, around the popliteal fossa above the knee | \nLateral knee area around the peroneal head | \n
Syringe | \nLuer-Lok, 3 mL | \nLuer-Lok, 3 mL | \nLuer-Lok, 5 mL | \nLuer-Lok, 5 mL | \n
Needle | \n23 G/25 mm | \n23 G/25 mm | \n21 G/50 mm | \n21 G/50 mm | \n
Direction | \nProximal-distal | \nBoth | \nProximal-distal | \nProximal-distal | \n
Intraneural vol. | \n2 mL | \n3 mL | \n3 mL | \n3 mL | \n
Perineural vol. | \n4 mL | \n6 mL | \n6 mL | \n6 mL | \n
Characteristics of platelet-rich plasma US-guided infiltrations for different nerves.
CTS, carpal tunnel syndrome; UTS, ulnar tunnel syndrome; Vol, volume.
\n
Preparation of the sterile field is required to maintain aseptic conditions throughout the treatment. The skin covering the affected nerve and the transducer of the US machine must be prepared following standard asepsis protocols.
Prior to the infiltrations, the nerve must be located by means of US in the pertinent areas. During this step, the US probe can be used in a long- as well as short-axis in respect to the nerve so that its examination can be as accurate as possible.
In the course of PRP injections, the needle is placed parallel to the US probe, and consequently its orientation in respect to the nerve has influence on the PRP diffusion. With the transductor in the long-axis in respect to the nerve, the needle is introduced almost parallel to it, spreading PRP along the nerve. If the US probe is placed in the short-axis, the needle is inserted at right angles to the nerve increasing the risk of injury axon. The spread is less than in the previous case, especially when the diameter of the nerve is large. However, this approach allows better visualization of the tissue. Therefore, we recommend using the US transductor that achieves a balance between diffusion and nerve visualization.
The proximal-distal direction is preferable so that PRP spreads through the nerve. In some cases as injections into ulnar nerve, the direction can also be from distal to proximal zone if the injured area is unapproachable.
Both intraneural and perineural injections are performed during the treatment. Activated PRP is injected softly and without rough movements of the needle to prevent nerve damage. As the PRP volume required for both infiltrations can exceed the capacity of the syringe, changes of syringes for loading them with PRP can be done without removing the needle from the injection site, thus avoiding repeated punctures.
Firstly, it is advisable to perform the intraneural infiltration with the needle reaching the intrafascicular epineurium of the nerve. During intraneural injection, PRP shows some hyperechoic signals under US control within the nerve.
Once intraneural injection is accomplished, the needle is gently retreated placing it just above the nerve to conduct the perineural injection around the nerve. The adjacent tissue to the nerve is detached when perineural infiltration is performed, appearing as a hypoechoic signal. This infiltration entails a hydrodissection that reduces nerve entrapment through a mechanical effect [42].
The dosage of these treatments is determined by the nerve size to be infiltrated, which is detailed in each case (Table 1). In all cases, it is recommended to carry out two treatments, with an interval of two between both visits.
The follow-up is conducted 4 weeks after finishing the treatment. Clinical examination is required in order to observe improvement in clinical parameters such as pain and paresthesia. Depending on the patient’s condition, we will follow different recommendation:
If the patient shows a significant improvement, no intervention will be performed. Six weeks after clinical follow-up, an electromyography (EMG) will be conducted to evaluate the state of the nerve and assess possible actions.
When the patient evolution has flat-lined or is not enough, neural infiltrations with PRP will be repeated again.
In case the patient has not experienced any improvement, infiltrations of PRP will be discarded and other treatment alternatives will be considered. An EMG study should be performed in the third month.
\n
PRP infiltrations into this nerve are indicated for compressive neuropathies such as pyramidal syndrome or deep gluteal syndrome.
The patient is placed as in the case of the sciatic nerve approach, namely in prone decubitus on a flat surface.
By means of US control, the nerve is located at the level popliteal fossa, and then the nerve path is followed until gluteal fold, where PRP injection in distal-proximal direction is conducted. If the nerve can be located in a more proximal area, the infiltration can also be performed following the proximal-distal direction.
The injection is conducted with 10 mL in a syringe fitted with an 18 G and 75 mm needle and US probe placed in the long axis.
Four ml of activated PRP is administered during intraneural infiltration and 8 mL of activated PRP is infiltrated around the nerve.
Traumatic neuroma follows different forms of nerve injury often as a result of surgery. They occur at the end of injured nerve fibers as a form of ineffective, unregulated nerve regeneration. Due to the peculiarities of these neuropathies, the volume of the product, the type of syringes and needles to infiltrate the PRP will largely depend on the nerve where the neuroma is located, which was described above. In addition, not only an intraneural and a perineural injection into neuroma are conducted but also in the proximal nerve close to the neuroma.
