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Patients demonstrate a droopy palate ipsilateral to the lesion and a mild hypernasality prostate artery embolization proscar 5mg sale. The hypoglossal nerve controls all of these muscles with the exception of one extrinsic tongue muscle, the palatoglossus muscle. The tongue deviates on protrusion, but there is only a mild impact on articulation. Multisystem Damage As discussed in this section, damage to one system leads to one or two types of dysarthria, whereas damage to another system leads to one or two other types of dysarthria. This flaccid-spastic subtype accounts for about 42% of mixed dysarthria cases (Duffy, 2013). Sometimes one form of dysarthria will characterize the beginning of the disease process and then the other form will appear as the disease progresses. Other conditions, such as traumatic brain injury or multiple strokes, can lead to mixed dysarthria. Many patients with dysarthria have the mixed form, because neurological injury often involves more than one neurological system component. Duffy (2013) found that mixed dysarthria accounted for nearly one-third of all dysarthric conditions. Sensory Pathways Important for Speech Ascending Sensory Pathways Descending neural pathways are motor in nature, whereas ascending neural pathways are sensory. Sense receptors in the skin and muscles send sensory signals to the dorsal root ganglion of the spinal nerve or the ganglia of sensory cranial nerves in the brainstem. Neurons in the spinal cord or brainstem then carry the signal through the thalamus to the postcentral gyrus of the parietal lobe. The sensory functions of this pathway include fine touch (as is found in the hands and mouth), vibratory sense, and proprioception. This sensory feedback is important to the speech process, and heightened awareness of it is often targeted in stuttering therapy. The intrinsic tongue muscles make up the tongue itself and are not visible in this view. The cerebellum is an important neural structure for our balance, and it uses proprioceptive information from the body to help us maintain our balance. Kinesthesia It is a common assumption that the brain uses only our sense of hearing as a source of feedback for how our motor speech system is performing. For example, if we mispronounce a word (as we all tend to do at times), we hear the error and make the appropriate corrections in order to say the word correctly. Auditory feedback is not the only sensory system the brain uses to monitor speech, however; if it were, how would a person who is deaf ever learn to speak The answer is that the brain also uses somatosensory information to achieve the precision needed in speech (Nasir & Ostry, 2006). Kinesthesia and joint position sense are the two components of proprioception (Konradsen, 2002). Deemphasizing auditory feedback and emphasizing kinesthetic feedback has been a standard tool for decades in treating stuttering. The spinothalamic tract is the primary route for pain information as well as temperature, pressure, and crude touch. This tract has the same origin as the previous two, but its final input is in the cerebellum. Its function is to relay proprioceptive information from the arms, legs, and trunk of the body to the cerebellum, where it is then Summary of Learning Objectives 259 who stutter, and relied solely on the kinesthetic feedback from his mouth. Often, delayed auditory feedback, rather than music, is used with people who stutter. In this therapeutic technique, the person who stutters wears headphones connected to a system (or a smartphone with an app) that sends auditory feedback back to him or her, but in a delayed fashion. Because it is delayed, it is of no use to the person because it does not match up with what is currently happening with the articulators. Delayed auditory feedback thus forces the person to depend on kinesthetic feedback rather than auditory feedback and helps to produce improved fluency. A seventh type, mixed dysarthria, results from diffuse brain damage that impacts multiple speech systems. As the disease progresses, the patient will eventually deteriorate to the point of having anarthria, which means no speech at all. The learner will connect different places of damage in the motor speech system to different forms of dysarthria. List the basic levels of the motor speech system beginning with the conceptual level. Write out the names of the seven types of dysarthria along with where damage occurs in the motor speech system to cause each. He also demonstrates tremors in both hands with the tremors being more pronounced on the