\r\n\tHowever, despite the positive outlook and trends in routing protocol design, there are still several open or unresolved challenges that researchers are still grappling with. Providing adequate responses to those challenges is essential for next-generation networks in order to maintain its reputation and sustain its preponderance in cyber and physical security. Some of the challenges include, but are not limited to, the following:
\r\n\t• Robustness and reliability of routing protocol
\r\n\t• Reduced dependencies on heterogeneous networks
\r\n\t• Security of routing protocols
\r\n\t• Dynamic Adhoc routing Protocols
\r\n\t• Routing in 5G Networks
\r\n\t• Routing IoT enabled networks
\r\n\t• Scalable and dependable routing system architectures
\r\n\t• QoS and QoE Models and Routing Architectures
\r\n\t• Context-Aware Services and Models
\r\n\t• Routing Mobile Edge Computing
\r\n\tThe goal of the book is to present the state of the art in routing protocol and report on new approaches, methods, findings, and technologies developed or being developed by the research community and the industry to address the aforementioned challenges.
\r\n\tThe book will focus on introducing fundamental principles and concepts of key enabling technologies for routing protocol applied for next-generation networks, disseminate recent research and development efforts in this fascinating area, investigate related trends and challenges, and present case studies and examples.
\r\n\tThe book also investigates the advances and future in research and development in Routing Protocols in the context of new generation communication networks.
The importance of the nanoporous materials has been well established historically by the extensive use of zeolite and activated carbon in separation and purification for industrial and clinical applications [1, 2]. Research on nanoporous materials for gas storage, drug delivery, catalysis, sensing, and optoelectronic applications are ongoing with the focus of using the properties of nanoporous materials to their fullest to improve nanotechnology to the state-of-the-art. In recent years, nanostructures of gold have gained great attention because of their broad range of potential applications in the fields of medicine and energy. Gold nanoparticles (AuNPs) have already been used in a clinical trial for the thermal ablation of solid tumors as a photothermal agent due to its unique optical properties [3]. It has also shown promising results in drug delivery and as a contrast agent for imaging to advance cancer therapy [4]. Gold nanorods (GNs) have also shown promising results in biosensing, drug delivery, photothermal therapy, and imaging.
Gold in the nanoporous form, so-called nanoporous gold (np-Au), has gathered considerable attention recently, as it is a robust 3-dimensional nanostructured form of gold with a very high surface area-to-volume ratio and still maintains the properties of AuNPs and GN [5]. The size of the pores and ligament of np-Au can be easily tuned and are in the range from few nanometers to few hundreds of nanometers [6]. The AuNPs and GNs easily aggregate if suitable conditions were not provided making them less useful for some nanotechnology applications. The np-Au not only circumvents this problem but is simple to prepare and easy to handle for wide varieties of applications.
Through this survey and discussion, we will demonstrate that there is a growing interest in this material, which is justified by its many emerging applications. As a support for enzyme immobilization, the material has accommodated a range of enzymes and is suitable for the development of enzyme reactors. Numerous biosensors for metabolites and for biomarkers have been introduced using np-Au as a support. The applications to catalysis have included many of the oxidation reactions suitable for gold nanoparticles, but with the advantage of possible use in a free-standing intact format. The support of surface plasmons by the material opens up possibilities for use in the development of optical biosensors.
This chapter will cover different synthetic strategies for the preparation of np-Au in different forms. We will also discuss the methods commonly used to characterize np-Au, including scanning electron microscopy, transmission electron microscopy, tomography, and gas adsorption isotherm measurements. Finally, we will focus on the broad range of applications of np-Au, including chemical sensing, electrochemical and optical biosensing, catalysis, and mechanical actuation.
The most common method of preparing np-Au is by dealloying [7]. It is a top-down approach where the alloy of gold containing other less noble metals is treated in a corrosive environment with or without applying a potential. The dealloying process selectively removes the less noble metal from Au-M alloy (M═Ag, Cu, Sn, Al, etc.) creating the nanoporous structure having interconnected ligaments [7, 8]. The shape and size of the alloy is important as the np-Au formed after the dealloying process maintains the shape and size of the alloy. The np-Au can be fabricated as a supported thin film or a free-standing structure. The supported np-Au is physically stable and easy to handle compared to the free-standing np-Au and is most commonly prepared for use as a working electrode in electrochemical experiments. Using supported np-Au, it is convenient to separate the interfacial boundary between np-Au and the clip holding the electrode. Figure 1A shows SEM images of the cross-section of np-Au supported on gold wire prepared by first forming the Au-Ag alloy using electrochemical deposition followed by dealloying in HNO3 for 24 h to selectively remove Ag [9]. Figure 1A′ is a low magnification SEM image of surface morphology of the as-prepared np-Au and the inset is the high magnification image [9]. Low magnification image shows crack formation throughout the surface due to the volume shrinkage during dealloying whereas high magnification image shows a porous structure having inter-ligament gap (pore size) of 27 ± 7 nm and ligament width of 26 ± 5 nm.
SEM images of np-Au in different form prepared by dealloying in concentrated HNO3. (A) Cross-section of Au supported np-Au obtained by 24 h selective dissolution of Ag from Au-Ag alloy, where the alloy was prepared by providing potential of −1.0 V (vs. Ag/AgCl) for 10 min on the gold wire. (A’) Top view of the as-prepared np-Au at low magnification. Insets are the corresponding high magnification images. Reproduced and slightly modified with permission from ref. [9], Copyright 2016, Elsevier. (B) np-Au plate dealloyed for 48 h. Reproduced from ref. [10]. (C) np-Au leaf (∼110 nm) dealloyed for 13 min. Reproduced with permission from ref. [11], Copyright 2011, Elsevier.
On the other hand, if the electrochemical connection is not desired, the free-standing np-Au is the material of choice for different applications, such as optical biosensing, solid-support organic synthesis, and protein separation. Free-standing np-Au plates, leaves and wires can be easily fabricated by simply dealloying the commercially available 10–12 Karat gold alloys in the desired form. The thicker the alloy, the longer should be the dealloying time for the effective removal of the sacrificial metals. Dealloying time is also important in determining the sizes of pores and ligaments. Figure 1B and C show the np-Au plate (∼250 μm thick) dealloyed for 48 h and np-Au leaf (∼110 nm thick) dealloyed for 13 min in HNO3, respectively [10, 12]. It was found that the structure and the composition of np-Au leaf after dealloying for 2 h in nitric acid are comparable to that of np-Au plate dealloyed for 48 h with the pores size nearly 30 nm and nearly 2 atomic percentage of residual silver [11, 13].
When desired, np-Au can also be created in wide varieties of free or surface bound micro and nanostructures. The micro and nanostructures of np-Au can be created using three strategies: (1) template (2) dewetting, and (3) solvent coarsening. The template-based strategy is the most common as wide varieties of desired structures can be created. Silver chloride (AgCl) can be used as a sacrificial template to prepare different types of zero-dimensional np-Au nanostructures, such as nanoframes, bowls and shells [14, 15, 22], Figure 2A and B. This solution phase synthetic strategy of np-Au can be performed by depositing Au nanoparticles from HAuCl4 precursor on to AgCl template using hydroquinone as a reducing agent and polyvinyl pyrrolidone (PVP) as a stabilizing agent. The sacrificial AgCl template can then be removed using concentrated NH4OH, and PVP can be removed by treating the np-Au with piranha solution. The adsorption of PVP on growing Au nanoparticle highly influences the growth of np-Au nanostructure.
SEM images of np-Au nano- and micro-structures prepared using different methods. (A) and (B) np-Au nanoframes and nanoshells prepared using AgCl as a template. The template used for C, D, E, and F are polystyrene beads, anodized Al2O3 films, and Ni macroporous foam, respectively. (G) Nanoparticles formed using dewetting technique on SiO2/Si surface from 20 nm thick Ag and 10 nm thick Au layer. (H) np-Au coarsened by immersion into concentrated HCl solution for 24 h. Top surface divided into “plots” by coarsened nanoporous walls. The typical side length of the “plots” was approximately from several micrometers to 20 μm. Reproduced with permission from Refs. [14, 15, 16, 17, 18, 19, 20, 21], respectively. (A) Copyright 2015, American Chemical Society, (B) Copyright 2014, Macmillan Publishers Limited, (C) Copyright 2007, American Chemical Society, (D) Copyright 2016, American Chemical Society, (E) Copyright 2014, The Royal Society of Chemistry, (F) Copyright 2008, American Chemical Society, (G) Copyright 2012, The Royal Society of Chemistry, and (H) Copyright 2006, American Chemical Society.
Polystyrene (PS) beads are frequently used as a template for np-Au preparation as they are readily available and can be easily removed using heat or chloroform. Nyce and co-workers used PS-bead to synthesize monoliths containing hollow np-Au of nearly 10 μm in diameter [17]. First, they created monolithic hollow Au/Ag alloy particle by subsequent electroless deposition of Au and Ag on PS-bead followed by casting and heat removal of the template. Finally, the hollow Au/Ag alloy was dealloyed in HNO3 to create monolithic hierarchical np-Au, Figure 2C. PS-bead can also be used as a mask to generate a semi-random array of np-Au disk on silicon or glass surface [16, 19]. For this, silicon or glass support is sputter deposited with gold and silver alloy on top of which the monolayer of PS-beads is prepared. Oxygen plasma treatment is then employed to shrink the immobilized PS-bead and separate it from the neighboring beads followed by sputter-etching in argon plasma to transfer the pattern of the bead to the alloy film. Finally, PS-beads were dissolved in chloroform to obtain the alloy disk and dealloyed in concentrated nitric acid to obtain the np-Au disk, Figure 2D.