\nIn many cases, surgical interventions are required for the treatment of neuropathies. Among these, the neurolysis is a standard procedure to separate the nerve from the surrounding tissues and try to solve problems related to compression and entrapment. In these cases, the use of PRP as a therapeutic adjuvant during surgery can stimulate and accelerate nerve recovery. Next, both endoscopic (Figure 7) and open neurolysis (Figure 8) of a median nerve are explained. Neurolysis in other nerves will be done in the same way but adapting to the particularities of each nerve.
\nEndoscopic neurolysis of median nerve. Endoscopic camera and cannula are introduced into the wrist (A). Carpal ligament (asterisk) is dissected and cut (B). PRP is infiltrated into the nerve (C) and a fibrin clot is placed between the nerve and the ligament (D).
Open neurolysis of median nerve. Median nerve and the transverse carpal ligament are observed after incision (A). Once median nerve is released, PRP is injected (B). Finally, fibrin membrane (C) is placed between the nerve and the ligament (D).
\n
After performing a small incision at the level of wrist crease, a cannula is introduced in order to observe structures in the wrist as the transverse carpal ligament with an endoscopic camera.
When the transverse carpal ligament is located and dissected, it is cut with endoscopic knife so that the median nerve is released.
Once the ligament is sectioned and nerve released, 2 mL of PRP is infiltrated into the nerve from the incision made for arthroscopy with a 30 G needle. A fibrin clot is placed in the open carpal tunnel before suturing.
\n
An incision at the level of wrist crease is conducted. The incision must be large enough to observe and access to the median nerve and the transverse carpal ligament.
Next, the median nerve and the transverse carpal ligament are located and dissected. During the surgery, the median nerve is released by cutting the transverse carpal ligament and removing all the adhesions present along the nerve.
Finally, intraneural and perineural injections of PRP are performed. In addition, a fibrin membrane is placed between the nerve and the ligament, to later suture the incision.
PRP products present a number of features that are quickening the application of this therapy in clinical practice, namely ease of use, reasonable biosafety and great versatility. Therefore, and although the PRP is still a recent technique, several clinical studies have emerging in the last decade (Table 2).
\nReference | \nCondition | \nTarget | \nIntervention | \nImprovement | \n
---|---|---|---|---|
Infiltrations | \n||||
[43] | \nCTS | \nMN | \nUS-guided perineural injection (1 × 1–2 mL) | \nPain and function | \n
[44] | \nCTS | \nMN | \nPerineural injection (1 × 2 mL) | \nPain and function | \n
[45] | \nLeprosy peripheral neuropathy | \nPTN and UN | \nPerineural injection (1 × 1 mL) | \nPain | \n
[46] | \nCTS | \nMN | \nUS-guided perineural injection (1 × 1–2 mL) | \nFunction | \n
[47] | \nPerinatal cerebral palsy | \nSystemic | \nIntravenous injection (1 × 25 mL) | \nFunction | \n
[48] | \nCTS | \nMN | \nInjection at the distal carpal crease (1 × 1 mL) | \nPain, function and EMG | \n
[49] | \nCTS | \nMN | \nUS-guided perineural injection (1 × 3 mL) | \nPain, function and EMG | \n
[50] | \nCPN palsy | \nCPN | \nUS-guided intraneural/perineural infiltrations (13 × 3–8 mL) | \nPain, function and EMG | \n
[51] | \nCTS | \nMN | \nUS-guided perineural injection (2 × 5 mL) | \nPain, function and EMG | \n
[52] | \nSection of RN | \nRN | \nUS-guided intraneural injections (5 × 4 mL) | \nFunction and EMG | \n
Surgery | \n||||
[53] | \nNerve gaps in extremities | \nNerves of the extremities | \nNerve gap bridged with a collagen tube with PRP fibrin | \nFunction | \n
[54] | \nPersistent pudendal neuralgia | \nPN | \nInjection after a transgluteal decompression | \nFunction | \n
[55] | \nBenign parotid gland tumor with facial muscles and nerve deficit | \nFN | \nPRP gel was applied around nerve endings during superficial parotidectomy | \nFunction | \n
Clinical research of PRP application for peripheral nerve injury.
CPN, common peroneal nerve; CTS, carpal tunnel syndrome; EMG, electromyography; FN, facial nerve; MN, median nerve; PRP, platelet-rich plasma; PTN, posterior tibial nerve; RN, radial nerve; UN, ulnar nerve; US, ultrasound.