right. What neurological condition do you think the neurologist diagnosed William as having Read the Libet studies found in the References and summarize his experimental design. Motor speech disorders: Substrates, differential diagnosis, and management (2nd ed. Motor speech disorders: Substrates, differential diagnosis, and management (3rd ed. Factors contributing to chronic ankle instability: Kinesthesia and joint position sense. Unconscious cerebral initiative and the role of conscious will in voluntary action. Time of conscious intention to act in relation to onset of cerebral activity (readiness-potential). We not only express language but also receive it through listening/comprehending and reading. Language is complex, and many brain regions appear to be involved in our production and comprehension of it. The learner will outline how language is thought to be neurologically processed in comprehending, reading, speaking, and writing. Students spend numerous hours learning at least one additional language to their native language; thus, language is not only something we use every day but also something we intentionally think about as we learn other languages. The purpose of this chapter is to define language, sketch out its components, discuss the neurology of language, and survey several language disorders. If person A wanted to communicate with person B, A could bring all the objects necessary and point to them to convey a thought, but language makes this task much easier. We use words to represent these real objects; thus we do not need objects at hand to talk about them. This word is an arbitrary set of phonemes that is understood to represent a furry, domesticated, four-legged creature that barks. For example, when I teach my classes, what I say one semester is never exactly what I say the next semester; I am always creating new sentences even though the topics are the same semester after semester. Old English developed into Middle English, then went through the Great Vowel Shift, and emerged into Modern English. Code Taking all these characteristics into consideration, a working definition of language can be developed before discussing the neural basis of language. Having defined language, it is now time to discuss the basic components of language before taking on the difficult task of outlining a neurology of language. The Neural Basis of Language 265 word dog, there is meaning attached to this word. Lastly, language use is also known as pragmatics, which refers to how we practically use language with other human beings. Just from laying out these three components and some of their subcomponents, one can see the incredible complexity of language. It is simply amazing that humans can produce such a complex feat and often with little thought behind how to do it. For example, in English phonology, we talk about three major features of consonants-manner, place, and voice. For the sign "mother," the fingers and thumb are flared out and the thumb taps the chin.

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It appeared therefore that the patient had a pyramidal syndrome of unknown etiology prostate cancer home remedies order 5 mg proscar with amex. Nine months following intake I reviewed this patient who has spastic paresis with a pseudobulbar affect and pseudobulbar signs. Bulbar evaluation has shown that he has dysphagia mainly for liquids, but he is able to cope as long as he drinks slowly. In neurology, it is also sometimes used to reduce saliva production to avoid choking, a sign of dysphagia. Medication that works as a muscle relaxer to improve spasticity, pain, and stiffness. Electrical potentials of the nervous system recorded following a presentation of a stimulus. Motor speech disorder involving muscular weakness, dyscoordination, and alteration of muscle tone. A laboratory technique to record the electrical activity (electric potential) of skeletal muscles. Electrical response arising from the nervous system after a stimulus is presented. A neurodegenerative disease involving abnormalities in heart rate, bladder control, etc. A disease that is caused by traumatic brain injury, infections, metabolic problems, etc. There is a variability of symptomatology that usually involves weakness, numbness, and pain in the limbs. Its symptoms involve stiffness, spasticity, weakness, hoarseness of voice, slow speech rate, and dysphagia. Involuntary crying or uncontrollable laughing caused secondarily by a neurological disorder. A disorder that involves a symptomatology of spasticity, weakness, hyperreflexia, etc. It is caused by a dysfunction in the corticospinal (pyramidal) tract of the spinal cord. Loss of stress patterns in speech arising from reduced variability in vocal intensity and fundamental frequency. Disorder involving symptoms such as progressive weakness, spasticity in the legs, exaggerated reflexes, and hyperreflexia. He demonstrated mild pharyngeal dysphagia but nothing significant, in that his weight has gone up by 2 kg. He was continued with the same medicaption (Rilutek, vitamin E, gabapentin, amp vitamin B12, magnesium, and inhalers). Over the years, there was a very slow progression and generally he was feeling more weakness in the upper and lower limbs. On examination, the spasticity was worse on the right side and generally he was not very weak. I believe that there was no change in his speech, and the palatal movements were not very affected. He was to continue the same medications and he was to be seen again in four months. The results showed a mild to moderate difficulty, resulting in scores in the "b-c" range. The patient complained about slow speech rate, increased effort to speak, fatigue when speaking, and poor control of emotional expression. The most deviant speech characteristics involved imprecise consonants, monopitch, reduced stress, and harshness. Meningeal linings of the spinal cord are attached to the vertebral column by means of. At the lower end of the spinal cord is a cone-shaped projection known as the. Motor fibers of the spinal cord that activate skeletal muscle exit through the root. The spinal cord is suspended by that arise from the pia mater and attach the spinal cord to the vertebral column. Afferent/efferent (circle one) pathways convey information from the cerebrum to the spinal cord. Afferent/efferent (circle one) pathways convey information from the periphery to the brain. Sensory pathways are in the dorsal/ventral (circle one) portion of the spinal cord. The funiculus contains the fasciculus gracilis and fasciculus cuneatus. The nuclei for the fasciculi gracilis and cuneatus are found in the medulla/pons/midbrain (circle one). The tract conveys sensation of light touch to the ventral posterolateral nucleus of the thalamus. The tract conveys pain and temperature sense from the lower body to the thalamus. Descending pathways from the cortex are the effector pathways that cause function. The pathways arise from pyramidal cells in the motor cortex, and include the corticospinal and corticobulbar tracts. At the level of the lower medulla, 75% to 90% of the fibers of the tract decussate at the pyramidal decussation and descend as the lateral corticospinal tract. The tract is the means by which all muscles of the face, mouth, and most of the neck are activated. The system controls inhibition of reflexes, maintenance of muscle tone, and control of graded antagonistic contraction in support of fine motor activity. The tract mediates rotation of the head in response to a visual stimulus. The tract arises from the vestibular nuclei of the pons and medulla level and is important in mediation of spinal reflexes and in extensor muscle tone, as well as maintaining posture and stabilizing the head. The tracts modulate spinal tract motor activity by inhibiting reflexive responses to facilitate voluntary motor activity. Muscle atrophy is prevented in patients with acute spinal cord injury using functional electrical stimulation. The corticopontine projection in the rhesus monkey: Origin and principles of organization. Etiology of impaired selective motor control: Emerging evidence and its implications for research and treatment in cerebral palsy. Disequilibrium in patients with atherosclerosis: Relevance of pontine ischemic rarefaction. A systematic review of electrical stimulation for pressure ulcer prevention and treatment in people with spinal cord injuries. Characterization of involuntary contractions after spinal cord injury reveals associations between physiological and selfreported measures of spasticity. Functional electrical stimulation after spinal cord injury: Current use, therapeutic effects and future directions. Prefrontal cortex projections to the basilar pons in rhesus monkey: Implications for the cerebellar contribution to higher function. Handbook of severe disability: A text for rehabilitation counselors, other vocational practitioners, and allied health professionals. Ischemia (cessation of blood flow) can result in irreversible brain damage within minutes, so a steady supply of blood is essential to the health of the brain. As we will see, the human brain has several redundant features that have the effect of partially protecting the brain from loss of nutrients.