Three-dimensional (3D) structures of metals and metal oxides can be used as a template for preparation of np-Au of different shapes and sizes. 3D-macroporous Ni foam was used as a template to prepare the three-dimensional np-Au film supported on Ni surface [19, 23]. In this method, Au-Sn alloy film was first electrodeposited onto the surface of Ni foam followed by removal of Sn in NaOH and H2O2 solution by treating for 3 days at room temperature, resulting in three-dimensional np-Au, Figure 2E. Significant advances in preparing monodisperse np-Au nanorods and nanowires of desired size have been made by using porous anodic aluminum oxide (AAO) as a template. The AAO having pore sizes of around 100–200 nm and wide varieties of thickness can be used as a template for preparing np-Au nanorods [18], nanowires [24], and nanotubes [25], Figure 2F. In this method, one side of the alumina template is closed by sputtering or evaporating a conducting copper film, followed by electrochemical cathodic deposition of gold and silver alloy through the template. The alloy nanostructures can be stripped as a free structure when Al2O3 and deposited Cu film is dissolved in suitable solutions. KOH can be used to dissolve Al2O3, and a mixture of CuCl2 and HCl can be used to dissolve the Cu film. Finally, removing Ag from Au-Ag alloy gives the nanoporous nanostructures. By decreasing or alternating gold/silver composition ratios to prepare the alloy on Al2O3 template followed by dealloying, step-like np-Au nanowires such as nano-cones and nano-barbells can be prepared [26].
Dewetting bilayers of gold and sacrificial less noble metal on SiO2 or TiO2 surface at elevated temperature leads to the inter-diffusion between bilayered metals to form an alloy while shrinking the volume to generate the isolated particles or droplets [20, 27, 28], Figure 2G. Removal of the sacrificial less noble metal using dealloying or etching creates the np-Au nanoparticle similar in shape and size to the alloy particle [29, 30]. Using this technique, ordered array of np-Au nanoparticles can be created on nanoimprint lithography prepatterned SiO2/Si substrates, where the size of the np-Au particles can be easily controlled by varying the metal layer thickness [31].
The np-Au ligaments and pores can be easily modified by keeping it in corrosive solvent for different period of time. It has been found that keeping np-Au in HNO3 for longer time creates the stress to the ligaments, which start merging at some locations decreasing the size of pores or completely closing the pore while at the other locations ligaments keeps separating further generating large pores. This process results into larger but fewer numbers of pores and ligaments [10]. We have found that after 42 days of dealloying in nitric acid, the average inter-ligament gaps and ligaments width increases to 115 ± 32 and 160 ± 47 nm, respectively from 27 ± 7 and 38 ± 8 nm obtained after 24 h dealloying. Interestingly, when np-Au is immersed in concentrated hydrochloric acid for 24 h, the ligaments of np-Au gets coarsened by several hundred nanometers and divides into regions of few micrometers to 20 μm in size, generating np-Au prism [21], Figure 2H.
Thin layer np-Au films can be created on the surface of gold electrodes by applying a potential with or without the use of sacrificial metals from electrolyte solution. Different strategies have been utilized to prepare np-Au using this method, including holding a high anodic potential for different times [32], ramping up the potential from 0 V to very high potential (>20 V) in few seconds [33, 34], cycling the potential between two points at a specific rate in suitable electrolyte [35], and using the combination of these methods. Chloride-containing electrolytes are commonly used for this technique, which create np-Au through electro-dissolution of Au into AuCl2− and AuCl4−, disproportion of AuCl2− to Au atom and AuCl4−, and deposition of Au atom back on gold electrode to form np-Au [32]. Deng and co-workers demonstrated that by simply holding the potential at 0.9 V (vs. Hg/Hg2SO4, sat.) in 2 M HCl, np-Au film can be created on the gold surface within a minute [32]. Later, the same group proved the effectiveness of the chloride ions for np-Au formation by taking 1 M KCl as an electrolyte. By providing 1.29 V versus saturated calomel electrode for 300 s the authors were able to create np-Au in neutral KCl solution [36]. The work has been further elaborated using 0.5 M NH4Cl as an electrolyte to prepare np-Au structure by providing the anodic potential of 1.32 V (vs. SCE) [37]. It has been found that the roughness factor, the ratio of the electrochemical active surface area to the geometric area, of np-Au depends on potential step time, which can be enhanced when hydroxylamine hydrochloride (NH2OH·HCl) solution is mixed with NH4Cl to prevent bubble formation during the np-Au formation step. Non-chloride-containing electrolytes like citric acid have also been used to prepare np-Au on gold rod by providing the anodic potential of 4.0 V for 3 h to create the ultra-high surface area with the roughness factor higher than 1000 [38].
Instead of simply sweeping the anodic potential linearly, multi-cycle potential scans can be used to prepare np-Au on the polished gold electrode using suitable electrolytes. In the cathodic potential scan, the sacrificial metal ions from the solution can be electrodeposited to create gold alloy in situ which on the subsequent anodic potential scan is removed from the surface of the gold electrode [39]. After the multiple cathodic/anodic cycles, np-Au with a high surface area can be generated, Figure 3. Hu and co-workers prepared a thin layer of np-Au on the gold electrode surface by etching the electrode by providing multiple electrochemical cycles in the potential range −0.72 to 1.88 V at 10 mV s−1 in benzyl alcohol electrolyte containing 1.5 M ZnCl2 at 120°C [35]. In this study, Zn plate and a Zn wire were used as the counter and reference electrodes, respectively.
(A) Schematic illustration of the formation of np-Au film electrode by a multicyclic electrochemical alloying/dealloying method. Step 1, electrodeposition of Zn and formation of Au-Zn alloy; step 2, electrochemical dealloying; step 3, electrodeposition of Zn and formation of Au-Zn alloy again; step 4, formation of np-Au film after multicyclic alloying/dealloying. (B) and (C) SEM images of np-Au electrodes after 30 cycles of alloying/dealloying in ZnCl2/BA electrolyte at 120°C, where (B) is cross-sectional view and (C) is planar view. The inset in (B) and (C) are the corresponding images with higher magnification. Reproduced with permission from Ref. [39], Copyright 2007, American Chemical Society.
Nanoporous gold can also be formed by first polarizing the pure gold electrode, holding it at a certain potential for specific time, and finally reversing the potential to clean the gold surface. By polarizing the gold electrode from 0.0 to 2.0 V at the scan rate of 0.02 V s−1 in 0.5 M H2SO4, holding the potential at 2.0 V for 60 min to form a gold oxide (orange-yellowish surface) followed by reverse potential scan to reduce the oxide layer on the gold surface (black surface), Sukeri et al. succeeded in preparing np-Au film on pure gold surface [40]. Similarly, Nishio and Masuda used oxalic acid to create the carbonaceous passivation film on gold surface by holding the potential at 1.8 V versus Hg/Hg2SO4 reference electrode, which on the reverse scan breaks down to form np-Au film with a uniform hole size of 20 nm [41]. The study has also shown that acidity is not the key factor for the np-Au formation by anodizing the sample in neutral sodium oxalate solution. Fang et al. used 1:1 (v/v) mixture of hydrofluoric acid and dimethylformamide as an etching electrolyte while suddenly ramping up the potential from 0 V to 40 V over 12 s or from 0 to 20 V over 24 s [33]. The latter slower voltage ramp was found to create the larger pores. On the other hand, the pore size created by directly holding the potential for 20 V or 40 V in the same electrolyte solution for similar time was found to create the smaller pore sizes. Xu and co-workers anodized the cleaned gold wire using potential of 5 V for 180 s in 0.15 M phosphate buffer to form oxides on electrode surface (evident by salmon pink color of the electrode surface) followed by reduction of gold oxide by 1 M ascorbic acid solution at room temperature to prepare np-Au (evident by change in color of the electrode surface to black) [42].
The shape and size of nano-and micro-structured np-Au along with their pores and ligaments size is characterized by scanning electron microscopy (SEM). SEM images are also important to determine the cracks on the surface of np-Au. For the very thin np-Au samples and for distinguishing the foreign elements incorporated within np-Au at high resolution, transmission electron microscopy (TEM) images are useful [43]. Filled nanoporous spaces by foreign elements appear dark on TEM images, which can be distinguished from the control np-Au appearing light. High-resolution transmission electron microscope (HRTEM) can further reveal the lattice spacing of the foreign element which may either vary significantly from that of the np-Au or show the epitaxial relationship with the continuous lattice fringes [44]. It can also reveal different kinds of lattice defects present within np-Au [7]. Transmission electron tomography can be used to generate bicontinuous 3D-structure of np-Au showing the internal structure of the np-Au [45].
Energy dispersive X-ray spectroscopy (EDS) can be used to confirm the removal of less noble metal from np-Au through which the time needed for the complete removal of sacrificial metals can be estimated. Change in grain size and crystal structures of alloy or np-Au are studied using X-ray/electron diffraction. Based on the appearance of the characteristic X-ray diffraction peaks, the np-Au hybrid electrode with wide varieties of metals can be prepared [23].
When sufficient mass of np-Au is available, the surface area and pore size of np-Au can be determined using nitrogen adsorption/desorption isotherms. BET surface area analysis and BJH pore size distribution analysis provide the information about surface area and pores, respectively [46]. These methods are mainly useful for characterizing unsupported np-Au monoliths. For the supported np-Au electrode, a simpler and easier method to determine the surface area is through the cyclic voltammetry (CV) using oxide stripping method. In this method, charge under the cathodic peak generated due to the stripping of oxide from the gold surface is used to calculate the actual surface area of np-Au. However, electrochemically active or accessible surface area of np-Au can be determined using CV of redox probes or mediators.