As in other pathologies, pain is one of the main problems of patients who suffer from peripheral nerve injuries. PRP showed to be a promising therapeutic tool for the relief or reduction of pain associated with neuropathies. Malahias et al. conducted a case series study where patients who suffered from carpal tunnel syndrome (CTS) were treated with one PRP US-guided injection around the median nerve [43]. At 3 months of follow-up, the pain was significantly alleviated in 11 out of 14 patients according to VAS score. A prospective controlled study carried out by Uzun et al. demonstrated the effectiveness of PRP in reducing the pain associated with CTS after one perineural injection of 2 mL of PRP [44]. These kinds of interventions were conducted not only over the median nerve but also over the ulnar nerve. Patients with peripheral neuropathy associated to leprosy received a perineural injection of 1 mL of PRP in the posterior tibial nerves and in the ulnar nerve. The results of this randomized control clinical trial showed a pain decrease 2 weeks after treatment [45].
\nThese results are also accompanied by a functional and clinical improvement, which has a positive impact on the quality of life of patients. Some of the patients mentioned above showed functional recovery together with reduction in pain [42, 43]. More clinical studies also showed improvement in clinical and functional symptomatology when applying PRP in different peripheral nerve lesions. Recently, a randomized clinical study demonstrated better functional outcomes in patients with mild to moderate CTS [46]. Patients who received one US-guided infiltration of PRP into the carpal tunnel achieved a better response that patients treated with saline 12 weeks after treatment. However, in this study, no differences in pain scores were found. A case report that described a 6-year-old boy with perinatal cerebral palsy should be noted [49]. After receiving an intravenous injection of 25 mL of PRP, an improvement in the cognitive sphere and language during the follow-up at 3 and 6 months was observed. Levels of GF maintained stable in plasma 3–5 times higher than average for his age group.
\nIt must be taken into consideration that some variables may have a certain subjective component or be influenced by other factors than the treatment administered. Thus, it is advisable to analyze more objective variables such as EMG. A randomized controlled study showed improvement in EMG parameters, such as sensory nerve action potential (SNAP) in CTS patients [48]. However, there were no differences between control group (splint) and PRP treatment. This could be because the infiltration performed in this study was conducted without US guidance or directly into the median nerve but in adjacent areas, hampering the biological effects of PRP on the nervous tissue. Wu et al. carried out other randomized controlled study of CTS patients achieving an enhancement in sensory nerve conduction velocity (SNCV) and distal motor latency (DML) [49]. Although these EMG values were not significantly better than control group, there were significant differences in terms of pain and other clinical symptoms. The authors observed this improvement 6 months after one US-guided injection of 3 mL of PRP in the median nerve. In a case report described by Sánchez et al., a patient with peroneal nerve palsy underwent serial US-guided intraneural and perineural injections for 33 months [50]. The patient not only achieved improvement related to pain and function but also showed EMG sings of reinnervation for the peroneus longus and tibialis anterior. Specifically, an increase in compound muscle action (CMAP) was reported. In another case report, a 56-year-old woman who suffered from severity of symptoms of CTS received a treatment consisted of two US-guided perineural injections of 5 mL of PRP [51]. During follow-up at 3 and 6 months after the treatment, she revealed significant improvements in the distal motor and sensory latencies as well as the sensory nerve action potential and CMAP amplitudes of the median nerves. Finally, García de Cortazar et al. reported a case that described a patient with a section of the radial nerve [52]. Four months after the trauma and consequent surgery without positive response, serial intraneural infiltrations of PRP were conducted with US guidance. Eleven months after the first injection, EMG showed a complete reinnervation of the musculature of the radial nerve dependent.
\nIn addition to the application of PRP in liquid form for neural infiltrations, its versatility allows it to formulate in different ways such as gel, scaffold or fibrin membrane to apply also in surgical interventions. (Figure 1). Kuffler et al. took advantage of these properties for patients with nerve gaps in their extremities [53]. In the surgical technique they conducted, collagen tubes filled with PRP formulated as fibrin membrane were used to bridge the nerve gaps. Patients of this case series reached sensory and motor recovery across nerve gap, reduction of pain and functional recovery. Hibner et al. observed in a retrospective analysis the efficacy of injecting PRP around the pudendal nerve after a transgluteal decompression to enclose the nerve in NeuroWrapNerve Protector [54]. The pain of these patients who suffered from persistent pudendal neuralgia after neurolysis and transposition was significantly alleviated. This success was also achieved in patients with facial muscle and nerve deficit associated with benign parotid gland tumor [55]. In this randomized control study, Scala et al. observed significant improvements in several clinical parameters in the group of patients where PRP gel was applied during superficial parotidectomy.
\nNeuropathies are very challenging pathologies whose treatment options include conservative procedures as well as surgical interventions. In both cases, PRP is a promising and safe therapeutic tool that can be used as liquid formulation for US-guided infiltrations or as fibrin scaffold for surgery. Its potential has been proved in diverse in vitro and in vivo studies, and there are constantly more treatments based on this therapy in humans also. The use of this technique allows physicians to take advantage of the biological processes required to achieve an optimal nerve repair and satisfactory clinical results.