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Neuroinflammation and neuroprotection in schizophrenia and autism spectrum disorder 83 prostate cancer diet order proscar 5 mg with amex. How environmental and genetic factors combine to cause autism: a redox/methylation hypothesis. Oxidative stress-related biomarkers in autism: systematic review and meta-analyses. Brain region-specific deficit in mitochondrial electron transport chain complexes in children with autism. The most common mood disorders are depression, bipolar disorder, and schizoaffective disorder. Mounting evidence suggests that impairments in neurotrophic factor expression or signaling contribute to these disorders and may be potential treatment targets. Defects at the cellular level associated with depression, such as reduced neurogenesis, elevated risk for neuroinflammation, and increased vulnerability to neurotoxicity, can all be explained by deficiencies in signaling through neurotrophic factors. Notably, many neurodegenerative diseases are associated with depression suggesting overlapping disease etiologies and neuropathological substrates. Neuroprotective roles of neurotrophic factors in depression comment on how impaired neuroprotection may contribute to symptoms of depression in neurodegenerative diseases associated with depressive disorders. We will discuss some of the ongoing efforts to target these defects in neurotrophic factor signaling for therapeutic treatment and explain what is needed to fully exploit altered neurotrophic factor signaling as a treatment target in depression and in neurodegenerative disorders with comorbid depression. The need for novel treatment strategies in depression Depression is a mood disorder associated with consistent feelings of sadness, worthlessness, and guilt, as well as the loss of interest and pleasure. Other symptoms include insomnia or hypersomnia, changes in appetite and weight, fatigue, inability to focus, and indecisiveness. Together, these symptoms have a huge negative impact on the quality of life of affected individuals and impair their relationships with family and friends as well as their productivity in the work force. Current therapeutic treatments for depression include antidepressant medications. Genetic and environmental factors, such as chronic stress and early-life adverse events, have been identified as disease contributors. The high incidence of depression in neurodegenerative disorders suggests shared underlying pathomechanisms of the two diseases, which may offer novel treatment targets. In this article, we will discuss current evidence that one of these shared etiologies may be impaired neuroprotection mediated by insufficient neurotrophic factor signaling. Neuropsychiatric disorders Evidence suggestive of impaired neuroprotection and neurotrophic factors 127 Evidence suggestive of impaired neuroprotection and neurotrophic factors signaling in depression A role for the loss of neuroprotection and altered neurotrophic factor signaling in depression has been supported by various findings in both humans and animal models. Those findings range from brain imaging, postmortem brain analyses, and quantification of blood serum levels of neurotrophic factors in humans with depression to genetic, molecular, and behavioral analyses in mouse and rat models of the disease. More recently, genetic studies have associated mutations in genes encoding neurotrophic factors with depression. Lastly, some preclinical studies in animal models suggest that enhancing neuroprotection may be a potential therapeutic strategy. The following paragraphs will provide a brief overview of these findings, which together, make a strong argument for the importance of neurotrophic factor-mediated neuroprotection in depression and other mood disorders. Altered brain volume, connectivity, and cellular atrophy in depression For decades, mood disorders have been associated with reduced brain activity, impaired synaptic plasticity, and reduced brain volume in structures of the prefrontal-limbic network, which is important for socioemotional development. Importantly, these findings were supported by postmortem analyses of cell density and cell soma size in these brain regions that pointed in a similar direction. Several studies reported reduced soma size or reduced numbers of pyramidal and granule neurons, interneurons, and glial cells in the brain. Examples are reduced soma size of hippocampal pyramidal neurons in autopsy tissue from individuals with depression compared with controls25 and reduced numbers of hippocampal dentate granule cells in brains of individuals with major depression not currently treated with antidepressants. Neuroprotective roles of neurotrophic factors in depression neuronal soma size were consistently shown to be reduced in several different studies in individuals with major depression27, 28 or bipolar disorder. A limitation of all of the described studies is that they did not assess whether the reduced size and density of neurons leading to reduced brain volume precedes the depressive phenotype or whether a depressed brain effects molecular changes, for example, in neurotrophic factor signaling, that may lead to these structural alterations. Answering this question will be important to determine if neurotrophic treatment strategies could alter disease progression by correcting disease-contributing mechanisms. Impaired neurogenesis in depression Adult neurogenesis, the