Self-assembled monolayers (SAMs) of thioalkyl derivatives on the planar gold surface are a well-studied field [47]. Different types of biomolecules, such as protein, DNA and carbohydrates can be strongly bound and presented on the surface of gold as a SAM mimicking the cell surface or their natural form [48]. Biomolecules can be either modified with the thiolated linker first and allowed to form a SAM or immobilized on the previously formed SAM by reacting with the terminal functional group. Np-Au surface can be modified with different types of SAM in the same way as done in a planar gold surface by immersing the np-Au on the ethanolic solution of desired SAM-forming molecules for few hours to overnight [9]. SAM formation on np-Au surface is of higher interest because high surface area of np-Au allows large number of desired molecules on the surface. However, SAM on np-Au is not as well organized as that on planar gold surface and chances of intermolecular interactions between the terminal functional group are higher [49]. The nature and size of the terminal group and length of the linker determine how deep the monolayers are formed and are functionally active in the interior of np-Au. When np-Au-based glucose sensor was constructed by immobilizing glucose oxidase (GOD) onto the SAMs of carboxylic acid terminated alkanethiol having different chain lengths, it was found that the sensitivity of the biosensor decreases with the increase in chain length [50]. This phenomenon has been explained by the better SAM formation of the longer chain length molecules on the np-Au surface, helping to immobilize higher number of enzymes and hence creating more difficulty for the electron transfer to occur. However, increase in thickness due to the longer chain length may also be the reason behind the difficulty for electron transfer to occur. The type of terminal functional group and chain length of SAM play vital roles in loading and releasing of drugs in np-Au. A negatively charged fluorescein (a small-molecule drug surrogate) shows lower loaded inside np-Au when np-Au surface was functionalized with carboxy-terminated SAM compared to when modified with amine-terminated SAM [51]. This is due to the repulsive interaction of negatively charged fluorescein with the carboxylic group and attractive interaction with the amine group. It was also found that increasing the chain length (11 carbons) of SAMs changed the pore area decreasing the access of fluorescein to the interior of np-Au and hence reducing loading capacity [51].
Modification or decoration of the np-Au surface with other metal or metal oxide can build up functionalities to the already versatile np-Au structures. Modifying the np-Au with a tiny amount of platinum, palladium and TiO2 nanoparticles not only greatly increase the effective surface area but also enhance the electrocatalytic performance toward methanol oxidation [52, 53, 54]. Modifying the np-Au with platinum and palladium also significantly improves the structural stability of np-Au whereas TiO2 suppresses the coarsening of the nanoporous structure after multiple uses. Modifying np-Au surface with metals and metal oxides, such as Pt, Pd, Cu, Ni, Ru, CuO, TiO2, and CoO have shown significantly enhanced sensitivity toward the nonenzymatic detection of glucose with very good selectivity in the biological matrix [55, 56, 57, 58, 59, 60, 61, 62]. When np-Au is modified with Ru to form np-Au/Ru nanocomposite and immobilized further into GCE with chitosan as a capping agent to create an electrode, it can act as a better nonenzymatic glucose sensor with good sensitivity and selectivity compared to bare np-Au [58]. The modified GC/np-Au-Ru/CHIT electrode shows six-fold higher amperometric sensitivity of 240 μA mM−1 cm−2. Modifying the np-Au with ultrathin nickel (Ni) film enables detection of glucose with the sensitivity as high as 5070.9 mA mM−1 cm−2, which is nearly 340 times higher compared to that on the polished gold electrode [63].
The immersion-electrodeposition method is one of the simplest methods to modify the np-Au surface with metals and metal oxides [52]. In this method, np-Au is immersed in a suitable salt solution, allowed to soak for certain time and electrodeposited by applying a suitable potential. Platinum was decorated on np-Au by first immersing np-Au in H2PtCl6 solution for 10 min followed by electrodeposition by sweeping the potential at 50 mV s−1 between 0 and 1.1 V (vs. RHE) for 3 cycles in 0.1 M HClO4 solution [52]. Similarly, iridium oxide was electrodeposited on np-Au using multiple cyclic voltammetry scans [64]. This method is suitable for modifying the external surface or thin films of np-Au with metal and metal oxides, but modifying the interior part of the thicker np-Au structure is challenging mainly because of the mass transport limitation leading to the closing of external pores before completely modifying the interior surface. There are different alternatives to overcome this situation. Underpotential deposition of the reactive metal to form a monolayer followed by galvanic displacement of the reactive metal by the atoms of desired metal can modify the np-Au surface while conserving the original structure of np-Au. Np-Au surface can be modified with Ni using galvanic displacement reaction of underpotential deposited zinc [63]. Similarly, Cu can be underpotential deposited on the np-Au surface to decorate it with Pt using a galvanic displacement reaction [43]. However, the residual metal such as silver, which is left while dealloying np-Au, can also be used in galvanic replacement reaction to decorate Pt using H2PtCl6 solution [65]. Water dispersed TiO2 nanoparticles were loaded inside np-Au followed by annealing to embed the TiO2 particles on the np-Au surface [53]. The desired noble metal can also be included as one of the constituents of the alloy, which remains on the np-Au surface after the dealloying process removing less noble metal/s [54].
Nanoporous gold without any further modification with other metals or biological molecules can act as a chemical sensor owing to its high surface area, ability to catalyze certain analytes at low potentials, resistance against surface fouling and pH, and fast mass transportation [66]. It has been successfully used to detect arsenic [As(III)], a toxic metal ion whose exposure can lead to many health issues including cancer, using square wave anodic stripping voltammetric technique to the concentration as low as 0.0315 ppb with the sensitivity of 44.64 μA cm−2 mM−1 [67]. World Health Organization’s recommended limit of arsenic in the drinking water is 10 ppb. Phenolic compounds, such as phenol and catechol have been considered as priority toxic pollutants by US-EPA but still extensively used by many chemical companies for various applications. A suitable detection method for these compounds is a need for monitoring its concentration in environment and food products. By applying a suitable detection potential, np-Au electrode can not only detect the phenolic compounds down to few micromolar range [68] but also selectively distinguish one from another [69]. However, np-Au can also be easily modified with biomolecules and different types of other metals for its use in bio/chemical sensing.
Nanoporous gold is a suitable solid support for the immobilization of enzymes because of its biocompatible nature, ability to form self-assembled monolayers on the surface, and high surface area-to-volume ratio [5]. Once the enzyme is immobilized on the electrode surface, it is very important that it maintains its enzymatic activity for further usage. Np-Au increases the stability and functionality of the immobilized or entrapped enzymes by decreasing their tendency to unfold due to its constrained environment [70, 71]. Lignin peroxidase (LiP) immobilized on np-Au was found to retain 55% of its initial activity after 2 h at 45°C whereas free LiP was completely deactivated under similar conditions [71]. Another study reported that alcohol dehydrogenase (ADH) or glucose oxidase (GOD) immobilized on np-Au lost only 5.0 and 4.2% of the original current response, respectively, after storage for 1 month at 4°C [70]. By creating the appropriate pore size of the np-Au, the leaching can also be drastically reduced from the electrode [70]. The larger the pore size of np-Au, the higher will be the leaching. On the other hand, smaller pores may block the enzymes from entering the np-Au interior portion. Fortunately, due to the ability of np-Au to form SAMs, enzymes can be strongly and covalently bound on np-Au surface increasing the loading and activity of the enzyme while decreasing the leaching [72, 73]. Nevertheless, physical adsorption of enzyme on np-Au is widely used to prepare the enzyme-based biosensor, because of comparative stability, the ease of preparation and few steps required [74]. The leakage of the physically immobilized enzymes can be reduced by using polymers like chitosan [75] and Nafion [70]. The high surface area of np-Au helps to amplify the response signal of the analyte during biosensing due to the large numbers of immobilized enzymes.
Supported np-Au is a suitable solid support for immobilization of different types of protein (e.g., antibodies, enzymes, and lectins), carbohydrates, and RNA/DNA molecules because of its clean surface, robust structure, high surface area and biocompatible nature [76]. These immobilized biomolecules on np-Au, called receptors, can be used as biosensors for the detection of various analytes, such as poisonous metal ions, small organic molecules, and other biomolecules. Because of the highly conductive nature of np-Au electrode, it can be used as a transducer for the detection of analytes using different electrochemical techniques. The commonly used electrochemical techniques for np-Au-based biosensing are cyclic voltammetry (CV), chronoamperometry (CA), chronocoulometry (CC), electrochemical impedance spectroscopy (EIS), differential pulse voltammetry (DPV) and square wave voltammetry (SWV). Except EIS which is based on the resistance of the electrode, all the other techniques are based on the measurement of current or charge whose signal is directly proportional to the concentration of the analyte. DPV and SWV are pulse-based techniques, which have the ability to discriminate against the charging current by only sampling the Faradaic current at the end of the pulse. As a result, a very small concentration of a sample can be detected precisely. Electrochemical biosensors can be classified as DNA aptasensor, enzymatic biosensor, and immunosensor based on the type of receptor molecule used. Recently, Zeng et al. prepared regenerable DPV-based aptasensor on the np-Au surface for the detection of Hg2+ with the limit of detection as low as 0.0036 nM [77]. The non-enzymatic amperometric glucose sensor is possible using np-Au electrode [11] or by modifying the np-Au surface with other metals or metal oxides [78]. However, np-Au surface can be modified with glucose oxidase to use the synergistic catalytic properties of both np-Au and glucose oxidase for the detection of glucose. In one such study, high sensitivity of 12.1 μA mM−1 cm−2 with the linear responses ranging from 50 μM to 10 mM was obtained with a low detection limit of 1.02 μM [79]. The prepared structure possesses strong anti-interference capability against many molecules present in human serum. Np-Au surface was used for detecting various cancer biomarkers based on sandwich-type immunosensing. Np-Au electrode immobilized on graphene surface was combined with horseradish peroxidase-encapsulated liposomes as labels and thionine as electron mediator for the detection of cancer antigen 15-3 using DPV [80]. The linear range of the immunoassay was found to be 2 × 10−5–40 U mL−1 with a limit of detection of 5 × 10−6 U mL−1. Similarly, DPV was used to detect carcinoembryonic antigen (CEA) by immobilizing anti-CEA on np-Au [81] and CV was used to detect prostate specific antigen (PSA) by immobilizing anti-PSA [82].