\nAlthough the PRP application for nerve pathologies is showing encouraging results and no negative side effects, apart from some painful episodes during injections, its use in these pathologies still has to be cautious. Although in some treatments normally the employed product has its importance, the way to use this product is also relevant to achieve a successful response. Elements such as a correct indication, an appropriate PRP elaboration and a suitable administration and application procedures are essential for the success of these treatments. Further studies and cases are needed to increase the knowledge not only of PRP for neuropathies but also of nerve biology, and thus improve protocols as well as clinical outcomes.
\nAlcohol is one of the most widely consumed psychoactive substances in the world, especially among adolescents and young adults [1, 2]. Many of these develop a pattern of alcohol consumption known as binge drinking (BD). BD has been defined by The National Institute on Alcohol Abuse and Alcoholism (NIAAA) as a pattern of drinking that elevates a person’s blood alcohol concentration (BAC) to 0.8 g/L or above [3]. This pattern involves the intake of large quantities of alcohol in a short period (about 2 h), followed by a period of abstinence, with a variability between 1 week and 1 month (see Figure 1). BD is the most common pattern of alcohol use among adolescents and young adults in Western countries. In Spain, the prevalence of BD pattern is similar in both sexes among 14–16 year-old adolescents and is more widespread among men than women in the age range of 17–18 years [4].
(a) Binge drinking pattern criteria. Quantity: intake of 50–56 g of pure alcohol in women and 60–70 g in men, in 2 h. Frequency: at least one BD episode per month. Intermittency: abstinence between BD episodes over time (minimum 1 week, maximum 1 month). (b) Number of drinks (1 drink = SDU, standard drink unit) in the USA and Europe for binge drinking’s BAC levels.
Individuals engaging in frequent BD have an increased risk to develop an alcohol use disorder (AUD) later in life. This risk has been suggested to be linked to executive deficits (e.g., [5]). The BD pattern of consumption seems to be especially associated with increased impulsivity and inhibitory control deficits (e.g., [6, 7, 8]). At the same time, this seems to be due to an attenuated frontal activation (e.g., [8, 9]). Thus, a higher incidence of BD has been related to decreased activation of dorsolateral prefrontal cortex, dorsomedial prefrontal cortex, and anterior cingulate cortex, brain regions strongly implicated in executive functioning [9]. The neurotoxic effects of BD on these regions can be less evident throughout adolescence, but if this alcohol consumption pattern persists, the executive dysfunction could be exacerbated. While individuals with AUD typically exhibit inhibitory control dysfunction, evidence of impaired inhibitory control among binge drinkers, who are at increased risk of developing an AUD, is mixed. Despite the variability in the literature, some findings point to mechanisms that may confer vulnerability for transition from binge drinking to AUD [6]. Therefore, inhibitory control deficits must be considered as an important factor that contributes to alcohol abuse.
On the other hand, important physical, social, and cognitive skills are acquired during adolescence and early youth. This period is also characterized by critical changes to the structural and functional development of brain areas related with these skills [10]. For example, the superior associative cortex (e.g., prefrontal cortex) undergoes myelination, pruning, and synaptic reorganization [11, 12], among other alterations. Significant changes in the volume and shape of the hippocampal complex, a brain region that plays an important role in memory functions, are also observed during this developmental period [13, 14, 15].
Due to this plasticity, the adolescent brain seems to be especially vulnerable to the neurotoxic effects of alcohol. In fact, alcohol-related performance deficits in tasks assessing cognitive processes, such as attention, memory, and executive functions, in the not-yet-adult brain are more evident during adolescence [16, 17] and become more pronounced with a BD pattern of consumption [12, 18].
The intermittence between BD episodes seems to be the most important factor involved, as the repeated alternation between intoxication and withdrawal is particularly deleterious for the brain, due to the excitotoxic cell death it provokes [19, 20]. Thus, it has been demonstrated that BD episodes can be more harmful for the brain than an equivalent amount of alcohol without withdrawal episodes [20, 21].
Therefore, the BD adolescent population constitutes a cohort at risk of brain damage, and any disruptive effects of alcohol on learning and memory abilities in this age group could have a particularly deep impact and last through to adulthood. Moreover, females would seem to be more vulnerable to these detrimental effects of alcohol [22].
In the following sections, the main insights provided by studies performed by our group and other researchers about the effects of BD on learning and memory performance will be discussed. We focus on the types of memory that are most damaged by alcohol: immediate visual memory (IVM) and working memory (WM). One distinctive contribution of this chapter is to evaluate, together, the impact of an acute BD episode and the sample’s history of consumption on learning and memory performance, as well as the possible gender differences at play.