The phenomenon of change in surface stress and strain of np-Au due to the adsorption or desorption of gas or water can be used to convert chemical energy into a mechanical response [83, 84]. One way to prepare such surface driven actuator is by alternate exposure to ozone and carbon monoxide on np-Au surface [85]. Exposure of ozone on np-Au surface leads to adsorption of oxygen on clean Au, whereas CO exposure cleans the Au surface by reacting with adsorbed oxygen to release carbon dioxide, Figure 4A and B. Another way to generate such stress on np-Au surface is by volumetric changes of np-Au by physical adsorption and desorption of polar water molecules [84]. This method can create reversible strain amplitudes up to 0.02% in response to a 15% change in relative humidity. The ligaments of np-Au actuator coarsen with time leading to a substantial loss in performance. In such case, np-Au can be modified with platinum or polyaniline to prepare a composite porous structure [83, 86]. Np-Au/Pt alloys prepared by dealloying ternary alloy of Ag-Au-Pt to create very small structure size and large specific surface area can significantly enhance the stress and strain in the bulk of the material reaching linear strain ∼1.3% [83].
(A) Illustration of surface-chemistry-driven actuation in np-Au. Au surfaces can be switched back and forth between an oxygen-covered and clean state by alternating exposure to ozone (O3) and carbon monoxide (CO). (B) Performance of a surface-chemistry-driven np-Au actuator. Strain versus time as the np-Au actuator is alternately exposed to a mixture of ∼7% O3 in O2 and pure CO. Between exposures, the sample compartment was purged for 3 min with ultrahigh-purity N2. Ozone exposure causes contraction, whereas CO exposure restores the original sample dimension. The response is mostly elastic, with only a small irreversible component. The system is very stable, and interrupting the exposure sequence for 1 h causes only a small drift of the signal. Reproduced with permission from Ref. [85], Copyright 2009, Macmillan Publishers Limited.
Propagating surface plasmon resonance (SPR) is the evanescent electromagnetic waves found in the interface of thin metal (e.g., Au and Ag)-dielectric interface, which propagates at the distance on the order of tens to hundreds of microns along x- and y-axis, but decays on the order of 200 nm along the z-axis [87]. However, if the oscillation of surface plasmons is confined within the surface of the nanostructures of the metal (e.g., Au and Ag), it is called LSPR [88]. Both the SPR and LSPR are sensitive to change in refractive index around the metal-dielectric interface. This property can be used to design a label-free, sensitive and high-throughput biosensor to study the interaction of biomolecules.
Thin films (∼100 nm) of np-Au can generate both the SPR and LSPR simultaneously [89]. Kim et al. studied biotin-streptavidin interaction on the surface of np-Au film fabricated by oblique angle deposition using SPR [90]. They found that there is an enhancement in SPR response due to np-Au compared to when studied on conventional bare gold film. The reason for enhancement in SPR response is attributed to excitation of local plasmon field and an increased surface area for the reaction. In the absorption spectra, two characteristic LSPR peaks can be observed for np-Au, one near 490 nm and other around 550–650 nm [91, 92]. The LSPR peak of np-Au at 490 nm is nearly independent of change in refractive index [92] and the peak at 550–650 nm is relatively wider compared to that obtained from Au nanoparticles and nanorods. The wide peak decreases the sensitivity of the biosensor limiting the use of np-Au in biosensing experiments. However, preparing np-Au nanostructures, such as np-Au disks can greatly enhance the plasmonic response due to high-density internal plasmonic “hot-spots” [19, 93]. By using these structures, the plasmonic bands can be tuned from 900 to 1850 nm by changing the diameter of the disk from 300 to 700 nm. The disk with a diameter of 300 nm shows the LSPR peak in relatively lower wavelength region and is sharper compared to the disk with higher diameter.
With the discovery of nanoparticles and nanoporous structures of gold, studies and understanding of the gold as a heterogeneous catalyst have been emerging. Heterogeneous catalysis is vital for (1) environmental waste management, as green chemistry reactions are possible and (2) synthesizing desired products, which is either not possible with homogeneous catalysis or requires poisonous chemicals if done without a catalyst. Gold nanoparticles, because of their high surface area and other unique properties, have shown promising results in heterogeneous catalysis. However, for the nanoparticles to be used in liquid phase catalysis, they should be functionalized with a suitable stabilizing agent or else they may undergo undesired aggregation decreasing the surface area and hence the catalytic activity. The functionalized stabilizing agent can also decrease the effective surface area and may passivate the surface faster. Unsupported np-Au, a bulk 3D-structure of gold having nanometer-sized pores and ligaments, can overcome these shortcomings. Besides having high surface area, it is easy to prepare, stable at harsh reaction conditions, and has less possibility of contamination. Furthermore, the structure can be easily reused and recycled, making it an ideal green catalyst for many reactions. Np-Au has already shown significant catalytic activity in many important gas-phase and liquid-phase reactions, such as oxidation of CO, alcohols, and carbohydrates. We will briefly discuss some of the reactions below.
CO-oxidation is one of the important reactions necessary in controlling air pollution, such as through automotive or industrial emission and in hydrogen purification in fuel cells [94]. One of the early experiments to show the use of unsupported np-Au in CO-oxidation was conducted independently by Xu et al. [95] and Zielasek et al. [96]. Their experiment not only presented some of the important information on CO-oxidation but also became a crucial step toward the use of unsupported np-Au for gas-phase heterogeneous catalysis. Unlike palladium and platinum-based catalysts, np-Au shows important catalytic activity for CO-oxidation even at very low temperature down to −30°C and are tolerant to CO poisoning [97], Figure 5. It was found that unlike in supported gold catalysts, preactivation steps by passing O2 at high temperature is not the necessary step for unsupported np-Au [95]. CO conversion rate of 99.5% and >85% could be achieved for nearly 20 h when reaction performed at room temperature and −30°C, respectively. However, catalytic efficiency was found to decrease faster at room temperature due to coarsening of the porous structure [95]. Residual silver [96] or Cu [98] in the np-Au have been linked to strongly influence the catalysis of CO, however, there is no evidence to support the ability of residual silver or copper alone on catalysis below 100°C. There is no consensus among the scientists over the exact mechanism of CO-oxidation over np-Au catalyst. Some suggest that the residual metal helps to activate the molecular oxygen and hence np-Au should be considered a bimetallic catalyst [97] while others think low coordinated gold atoms present on the ligaments surface due to various steps and kinks are responsible for activating molecular oxygen [6]. Long-term stability of the np-Au catalysts for CO-oxidation at room temperature is still a challenge.
Catalysis: (A) CO2 signal typically detected at the reactor out during activation of a np-Au disk; (B) CO2 signal (outlet) for increasing O2 concentration at the reactor inlet (CO as carrier gas, reactor temperature 20°C). Reproduced with permission from Ref. [97], copyright 2009, American Chemical Society.
Methyl formate is an important precursor for the manufacture of formic acid, formamide, and dimethyl formamide, which is prepared in the industry at thousands of tons each year by combining poisonous carbon monoxide gas with methanol for the better selectivity [99]. However, it is possible to synthesize methyl formate from partial oxidation of methanol using suitable catalyst without using CO [100]. Monolithic unsupported np-Au has shown promising potential to be used in a gas-phase catalysis for selective conversion of methanol to methyl formate [101]. This is due to its high surface area, presence of considerable number of low-coordinated surface Au atoms, and availability of small percentage of Ag as a residual atom [101, 102]. Unlike nanoparticles, nanoporous structures are highly resistance to sintering and are successful in circumventing the limitation of bulk structure for dissociating the bound oxygen on its surface [103]. Strongly bound oxygen on the surface decreases the catalytic efficiency of the gold. Wittstock et al. used unsupported monolithic np-Au disc for the selective gas-phase oxidative coupling of methanol to methyl formate at low temperature with selectivity above 97% and high turnover frequencies [103]. Thin film of supported np-Au prepared on aluminum microfiber to form a composite structure was found to be cost effective, highly active, selective, and stable for oxidative coupling of methanol to methyl formate [104]. The composite structure is capable of achieving ∼100% methyl formate selectivity with ∼25% methanol conversion at 100°C and stable for more than 300 h without any sign of sintering.
On the other hand, the electrocatalytic oxidation of methanol using precious metal catalysts is of great interest for its use in direct methanol fuel cells. Pt-based catalyst strongly chemisorbs the intermediate species generated during electrooxidation of methanol poising the catalyst. However, these intermediate species have weak interactions with gold surface. Np-Au has high surface area and can transfer electrons better than the bulk and Au nanoparticle-supported electrode, making it a suitable catalyst for electrochemical oxidation of methanol [105]. Unfortunately, it was observed that the np-Au structures are coarsened quickly with the multi-cycling of the potential [52]. However, decorating the surface of np-Au by small amount of Pt to form nanoporous bimetallic Au-Pt alloy nanocomposites can greatly enhance the structural stability and the electrocatalytic activity toward methanol oxidation [106]. The nanoporous bimetallic Au-Pt alloy nanocomposites can also be prepared by dealloying the ternary alloy of gold, platinum, and other less noble metal [107]. This type of modified np-Au can work as a suitable catalyst for electrooxidation of other small organic molecules, such as formic acid, formaldehyde, and ethanol [108].
Recent works have proved that np-Au has remarkable catalytic activity in liquid-phase catalytic reactions. This type of reactions are not only selective but also work without any additives or stabilizing agents while avoiding cumbersome work-up procedures like filtration or centrifugation. Yin et al. used unsupported np-Au for the aerobic oxidation of
A substantial progress has been made during the last two decades in the synthesis, modification and functionalization of np-Au due to their many important and unique properties. Chemical dealloying is a quick and easy means of creating np-Au whether it is a self-supported bulk or solid-supported thin film; however, electrochemical dealloying is useful for control tuning of pores and ligament size of the thin films and might not be as useful for dealloying bulk structures. Recent knowledge on techniques to control the shape and size of np-Au and size of its pores and ligament has increased its importance in wide range of disciplines, including catalysis, optical and electrochemical chemical and biomolecules sensing, actuator, bioreactors, biomedicine, and energy.
In summary, np-Au is a versatile nanostructured framework that has diverse application not only as a pure material but also by functionalizing it with diverse types of organic molecules and metal or metal oxide nanostructures to convert it into multifunctional composite material. Converting np-Au into the multifunctional nanostructures can greatly increase its potential applications in different other fields of nanotechnology that were not previously envisioned.
The authors acknowledge recent support of their work in this area by University of Missouri – St. Louis and by the NIGMS awards R01-GM090254 and R01-GM111835.
Stroke is one of the leading causes of long-term disability in the United States and is the third leading cause of mortality [1]. Brain parenchyma is densely packed with millions of neurons, where any assault such as an ischemic or hemorrhagic stroke can leave a patient with debilitating deficits [2]. A few of these deficits include the inability to speak or understand language; loss of vision, complete paralysis of one side of the body, quadriplegia, persistent balance issues, and loss of the ability swallow independently. Neuropsychological changes are also very common and well documented in poststroke patients; however, the number of patients that suffer from these changes are grossly underestimated [3].
More than one-third of all stroke survivors experience some form of depression [4]. Depression after a stroke can manifest in many different ways including feelings of anger, frustration, hopelessness, guilt, mental slowing, fatigue, irritability, changes in appetite, social withdrawal, loss of interest in activities they once found enjoyable (also known as anhedonia), or even suicidal thoughts [2]. Patients that suffer from poststroke depression, often have these symptoms missed or undertreated. Recovery and rehabilitation can be adversely affected if post stroke depression is not adequately treated. This can result in increased length of stay at postacute care facilities, increased morbidity, decreased quality of life and even increased mortality [5]. Numerous depression scales have been used to define poststroke depression including the Beck Depression Inventory (BDI), Montgomery-Åsberg Depression Rating Scale (MADRS), Centre for Epidemiologic Studies Depression scale (CES-D), Zung self-rating depression scale and the Hamilton Depression Rating Scale (HDRS) [5]. Post stroke depression has a great impact on the healthcare system as well as on the individual patient. In this chapter, we will examine all aspect of depression as it relates to stroke by using these scales and large meta-analyses to define post-stroke depression, and assess how it relates to stroke and recovery.
Advancements in acute medical therapies have led to the reduction of mortality due to acute ischemic or hemorrhagic stroke [5]. Studies have shown that 10% of patients recover without any residual deficits, a quarter have mild residual deficits, while 50% are severely disabled or require skilled nursing care within a medical facility able to manage their needs [6]. Along with severe physical disability, patients that suffer from a stroke also experience neuropsychiatric changes. The most common neuropsychiatric sequelae, post-stroke, are depression and anxiety [7]. Patients that survive stroke often experience anxiety and depression related to making adjustments to their new reality [7]. With more patients surviving stroke, quality of life becomes an area of focus. Poststroke depression has been regarded as one of the most important measures for quality of life after an acute stroke. The presence of depression after stroke results in impaired recovery, decreased participation in rehab efforts, impaired cognition, and even increased mortality. The majority of the expressed concern from patients is related to their ability to work and provide financial stability for themselves/their families, the ability to manage their activities of daily living, and the loss of their functional independence [7].
The term poststroke depression puts a focus on ischemic rather than hemorrhagic strokes, which is mostly due to the fact that ischemic strokes have been studied more in the literature, and thus will be the focus of this chapter [8]. Poststroke depression can occur anywhere from days to years after an acute ischemic event with the peak incidence of poststroke depression occurring between 3 months and 2 years, even if the patient’s symptoms are improving [9]. Patients that experience the onset of poststroke depression at or after 7 weeks from the acute event are less likely to have a spontaneous remission of this depression [9]. In the acute phase, patients that had a longer inpatient hospital stay were seen to score higher on the Beck Depression Inventory than those that were in the community or in a rehabilitation facility. However, many of these studies have excluded patients that are aphasic, have cognitive impairment, or experienced pre-stroke depression. This may be one of the main reasons that poststroke depression may be underdiagnosed and undertreated [10].
Patients younger than 60 are seen to have higher depression scores poststroke. In the general population, major depression is more prevalent in patients younger than 65 years old [11]. In multiple studies that adjusted for pre-stroke depression it was found that more than 30% of the patients younger than 65 could be diagnosed as having clinical depression using the Center for Epidemiologic Studies Depression Scale (CES-D). It was found that within this younger age group there was a higher rate of depression associated with lower socioeconomic status, familial stress, and the ability to provide financial stability [7, 11]. However, having good social support has been found to be protective against poststroke depression [7, 11]. Adults over the age of 65 represent the majority of stroke patients, which can skew the data. However, multiple meta-analyses have shown that when controlling for other variables such as sex, patients younger than 65 experienced more poststroke depression, and more obvious depressive phenotype [6, 11].
Biologic sex and poststroke depression is a controversial issue. Numerous meta-analyses have looked at the relationship between ‘gender’ and how it affects or predicts poststroke depression. The results were mixed when looking at data from across the globe. In some studies, women have been found to experience double the risk of poststroke depression compared to men [12, 38]. The gender disparity may be related to how each sex reacts to stressful life events. Women have been demonstrated to have more stress in reaction to negative life events, such as a stroke, which results in feelings of depression [12]. On self-reported survey, women were seen to indicate they have more depressive symptoms, compared to men, when age was controlled for [12]. The risk factors for women developing depression after an acute stroke were: pre-stroke psychiatric comorbidity, age younger than 65, and impairment in cognition [13]. Similarly, men with higher level of physical disability after a stroke had more depressive symptoms than women, or men with less physical disability. In multicenter analysis from China, and India, these studies found that male sex had a higher correlation with poststroke depression [10, 15]. However, there may be confounding factors when evaluating sex differences and poststroke depression. For example, in China there may be a higher number of men in the general population [14]. In the Indian study there were more men in the study [10]. In the USA, it is possible that there is a higher rate of self-reporting by women, as well as under reporting of depressive symptoms in men, based on their level of physical disability [14]. Therefore, more studies need to be done in this area to determine if gender is a definitive predictor of poststroke depression.
Socioeconomic status and education related to poststroke depression is also difficult to measure, due to multiple confounders and conflicting data. However, reviewing the meta-analysis of patient demographics and poststroke depression has shown that patients with lower overall education levels have an increased risk for poststroke depression with mild depressive symptoms [13]. A large meta-analysis of the literature found that there is an association between more years of education and lower risk for depression after a stroke. This study demonstrated that on average the participants in the study without poststroke depression had 0.32 years of education more than those that did have depressive symptoms after their stroke [16]. The symptoms that were seen in this data set were defined as mild depressive symptoms, but could not be classified as clinically depressed. However, this may also have confounding factors in this category. Patients that have lower socioeconomic status have been shown to have lower levels of education [16]. They may also be exposed to environmental factors that put them at increased risk for stroke, such as unhealthy diet, unhealthy lifestyle, more perceived stress, exposure to second hand smoke, and pollution in urban areas [10, 13, 16]. These factors may increase their risk of stroke, and thus their risk for poststroke depression.
Comorbid conditions prior to a stroke can affect the development of depression after an acute ischemic event. Conditions such as diabetes, and preexisting psychiatric disorders like depression, anxiety, and bipolar disorder can all have an effect on poststroke depression [17, 18]. One meta-analysis has demonstrated that patients that have vascular risk factors such as diabetes are at a higher risk for developing poststroke depression [17]. This is not thought to be related to the vascular depression theory, which will be discussed later in this chapter. In a Chinese study, it was shown that at 3 months after an acute stroke, patients with diabetes were more likely to develop poststroke depression. This was an independent risk factor for the development of poststroke depression at or after 3 months [17]. The hypothesis behind this is based on the pathophysiology behind both diabetes and poststroke depression, which involves the inflammatory pathway, and the hypothalamic pituitary access. This will be discussed later in the chapter.
Preexisting psychiatric disorders such as depression, anxiety, and bipolar disorder can also predispose patients to worse poststroke depression in the subacute phase, which is within 3 months [17]. One meta-analysis that looked at predictors of poststroke depression found that of the patients that had a preexisting mood disorders such as dysthymia, major depression, minor depression, anxiety, agoraphobia and adjustment disorder were all associated with increased risk of worsening depression after a stroke. Of 1058 patients with reported depression prior to their stroke, 27% had worse depressive symptoms after the acute ischemic event [18]. Premorbid anxiety was also predictive of worsening anxiety after the stroke. Anxiety poststroke results in impaired response to adverse events increased perceived stress and more depressive symptoms [18].