For this review, we conducted a literature search of three databases: Web of Science, PsycINFO, and PubMed. The following combination of key terms was used: binge/heavy/social OR adolescent/young OR blood alcohol OR immediate/working/memory OR alcohol/ethanol OR cognitive AND acute alcohol. These keywords were examined in the “title” section for Web of Science and PsycINFO and “title/abstract” sections for PubMed. We considered studies published in English since 2000 (1 January 2000–30 November 2018) in humans. The total number of studies identified through the initial database searching was 677 (Web of Science, 284 records; PsycINFO, 215 records; PubMed, 178 records). Duplicated records were removed, and other articles were excluded using strict exclusion criteria: no BD pattern, out of age range (18–35 years old), psychiatric disorders, and other criteria described in the “methods” section. Eventually, 15 full-text articles were included in this review (see Figure 2 and Table 1). This review is limited by the publication bias (databases not included), procedure of selection bias, and unavailable data.
Preferred reporting items for systematic reviews and meta-analyses (PRISMA) flow diagram showing how articles were selected for review.
The experimental subjects in our studies (e.g., [23, 24]) were adolescent university students, who filled in a self-report questionnaire about consumption of drugs, frequency and level of alcohol consumption, hours and quality of sleep, and physical and psychological health. They were recruited based on strict inclusion and exclusion criteria. The inclusion criteria used were 18–19 years old, a healthy body mass index (between 20 and 25), and good health (without major medical problems). The subjects had to be refrainers (or very occasional alcohol consumers) or binge drinkers. The exclusion criteria were as follows: on medication; a history of mental disorders (diagnosed by a health professional according to DSM criteria); an irregular sleep pattern (non-restorative sleep and/or irregular schedule); having consumed, albeit sporadically, any drug (apart from alcohol) or having a history of substance abuse, including caffeine (our criterion: ≤2 stimulant drinks/day), tobacco (our criterion: ≤10 cigarettes/day), and alcohol (except for the BD consumption pattern); and having first-degree relatives with a history of alcoholism.
Other studies reviewed in this chapter included adolescents and young adults (18–35 years old) selected by similar or less restrictive inclusion/exclusion criteria, considering the alcohol use of subjects (history of problems due to alcohol use) and a history of mental health treatment (e.g., [25]).
Gender differences in the effects of alcohol have been reported, supporting the view that the brains of male and female adolescents are differentially affected by alcohol use [22]. There is evidence suggesting that female adolescents are more vulnerable to the neurotoxic effects of alcohol on cognition [22, 26, 27], since the cognitive tolerance effect of alcohol on IVM develops in BD women but not in BD men [24]. Other authors have found that men generally report lower sensitivity to alcohol (individuals need more alcohol to experience the same sensations or impairments) than women, and reactivity to alcohol-related cues is more pronounced in male than in female binge drinkers (e.g., [11]). These results might at least partially explain why men typically show a higher prevalence of alcohol consumption than women. However, in Spain at least, the incidence of alcohol consumption in 14–18-year-old adolescents is higher among females than males [4], while the BD pattern during adolescence is similar in 14–16-year-old adolescents and is more common among men than women in the age range of 17–18 years [4].
Gender differences in WM have also been reported in healthy young subjects, showing an advantage in this memory among males, with females exhibiting disadvantages manifested by a small effect size in both verbal and visuospatial WM [28]. This male advantage could be due to the activating effects of testosterone [29], though age and specific task modulate the magnitude and direction of the effects (e.g., [28, 30]). However, there are reviews in literature that explore the history of BD consumption but not the acute effects it exerts and which does not support the existence of gender differences in the effects of alcohol on this type of memory (e.g., [31]).
In the light of these data, it would seem crucial to consider (a) including both sexes, men and women, in any studies carried out and (b) evaluating potential gender differences in the relationship between BD and memory in adolescents and young adults.
Selected subjects were invited to participate in our studies if they reported refraining from alcohol consumption (or having indulged in very sporadic consumption) or a history of alcohol use classified as a BD pattern according to the NIAAA criteria for Spain (see [12]). Subsequently, the participants were classified as fulfilling a BD pattern if they had drunk six or more standard drink units (SDU) in the case of men or five or more SDU in the case of women on a minimum of two or three occasions per month throughout the 12 months prior to the survey. In Spain a SDU = 10 g of alcohol of distilled spirits (alcohol content ≥40% vol.). It is important to clarify that a stable BD pattern maintained over the time (12 months in the case of our studies) is a crucial criterion, because repeated alternation between intoxication and abstinence has been shown to be particularly harmful to the developing brain [19, 20]. Participants were classified as refrainers if they had never consumed alcoholic beverages or had drunk very sporadically (<1 SDU on <3 occasions per year, for example, 250 ml of beer, per occasion) since the onset of their alcohol use.