Poststroke depression has been defined as a mood disorder resulting from a general medical condition, by the Diagnostic and Statistical Manual of Mental Disorders (DSM) IV, meaning it does not carry with it the same definition of major depression [16]. There has been some debate about the etiology of poststroke depression, where multiple hypotheses exist, including but not limited to disruption to monoamine pathways, inflammatory cytokines, and hypothalamic–pituitary axis within the brain that modulates mood. The other belief is based on a psychosocial model, where depression develops after a stroke due to inability to adjust to new life circumstances, inability to care for oneself, fear of recurrence, financial insecurity and carrying a new diagnosis [7].
One question that has been analyzed extensively with no definite answers is the location of a stroke as a predictor of poststroke depression. These studies used techniques such as voxel-based symptom lesion mapping, diffusion tensor imaging (DTI), functional magnetic resonance imaging (MRI), and positron emission tomography (PET) scans [19]. Functional neuroimaging has sought to determine neuronal circuitry to discover how damage to these circuits results in mood or personality changes. These imaging modalities demonstrate that there is less activity in the frontal cortex, anterior cingulate, dorsolateral and caudate nucleus, in patients that are experiencing depression. In pilot studies using DTI, there has been some data demonstrating that damage to the fronto-striato thalamic pathway and pathways involving emotional control, reward systems and decision making can lead to increased risk of poststroke depression [19]. DTI changes were seen in stroke patients that had damage to the genu and splenium of the corpus callosum, frontal lobe white matter and anterior left corona radiata, resulting in increased levels of apathy [20]. A few theories about lesion location and depressive symptoms include-anhedonia as associated with the stroke volume affecting the hypothalamic-pituitary-adrenal axis, and increased risk for depression in patients with basal ganglia, and frontal lobe strokes [20]. A study by Paradiso and colleagues demonstrated that patients who had left hemispheric strokes were likely to have more depressive symptoms [19]. They proposed that right hemispheric strokes experience fewer depressive symptoms due to anosognosia. If the patient is unaware of his or her deficits, they will less likely feel depression related to their loss of function. Left hemispheric strokes have also been seen to have an earlier onset of poststroke depression, usually in the first 6 months poststroke [13].
One of the models that have been proposed is that subcortical strokes like those in the basal ganglia, and strokes in the frontal lobes can result in disrupted serotoninergic and norepinephrinergic pathways that can be associated with poststroke depression [21]. The belief is that strokes that affected the amine-containing axons between the brainstem and specifically the left cerebral cortex would result in decreased production of serotonin (5-HT) and norepinephrine [22]. A reduction of these neurotransmitters in the frontal and temporal lobe limbic structures, and in the basal ganglia could result in difficulty with mood regulation [19]. This theory was supported by the finding that there were low levels of the 5-HT metabolite, 5-hydroxyindoleacetic acid in the cerebrospinal fluid (CSF).
Inflammatory cytokines were also thought to be related to the development of poststroke depression [23, 24]. Jioa and colleagues found that interleukin (IL)-6 was elevated in patients with post-stroke depression, even after controlling for confounders, with a confidence interval of 95% [23]. The elevation of IL-6 in patients that have strokes could possibly predict the development of poststroke depression [23, 24]. In another meta-analysis, brain-derived neurotrophic factor (BDNF) was found to be involved in the development of depression and poststroke depression [25, 26]. In these studies, a low serum level of BDNF in the acute phase after a stroke was associated with the development of poststroke depression. BDNF is inherently involved in hippocampal plasticity and memory [27]. One study found a significant negative relationship between BDNF and NIHSS [25, 26, 27]. In rodent models, low levels of BDNF in the hippocampus that had an acute stroke exhibited depressed behavior, however if BDNF was overexpressed there was a marked decrease in depressed behavior [21]. Increased BDNF in the rodent model also resulted in reduced infarct size and improved functionality of the rodent [25].
Increased serum level of C-reactive protein (CRP), neopterin, ferritin, and glutamate could also be related to poststroke depression [24]. Proinflammatory markers such as tumor necrosis factor (TNF)-α, interleukins (IL)-1β, IL-6, IL-1, and interferon gamma (IFN-γ) were associated with the development of poststroke depression [23, 24]. Additionally, inflammatory cytokines can activate the hypothalamic pituitary adrenal axis [24]. Activation of the HPA access can also lead to the downstream release of glucocorticoids, which can also result in increased blood glucose levels, and potentially diabetes if this is a chronic process. After an acute stroke, patients often exhibit increased levels of serum adrenocorticotropic hormone, and cortisol. These hormones result in higher mortality and worse neurologic outcome [23]. Increased cytokine activity could also result in greater expression of genes involved in the metabolism of tryptophan such as indoleamine 2,3 dioxygenase (IDO) [27]. If IDO expression increases, tryptophan will be converted to kynurenine and not 5-HT. The downstream effect could result in decreased levels of 5-HT in the limbic system, temporal lobes, frontal lobes, and basal ganglia, which could potentially result in depression [27].
There have also been studies that have shown a genetic contribution to poststroke depression. Multiple studies have evaluated the 5-HT gene located on chromosome 17q11.1-17q12, which encodes the serotonin transporter [25, 26, 27]. In a meta-analysis of 7 studies, there was a significant relationship between 5-HTTLPR polymorphism and the development of poststroke depression symptoms. 5-HTTLPR is an exon of the 5-HT transporter gene polymorphism [25, 26]. The hypothesis is that this gene polymorphism responds to the increased activity of the amygdala when responding to negative stimuli. An increase in 5-HTTLPR serum level has been positively associated with threefold increased risk of developing poststroke depression [25, 26, 27, 28]. Another 5-HT polymorphism that has been analyzed is the STin2 VNTR, which is located within intron 2. It has variable number tandem repeats 9, 10, or 12. Repeats of the 9-allele have been well documented to be associated with multiple psychiatric disorders such as bipolar disorder, and major depression [25, 26, 27, 28]. Repeats of the twelfth allele have been linked to the development of schizophrenia and bipolar affective disorder. It has been demonstrated that patients with variable tandem repeats of 9/12 and 12/12 were likely to have more depression after a stroke [25, 26, 27, 28].
Lastly, psychosocial factors must be considered when assessing who is at risk for poststroke depression. After suffering a life-altering event such as a stroke, even if there are no severe deficits, patients can undergo an adjustment period. They may feel depressed about the new diagnosis of a stroke. There is also the concern of getting back to their normal life routine such as working, caring for dependents, and caring for their own activities of daily living (ADLS) [11, 12]. Patients that do not have good social support tend to experience more depression after a stroke due to feeling helpless, and alone. Patients may also experience anxiety, related to the fear that another stroke may occur. Financial costs of health care also play a role in postacute stroke depression. If a patient is unable to work there may be a concern about medication compliance, affording medication, affording postacute special services like physical therapy or occupational therapy [11, 12].
Although there is a growing prevalence of stroke in patients aged 65 and younger, the majority of strokes affect patients that are elderly. With the prolonged life expectancy, there is an increased risk for stroke in the aging population, with 70% risk being after the age of 65 [29]. In patients older than 80 years old that suffer from strokes, there is a greater risk of fatality, prolonged hospitalization, complications, and increased postacute care needs [30]. In elderly patients that suffer from stroke, depression may be difficult to diagnose. This is largely due to the symptoms being a vegetative phenotype. It is also confounded because depression is the most common psychiatric disorder among the elderly—with 1% of the elderly population having a formal diagnosis of major depression, and 15% with depressive symptoms according to the National Institutes of Health Consensus development conference [31]. This poses a challenge that practitioners face in distinguishing between premorbid depression, inherent stroke symptoms and poststroke depression, given that many of the features overlap. Some such features include cognitive impairment, psychomotor retardation, and social withdrawal [29]. One measure used to assess poststroke depression in the elderly is the geriatric depression scale (GDS) [32]. This is a self-reported scale where patients answer yes and no questions to determine if a patient is experiencing some form of depression. A score greater than 6 indicates that the patient is likely experiencing some form of depression. This scale is highly sensitive and predictive of poststroke depression in the geriatric population [32]. However, the GDS cannot be used by aphasic stroke patients or those with cognitive impairments caused by a stroke.
Alexopoulos and colleagues found that elderly stroke patients that suffered ischemic strokes demonstrated increased encephalomalacia and MRI hyperintensities that would predispose these patients to develop depression [33]. Their study suggested that these changes were not seen in elderly patients that had depression without vascular risk factors. Elderly patients that have been observed to have signs of depression, but do not have any vascular risk factors were found to have less white matter hyperintensities on MRI, which were similar to the nondepressed controls [31]. It has also been demonstrated that patients that suffered from depression without vascular insult had phenotypically different depression with features of more agitation, aggression, feelings of guilt and dysphoria. This is the theory of vascular depression in the elderly [33]. The hypothesis behind vascular depression states that chronic small vessel changes or non-symptomatic cerebrovascular events accumulate over time, resulting in the disruption of cortico-striato-pallido-thalamo-cortical (CSPTC) pathways [31]. Vascular dementia is described as a subcortical phenomenon. This type of depression differs from poststroke depression, in that they are silent, and the patient is not aware that they have suffered a stroke [31]. In a Japanese sample, greater than 80% of the patients that had major depression had MRI evidence of multiple silent infarcts [32]. Up to 75% of these depressed patients had lesions in the basal ganglia and thalamus [31, 33].
Three pathways associated with CSPTC were proposed in the way that vascular depression can present phenotypically. Within the CSPTC are the orbitofrontal pathway, the cingulate pathway, and the dorsolateral pathway. Injury over time to the orbitofrontal pathway can result in irritability and disinhibition [31]. The cingulate pathway can cause apathy, and lack of initiative if injured, and lastly, injury to the dorsolateral pathway can result in poor speech productions, and inability to learn. These symptoms can all be seen in elderly depression. Prefrontal dysfunction has shown to have a poor or delayed response to antidepressants in elderly patients [31, 33]. However, early administration of antidepressants, particularly selective serotonin reuptake inhibitors have been shown to improve neuropsychological rehabilitation in elderly stroke patients.
Lacunar infarcts have been seen to result in more depression among Alzheimer patients especially basal ganglia strokes and cortical strokes were found to have more cognitive impairment [31]. Severe cognitive impairment was also seen to be one of the leading causes of depression in the elderly. There are some questions of whether cognitive impairment or dementia can increase the risk of stroke, and thus poststroke depression among the elderly, or do strokes result in cognitive decline and vascular depression [31]. Dementia and depression can be difficult to differentiate. In the elderly, pseudodementia can be secondary to depression however, the opposite is also true. This is a “what came first” type of scenario with dementia, stroke and vascular depression [31].
Although vascular depression and poststroke depression are different in the way they affect a patient, they likely lay on a continuum. Both are secondary to a vascular event, and both result in depression. Vascular depression has a higher incidence in elderly patients as they have an accumulation of more subcortical white matter changes that are seen as hyperintensities on MRI FLAIR. Poststroke depression is less subtle since the patient is usually aware that they have had a stroke [31, 33]. There may be a growing incidence of vascular depression among young patients, due to poorly controlled hypertension, tobacco, diabetes, drug use, and poor diet and lifestyle choices causing small vessel disease. These risk factors put all patients at risk for an acute stroke, and chronic small vessel disease.
In patients that suffer from large ischemic or hemorrhagic strokes, they are often left with a serious physical disability [2]. A proximal middle cerebral artery occlusion can result in severe expressive, or receptive aphasias, hemiparesis, facial weakness, sensory loss inability to swallow, neglect, apraxia, and a propensity toward developing seizures [34]. If the patient is relatively young, the probability of cerebral edema is high, which could result in complications such as brain herniation if a hemicraniectomy is not performed. Intracerebral hemorrhage in these vascular territories can result in similar findings that may necessitate an extra ventricular drain to remove blood from the ventricles, or a decompressive hemicraniectomy to evacuate the hemorrhage [34]. A patient with a large stroke in the posterior circulation can result in the patient being obtunded, having chronic balance issues, hemiparesis, vision loss, and ataxia [3].
Patients that survive these large strokes often experience the most debility, with the majority becoming bedbound, requiring a percutaneous endoscopic gastrostomy tube for nutrition and tracheostomy tube for assistance with breathing. Due to the severity of their disability, these patients require 24-hour care, by their families or nursing professionals. The majority of these patients experience severe depression and guilt, due to feeling like a financial or physical burden on their loved ones [35]. They also experience loss of autonomy due to their deficits. They are no longer able to manage their own activities of daily living, which results in feelings of inadequacy, and resentment for those that are doing the caregiving. Depression has also seen to be positively correlated with the national institute of health stroke scale (NIHSS) which measures stroke severity, wherein the higher the stroke scale, the more severe the depressive symptoms [36].
Patients with large strokes and increased debility often require management in a skilled nursing facility (SNF). At SNF, the patients do not participate in as much rehabilitation activities, as compared to other stroke patients in an inpatient rehabilitation setting [32]. These patients are therefore at disadvantage because their exposure to rehabilitation is limited. The combination of decreased functionality, less access to rehabilitation, and depression impairs the recovery for these patients. They too lose the desire to participate in meaningful interaction due to their disability [32].
Diagnosing depression after a stroke may be difficult for practitioners given that stroke patients can have complex symptoms. The physicians that treat stroke patients should be aware that over a third of patients experience depression after a stroke, and to note that even subtle changes in behavior could represent an aspect of poststroke depression [17]. Small changes like irritability, frustration, extreme fatiguability, and refusing to partake in physical therapy and occupational therapy. Another challenge is that many symptoms of stroke and depression overlap, such as fatigue, pain, decreased motor activity, and decreased verbal output [7]. Only a few of the depression scales used to assess poststroke depression include somatic symptoms in their evaluation. The Beck Depression Inventory is one such scale. However, again some somatic symptoms from the stroke itself can be mistaken as a positive finding on a depression scale. It is important to be able to tease apart what symptoms are due to a stroke and what symptoms are related to depression. If a diagnosis of poststroke depression is missed, it can negatively affect how the patient recovers, and even affect their mortality.
The symptoms that make the diagnosis of poststroke depression the most difficult are aphasia, anosognosia, neglect, abulia and cognitive disabilities that result from their stroke [37]. Unfortunately, the majority of studies that evaluate poststroke depression exclude patients with these symptoms. This is largely due to their inability to answer questions, fill out questionnaires, or because it is difficult for medical staff to assign a score to the patient based on their daily interactions. Aphasia is independently associated with an increased risk of developing poststroke depression [37]. However, three scales have been developed to assess depression in aphasic patients. These scales include the Stroke Aphasic Depression Questionnaire-10 (SADQ-10), the Aphasia Depression Rating Scale (ADRS), and the Perceived Stress Scale (PSS). The (SADQ/SADQ-10/SADQH-10) and the Aphasia Depression Rating Scale are based on the observation of other people to determine if the patient being assessed is in fact depressed or not. The SADQ-10 used caregivers as the observers, with non-aphasic patients as the controls [37]. A value of 14/30 or higher was correlated with the development of depression and depressive symptoms with a sensitivity of 70% and specificity of 77%. The ADRS scoring system used external signs that could be observed such as fatigue, insomnia, changes in weight, and signs of anxiety. A score of 9/30 or higher was associated with the development of depression with a sensitivity of 83% and specificity of 71% [37]. After a comparative analysis, it was determined that either one of these tools could be used for assessing depression in aphasic patients. A review of the current studies could be more generalizable if aphasic patients were included and analyzed with these scales.
Poststroke depression was found to be an independent predictor of symptom severity after a stroke, and difficulty with managing activities of daily living [35]. In a meta-analysis of seven studies, poststroke depression was found to have an association with increased mortality [39]. Specifically, patients that experienced early poststroke depression as defined to be within 3 months of stroke onset, were found to have 1.5 increased risk of death. A literature review by Robinson and colleagues, found that using the Hospital Anxiety and Depression scale (HADS), patients that had a score greater than 7 at 3 months had increased mortality than those with a score less than 7 [38]. These scores were evaluated up to 5 years poststroke, and the hazard ratio was found to be 1.41. It was seen that mortality was increased in patients with poststroke depression that were younger than 65 years old [38]. Their study also demonstrated that in greater than 50,000 veterans that suffered an ischemic stroke, those that developed poststroke depression had higher rates of mortality within 3 years of that acute event. The hypothesis behind this being that early poststroke depression can occur in a patient with a severe disability such as neurocognitive decline, paralysis, aphasia, or dysphagia [38]. Due to the severity of their post-stroke symptoms these patients may be at increased risk of death due to complications like pneumonia secondary to dysphasia or infection from decubitus ulcers. Another hypothesis is that patients that are suffering from poststroke depression may be less likely to be compliant with medical recommendations, such as healthy diet, avoiding tobacco, alcohol, drug use, scheduled follow up appointments and medication compliance [37, 38]. These factors can increase the risk of mortality. Another theory states that mortality associated with poststroke depression may be related to cardiovascular mortality [38, 39]. There is an association between depression and myocardial infarction, where it was found that depressed patients had less heart rate variability. This finding was also seen in patients with poststroke depression. This could put these patients at risk for myocardial infarction and subsequently, death. This meta-analysis also highlighted the idea that pharmacologic antidepressants have a mixed response in poststroke depression [38].
In order to treat poststroke depression, it needs to be accurately diagnosed. Currently the DSM IV is used to diagnose this disorder, along with multiple depression rating scales such as the Hamilton Rating Scale for Depression, Beck Depression Inventory, Montgomery-Åsberg Depression Rating Scale, Center for Epidemiological Studies Depression Scale, Zung self-rating depression scale and the Post-Stroke Depression Rating Scale [5]. There are many challenges in diagnosing depression in a patient after an acute stroke. Many of these patients have a somatic component to their symptoms, like pain, fatigue, or limited speech after a cerebrovascular event. These symptoms can confound a depression scale that account for somatic symptoms—like the Beck Depression Index [5]. Depending on which scale is used to measure depression in these patients, there may be an overestimation or underestimation of depression. Since the hypothesis that stroke results in disruption of the monoamine pathways, there has been a focus on antidepressants like selective serotonin reuptake inhibitors, or tricyclic antidepressants to target poststroke depression. However, the role of antidepressants has been debated. There are some studies that show efficacy and reduction in mortality, and some that show a minimal effect or even adverse side effects [38, 39, 40]. Selective serotonin reuptake inhibitors (SSRIs) are well tolerated and can lead to fewer symptoms of depression at 3 weeks of use [40]. It is one therapy that is thought to work well in all age groups, regardless of comorbid conditions. SSRIs are better tolerated in all populations, compared to tricyclic antidepressants (TCA) [39, 40]. One endpoint found that patients that were started on SSRI early had decreased risk of myocardial infarction and recurrent stroke [40]. In a meta-analysis by Robinson and colleagues, the use of nortriptyline or fluoxetine demonstrated improvement in activities of daily living in poststroke depression compared to patients on placebo [38]. This study also demonstrated that the continued use over 12 weeks resulted in improved cognition in patients with poststroke depression, where the effect could last up to 2 years. Not only do SSRI inhibit reuptake of serotonin, but it was demonstrated in rodent models that SSRIs can decrease infarct volumes, reduced inflammation and increase neuroplasticity by modulating BDNF expression [38]. SSRI was also found to increase neurogenesis in the hippocampus, and improve cerebral blood flow autoregulation which is thought to be related to the upregulation of BDNF [27, 38].