Therefore, in the studies reviewed in this chapter, including ours:
The experimental subjects were nondependent individuals indulging in alcohol use, usually evaluated by the Alcohol Use Disorders Identification Test (AUDIT) or others, such as the brief Michigan Alcoholism Screening test (e.g., [25]).
A very noticeable factor is the variability both in the samples’ history (refrainers, habitual consumers, binge drinkers, light binge drinkers, etc.) and in the acute administration of alcohol that leads to a BAC of 0.8 g/L (see Table 1 “sample’s history of consumption” and “cognitive performance—with (BAC)—” entries for details).
Depending on the study, performance in the memory task was registered as either rising or declining BACs.
Taking into account the scarcity of studies evaluating acute alcohol consumption in adolescent and young adult refrainers or occasional consumers (e.g., [23]), the present chapter provides unique insights into this field of research.
In our studies, the third edition of the Wechsler Memory Scale (WMS-III; version adapted for the Spanish population) [32] was used to assess IVM and WM. The IVM subscales require the respondent to recognize faces and remember scenes, while the WM subscales require the respondent to put letter-number sets in order and to reproduce visual-spatial sequences. The literature reports a poorer performance in these types of memory under the acute effects of alcohol (e.g., [24, 33]) and especially in WM associated with a stable BD maintained in time (e.g., [34]).
Other scales used for the evaluation of these or similar types of memory are:
The Cambridge Neuropsychological Test Automated Battery (CANTAB) for evaluating spatial recognition memory. The CANTAB is a computer-based cognitive assessment system consisting of a battery of neuropsychological tests, administered to subjects using a touch screen computer. This battery evaluates several areas of cognitive function using nonverbal stimuli in the majority of its tests, including the pattern recognition memory, a test of visual recognition memory in a two-choice forced discrimination paradigm.
The Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) for evaluating long- and short-term memory, working memory, and declarative memory. The ImPACT is a computer-based program for assessing neurocognitive function and concussion symptoms. This neurocognitive test battery consists of several modules for evaluating attentional processes, verbal recognition memory, visual working memory, visual processing speed, reaction time, and numerical sequencing ability.
The Wechsler Adult Intelligence Scale (WAIS-R) with the digit symbol substitution test (DSST) for evaluating short-term memory. The WAIS-R (revised form of the WAIS, a test designed to measure intelligence and cognitive ability in adults and older adolescents) consisted of six verbal and five performance subtests, including the DSST. This subtest (DSST-WAIS-R) consists of digit-symbol pairs followed by a list of digits; under each digit the subject must write down the corresponding symbol as fast as possible within the allowed time.
Obviously, the use of different tests/batteries for evaluating memory contributes to the heterogeneity of results in this field of research.
In our procedure, all participants signed an informed consent and a data confidentiality agreement on arrival at the laboratory. BAC was measured in all subjects with an alcoholmeter to ensure that they had not previously drunk alcohol on the day in question, and the alcohol use of the BD adolescent subjects was assessed using the AUDIT test (none of the subjects was assessed as alcohol-dependent). Next, refrainers and binge drinkers drank 330 ml of lime- or orange-flavored refreshment (control groups), and binge drinkers’ drank a high dose of alcohol. Alcohol was administered in a fixed dose of 120 ml (38.4 g) consisting of vodka mixed with the abovementioned refreshment for both genders or in function of their body weight (0.9 g alcohol/kg body weight in men and 0.8 g alcohol/kg body weight in women). The subjects were instructed to consume their drink within a period of 20 min. After finishing the drink, all subjects rinsed their mouths with water, and BAC was repeatedly measured every 5 min throughout the waiting period, until it reached a peak (approximately 20 min after consuming the drink). This peak of BAC was considered the value with which to classify the participants into the different experimental groups. The subjects performed the IVM and WM tests, while BAC was descendent. BAC was measured once again at the beginning of the tests, between the tests and at the end of the experiment. The BACs registered for the male and female subjects (separately or together) in the different experimental groups were:
0.0 g/L, in refrainers men (n = 17) and women (n = 24) or BD men (n = 23) and women (n = 27). These are control groups receiving a nonalcoholic drink.
0.33 g/L, in refrainers men (n = 17) or BD men (n = 22).
0.38 g/L, in refrainers men (n = 11) and women (n = 11) or BD men (n = 11) and women (n = 11).
0.5 g/L, in refrainers (n = 18) or BD women (n = 24).
0.3–0.5 g/L (mean = 0.4 g/L), in BD men (n = 12) and women (n = 12).
0.54–1.1 g/L (mean = 0.8 g/L), in BD men (n = 14) and women (n = 24).
(Note: The A, B, C, and D experimental groups belong to Ref. 23; and the A, E, and F experimental groups belong to Ref. 24).
All tests were performed between 4:00 pm and 8:00 pm, and the subjects that received alcohol remained on the premises until their alcohol concentration dropped to legal limits for driving (<0.3 g/L).
Similar procedures were applied in the other reviewed studies, where cognitive performance—with (BAC)—was evaluated after alcohol intake administered in fixed doses or according to body weight. Participants also abstained from alcohol for at least 12 h prior to the experiment, as well as drinking coffee or tea on the mornings prior to the experiment, and were instructed to eat a low-fat breakfast and lunch on the day on which tests were performed (e.g., [35]).
The main findings obtained in our experimental investigations and those of other groups are summarized in Table 1. The effects of acute alcohol consumption—one BD episode with different BACs—on different types of memory are reviewed.
A total number of 15 studies are summarized. Only three of them included adolescent male and females (18–20 years old) [23, 24, 33]; the participants in the rest of the studies were in the 18–35-year-old group, without studies comparing adolescents and young adults.
The sample’s history of consumption encompasses a range from refrainers to heavy binge drinkers, including habitual consumers/moderate drinkers and light binge drinkers. This variability in the samples of the reviewed studies gives us a more specific view of the acute effects of alcohol in different types of consumers and not only in binge drinkers.
In general, the results obtained in the evaluated memory tasks confirm the deleterious effects of alcohol use. Significant impairments were observed in spatial recognition memory, WM, associative learning, word fragment completion, free recall, long-term memory, short-term memory, and IVM. However, an absence of effects has also been observed with respect to some of these memories, such as visual memory, short-term memory, WM, and IVM. It is possible that the impairing effects observed are conditioned by BAC (ascendant BAC, BAC peak, descendant BAC) in the case of some types of memory. Thus, in studies in which there were ascendant and descendant BACs, impairment was reported in long-term memory, short-term memory, and WM declarative memory with ascendant BAC but not with descendant BAC.
Finally, the values for cognitive performance—with (BAC)—in Table 1 show the absence of effects or impairing effects in every sample, including for BAC of 0.0 g/L (refrainers and binge drinkers consuming refreshment/placebo). For example, in Vinader-Caerols et al. [23], male IVM performance was refrainers (0.0 g/L) = refrainers (0.33 g/L) = BD (0.0 g/L) = BD (0.33 g/L) and women’s performance was BD (0.0 g/L) < refrainers (0.0 g/L).
The key findings of this review will now be discussed. Among the types of memory reviewed, word fragment completion, free recall, and IVM appear to be the most sensitive to the effects of acute alcohol, as they are affected by moderate doses of alcohol (BAC = 0.3–0.38 g/L) in adolescents and young adults (e.g., [23, 38]). However, higher doses of alcohol (BAC levels of BD, i.e., around 0.8 g/L) are necessary for a significant impairment in other memories, such as WM (e.g., [24]) and short-term memory (e.g., [40]). A plausible explanation for the lack of effects reported with BACs under 0.8 g/L (e.g., [23, 25, 40, 44, 45]) is that the brain of binge drinkers employs compensatory mechanisms in additional brain areas to perform the tasks adequately and that these resources are undermined at higher BACs (e.g., [24, 33, 36, 40, 41]).
In contrast to the present review, others have attempted to provide an overview of affected (and unaffected) neuropsychological functions in adolescents and young binge drinkers, without evaluating the acute effects of alcohol and considering only the subjects’ history of BD (e.g., [31]). However, the interaction between a BD history of consumption and the effects of acute alcohol exposure on learning and memory needs to be studied, as some long-term effects of repeated alcohol exposure in adolescents (such as alcohol tolerance or damaged cognitive abilities) are observed more readily—if at all—following an acute dose of alcohol [23].
It is known that tolerance can develop early in adolescents and young adults without alcohol use disorder [47, 48]. Considering the scarcity of studies that have evaluated the phenomenon of tolerance in healthy adolescents and the potential vulnerability of females to the neurotoxic effects of alcohol, we performed a study [23] in which we observed that binge drinkers performed better in IVM than refrainers when given alcohol (showing the development of alcohol tolerance) and binge drinkers performed worse than refrainers after consuming a nonalcoholic control drink (as their memory would have been damaged). Thus, adolescent women are more vulnerable to the neurotoxic effects of alcohol than men, because the cognitive tolerance effect of alcohol on IVM develops in BD women but not in BD men. The phenomenon of women beginning to drink earlier and progressing more rapidly than men from drinking onset to problematic drinking, known as the “telescoping effect” [49, 50, 51], would explain why adolescent women develop cognitive tolerance earlier than men.