In the fluoxetine in motor recovery of patients with acute ischemic stroke (FLAME) trial, fluoxetine use for 3 months was tested to see if it would improve motor recovery in patients with hemiparesis [41]. This trial was used to assess if the use of fluoxetine would change the Fugl-Meyer motor scale (FMMS) score which is an index used to test motor recovery, with a score of 100 representing complete motor function without any deficit. Two groups were analyzed a fluoxetine dose of 20 mg was the placebo and a 40 mg dose was used as the test treatment. At 3 months there was a significant improvement in motor function among the patients in the treatment arm [41]. At 90 days modified rankin scale (MRS) scores were better in the treatment arm as well. The frequency of depression was lower in the treatment arm when assessed with the MADRS score at 90 days. Even in patients that did not receive intravenous thrombolysis, their FMMS scores at 90 days were higher in the treatment arm. Patients that were assessed to be depressed at the onset of the trial, based on MADRS score, were excluded from this trial [41]. Pretreatment with SSRI prior to stroke was also an exclusion criterion. Although the FLAME trial seemed to be promising for improving motor function in poststroke patients and reducing depression within that 3-month period, newer studies have shown the use of SSRI prior to stroke, was negatively associated with ambulation poststroke [8].
In a study by Etherton et al., it was found that the use of SSRI prior to an acute stroke was associated with a decrease in discharges back to the patient’s home, and increasing need for ambulatory aids [8]. When examining the patients in the two groups: pre-SSRI/spread vs. non antidepressant, there were no significant difference in admission NIHSS or length of hospital stay. The authors thought this may be due to the possibility that patients that were on SSRI or antidepressants prior to admission for their stroke event may have suffered a stroke before or TIA, resulting in a larger stroke burden. Another ischemic event could cause recrudescence of old stroke symptoms due to an increased burden on that area that was receiving adequate blood flow, which could lead to the patient having more needs such as rehabilitation at discharge. Pre-SSRI use was also associated with increased mortality at 30 days, and worse stroke severity in patients with hemorrhagic stroke [8].
Another criticism for the use of SSRIs was due to the increase in the risk of major bleeding or death. In a meta-analysis of 31 case-controlled studies, it was found that SSRI use was associated with risk of major bleeding events, with the increased risk being 41% [40, 42]. This meta-analysis also examined cohort studies that evaluated the use of SSRI vs. non-SSRI in association with major bleeding risk of 36%. The pooled data from the meta-analysis found that SSRI was associated with major bleeding risk with an odds ratio of 1.41. Gastrointestinal bleeding accounted for the majority of these major bleeding events, with a few intracerebral hemorrhage cases [42]. The hypothesis behind the increased bleeding risk is that platelet activity is inhibited by serotonin. This hypothesis is strengthened by the idea that patients taking SSRI have less myocardial infarctions and fewer strokes. The major bleeding risk associated with SSRI are amplified with adjunct use of non-steroidal anti-inflammatory drugs (NSAIDS) [42].
Overall, antidepressants such as SSRI and TCA have been thought to be the best initial treatment for post-stroke depression. SSRI are overall better tolerated in all populations [40]. These antidepressants can help patients combat poststroke depression enough to allow them to participate in rehabilitation efforts. Psychotherapies such as cognitive behavioral therapy (CBT) have been studied to assess if it would be beneficial in the treatment of poststroke depression. Due to the small sample size of the studies, and other limitations there was no real effect seen with CBT [5]. It may be an area of adjunct therapy for patients with severe poststroke depression that need more than pharmaceutical treatment. However, the use of CBT should not delay the initiation of treatment with antidepressants.
Depression after stroke strongly affects the way patients participate in and respond to rehabilitation. Depression has been linked with decreased participation in rehabilitation efforts which in turn results in more increased morbidity and mortality and decreased quality of life. In a Japanese study that evaluated poststroke depression in patients admitted to a rehabilitation center, their results demonstrated that the patients that were identified as having poststroke depression had less response to rehab and minimal improvement in activities of daily living and functional independence measures [32]. This study found that the level of independence in the activities of daily living at the time of discharge from rehab was related to the severity of poststroke depression at the time of admission. Poststroke depression had a negative 5-year correlation with the ADL. Psychological factors accounted for a large part of how patients responded to rehabilitation [32]. This study found that patients with poststroke depression experience feelings of hopelessness and were thus not motivated to participate in rehabilitation. Depression in these patients also leads to listlessness and inattention, which predisposed the patients with poststroke depression to falls. Thus, another reason why mortality is higher in patients with poststroke depression. Falling was also correlated with a decreased ability to manage their ADL [32].
Another study on depression and rehabilitation found that patients with hemiparesis and poststroke depression had 51% less participation in rehabilitation activities [43]. This study showed that any amount of depression after a stroke can affect a patient’s quality of life despite the severity of the stroke. This is because each patient has a unique response to acute stress. The perceived stress score is valuable in rehabilitation because it helps practitioners identify which patients are more at risk of developing depression. If they are identified early, treatment of depression can be initiated, and rehabilitation does not need to be adversely affected. Some of the indexes used to measure the quality of life in patients with poststroke depression include the Stroke Specific Quality of Life Scale SS-QOL, stroke impact scale, Barthel index of ADL as well as the multiple depression rating scales [43]. The Scandinavian Stroke Scale (SSS) and Bergman Balance Scale (BBS) are measures used to assess the progress of rehabilitation, which is more encompassing than the Modified Rankin Score [10]. If patients are able to meaningfully participate in rehabilitation, studies have proven that symptoms of depression can improve, and their quality of life scores increase as well [43]. This coupled with the use of antidepressants can help patients with depression poststroke manage their symptoms of depression and improve their functional outcome. It could also help prevent a subsequent ischemic event [43].
Depression has also been found to be a risk factor for stroke [44]. This has been demonstrated even when controlling for confounders like tobacco use or substance use. Patients with psychosocial stressors put patients at an increased risk of stroke [11, 12, 44, 45]. Not only do these patients have an increased risk of hypertension, and diabetes, but also have an increased prevalence of tobacco use and substance use that also put them at greater risk for an ischemic stroke [44]. A meta-analysis by Dong and colleagues, looked at 17 prospective studies that included greater than 200,000 patients [45]. Of this subset of patients, greater than 6000 had a positive association between depression and a second stroke. A depressed patient had 34% higher risk of developing stroke, even when age and sex were controlled for [45]. Thus, stroke and depression may be a part of a vicious cycle where a stroke results in depression and then depression results in another stroke. This process repeats and, in turn, hinders recovery and rehabilitation. Thus, proving again why it is important to diagnose depression after a stroke, and treat it adequately.
Poststroke depression can increase the burden on the healthcare system. In two literature reviews the effect of depression after a stroke was assessed by looking at large veteran populations [46, 47]. These studies demonstrated that patients that suffered from poststroke depression had on average a longer hospital stay, as well as increased outpatient and inpatient physician visits over 1 year. These patients also had a higher likelihood of having significant deficits such as dysphagia after their stroke, and complex comorbidities that required frequent hospital visits, or prolonged stays in nursing facilities/rehabilitation centers [47]. They were also noted to have higher risk of a subsequent stroke within 1 year of their first stroke, and readmissions for complications related to their strokes such as aspiration pneumonia, or falls [47]. In Husaini and colleague’s analysis of 17,010 patients from Tennessee, their study demonstrated that patients with stroke and depression had higher average health care costs than patients with only stroke, or stroke with another comorbid psychiatric disorder, even while controlling for age, sex and race [48]. On average stroke patients with depression had a healthcare cost of $77,864, compared to $47,790 in patients with stroke only these costs are due to increase use of diagnostic tests, increased pharmacologic interventions, and addition therapist and physician consultations [47, 48]. If poststroke depression could be identified early, and treated it could reduce the total cost to the patient, and could decrease the overall healthcare burden (Figure 1).
The diagnostic and treatment procedures of PSD. MDD = major depressive disorder; PSD = poststroke depression [49].
Depression and stroke have a bidirectional relationship where one acts as a risk for the other. Poststroke depression is an area of study that has evolved over the years. New studies on its etiology have been discovered, and continued research efforts are providing more insight on the questions we still have, such as the associations of lesion location, the role of inflammation, neuroplasticity, and even genetics. Some patients are more at risk than others for developing poststroke depression, but the main goal is detection, management, and rehabilitation. Detecting poststroke depression is important, so treatment can be initiated as soon as possible, thus reducing morbidity, mortality, and assisting these patients with participating in rehabilitation efforts. Rehabilitation not only improves function in these patients, but also has beneficial effects on depression as well. If patients can effectively partake in rehabilitation efforts, their quality of life scores have been shown to improve (with quality of life being a measure for depression in these patients). Improvements in perceived quality of life can have downstream effects resulting in a reduction of readmissions to the hospital, and outpatient visits, and thus a reduction in the healthcare burden caused by this disease process. If depression can be effectively managed, patients will be more likely to have meaningful participation in poststroke rehabilitation, and reduce the risk of morbidity and mortality associated with their stroke.
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