Although men and women have been included in some of the reviewed studies, only ours [23, 24] were carried out in order to specifically evaluate these gender differences in adolescents. In our second study [24], although the tolerance phenomenon was not evaluated (because refrainers did not consume an acute dose of alcohol), no gender differences were detected in IVM and WM performance with BAC > 0.5 mg/L. We suspect that an increased BAC overrides these cognitive differences between men and women. At the same time, the BAC is dependent on several factors such as rates of absorption, distribution, and elimination, as well as gender, body mass and composition, food effects, and type of alcohol. Therefore, careful extrapolation and interpretation of the BAC is needed [52].
The findings of the present review would be bolstered with a tighter control of factors that contribute to heterogeneity of results, such as:
Not taking into account the gender factor. The inclusion of men and women in study samples is more representative of the population.
Variability in the sample’s history of consumption, which can encompass a wide range (refrainers, habitual consumers/moderate drinkers, light binge drinkers, heavy binge drinkers, etc.).
The use of different tests/batteries for evaluating similar memories (e.g., CANTAB, ImPACT, WAIS-R).
The registration of performance in ascendant/descendant BACs. For example, more deleterious effects are observed in ascendant BAC versus descendant BAC. Most of the studies either they evaluate memory performance in descendant BAC or they do not specify whether the BAC is ascendant or descendant.
Variability in the age ranges in the studies. This variability (see Table 1), without a neat separation between adolescents and young adults, does not allow to properly compare these periods in order to find potential differences. Actually, there are not studies directly evaluating possible differences in the effects of acute BD on memory, comparing adolescents and young adults.
Several studies, using different paradigms (e.g., Stroop task, Go/No-Go task), have also shown that BD during adolescence is associated with poor inhibitory control (e.g., [7, 53]). Inhibitory control processes are developing during adolescence and youth, and a poor inhibitory function may predispose the individual to alcohol misuse [53]. Thus, impaired inhibitory control has been related to increased loss of control over drinking (i.e., a greater number of drinks per episode) [7], and this impairment seems to be related to the severity of alcohol-related problems [54, 55]. Likewise, acute and binge alcohol drinking may impair the inhibitory control and compromise the ability to prevent or stop behavior related to alcohol use. Then, poor inhibitory control can be both the cause and the consequence of excessive alcohol use. Adolescence and young adulthood may be a particularly vulnerable period due to the following reasons: (a) the weak or immature inhibitory functioning typical of this stage may contribute to the inability of the individual to control alcohol use and (b) alcohol consumption per se may alter or interrupt the proper development of inhibitory control leading to a reduced ability to regulate alcohol intake [53]. Therefore, inhibitory control training is a potential effective component of a comprehensive protocol for intervention strategies focused on this at-risk group of young adults who continue a BD trajectory into adulthood. Interventions targeting binge-drinking behavior should aim to inhibitory control training.
Increasing the knowledge about the effects of BD alcohol consumption pattern on memory and other executive functions in adolescents and young adults is also instrumental to designing programs and policy to reduce the impact of drinking in this highly vulnerable population in order to diminish the likelihood of participation in risky behaviors.
After reviewing the literature concerning the effects of one BD episode (with different BACs) on learning and memory performance in adolescents and young adults, the following conclusions can be drawn:
Alcohol BD has differential effects depending on the type of memory. For example, IVM is more sensitive than other memories to the neurotoxic effects of acute doses of alcohol in adolescents and young adults with a BD history (IVM is affected by a moderate BAC, while WM score is undermined only by BAC levels of BD).
BAC is an important factor to take into account when evaluating the acute effects of BD alcohol on memory performance in this type of studies.
Women are more vulnerable to some of the detrimental effects of alcohol than men are. For example, an effect of cognitive alcohol tolerance on IVM has been observed in women but not in men. These gender differences emphasize the need to include females in studies when investigating the neurotoxic effects of alcohol in adolescents and youths.
Further research, particularly longitudinal studies, is necessary in order to confirm the abovementioned findings and to consolidate these conclusions.
In relation to the inhibitory control in binge drinkers, taking into account the scarcity of studies evaluating inhibitory control training on alcohol consumption (e.g., [56, 57, 58]) and the lack of them evaluating this kind of training on BD, future research should investigate long-term implementation of inhibitory control training, emphasizing the importance of this training as part of the intervention strategies focused on this at-risk group.
The authors wish to thank the “Generalitat Valenciana” [PROMETEO-II/2015/020] and the “Universitat de València” [UV-INV_AE18-779336] for the funding part of the work reviewed herein. They also wish to thank Mr. Brian Normanly for his editorial assistance.
The authors have no conflict of interest to declare.
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
\n\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
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