capability of certain areas in the brain to produce new neurons throughout adulthood, has been observed in many different mammals, including humans. Yet, the question of whether impaired neurogenesis is an underlying cause of depression is still mired in controversy. For example, most behaviors usually tested to establish a depressive-like phenotype in mice, such as the forced swim test,40 were not affected by ablation of neurogenesis using antimitotic agents or cranial irradiation. In line with this notion, it was recently proposed that adult neurogenesis is required for cognitive flexibility, deficiency of which may affect resilience to stress and induce depression. There are only a few studies in humans addressing impaired neurogenesis in depression. In summary, keeping in mind the issues with modeling complex brain disorders like depression in rodents54 and the recent research suggesting differences in adult neurogenesis between humans and other mammals, a clear assessment of the role of neurogenesis in depression is difficult based on current knowledge and requires more research. Impaired adult neurogenesis in individuals with depression and its requirement for antidepressant efficacy, if confirmed, would support the hypothesis that neurotrophic factor signaling, an important driver of neuronal maturation, is diminished in depression. In the brain, neuroinflammation as an acute response to viral infections and injury, for example, can have both beneficial and adverse effects. Altered neurotrophic factor signaling in depression the most direct evidence supporting impaired neuroprotection has been provided by studies that identified impaired levels or activity of neurotrophic factors and their receptors in depression. They can bind and activate two different classes of transmembrane receptor proteins, the p75 neurotrophin receptor and the tropomyosin receptor kinases (Trk) A, B, and C. In contrast to the high-affinity Trk receptors, the p75 receptor does not have an intrinsic catalytic domain and thus mainly functions via interactions with effector proteins, for example, other membrane receptors, including Trk receptors. Neuropsychiatric disorders Evidence suggestive of impaired neuroprotection and neurotrophic factors 131 plasticity, and neuroinflammation. Defects in neurotrophin signaling are thus expected to have profound consequences on neuronal circuits and brain functioning. Following is a summary of findings associating reduced neurotrophin signaling with depression. Notably, these effects are not limited to one type of neurotrophic factor but rather affect all four neurotrophin family members. The aforementioned studies differ in age, gender distribution, and medication usage. Nonetheless, there seems to be a broad consensus that depression in humans is associated with altered neurotrophin expression, and in most cases, reduced levels of neurotrophins were found. Evidence from genetic studies supporting impaired neurotrophic factor signaling in depression Depression is thought to be caused by the interplay of mutations in genes that increase susceptibility to depression and environmental factors, such as adverse childhood events. Neuroprotective roles of neurotrophic factors in depression interactions between childhood adversity and susceptibility genes lead to more severe changes in brain structure than either of these factors alone. Larger, well-controlled studies are needed to further assess genetic and epigenetic susceptibilities in neurotrophin signaling in depression. Stress and stress-induced depression and neurotrophic factor signaling in mouse and rat models As already alluded to , chronic stress or stress induced by early-life adverse events often contributes to or can even elicit depression. On a molecular level, similar pathways seem to be affected by both conditions, suggesting common underlying pathological mechanisms for stress and depression. Neuropsychiatric disorders Evidence suggestive of impaired neuroprotection and neurotrophic factors 133 background and environmental influences, which should make the data better interpretable and more consistent. As described in more detail in the succeeding text, work in these rodent models showed that both acute stress and depressive phenotype-inducing chronic stress lead to alterations in neurotrophic factor signaling. The models encompassed different time frames, such as chronic stress and acute stress, and a variety of different stressors, including immobilization, social defeat, foot shock, and swimming. These discrepancies could be due to the type of stressor used or the genetic background or age of the animal model. The relevance of altered neurotrophic factor signaling in stress is further supported by a few animal studies that quantified the levels of components of other neurotrophic factor signaling pathways and showed that they are affected similarly. Neuroprotective roles of neurotrophic factors in depression appeared to be more sensitive to stress. Similarly, increased sensitivity to stress-induced behavioral alterations was observed in female mice with inducible Bdnf knockout in the forebrain. Evidence for enhanced neuroprotection as an underlying mechanism of current successful therapeutic strategies in depression Except for research done with genetic mouse models, the studies described earlier showed mainly correlative evidence for altered neurotrophic factor signaling and neuroprotection in depression. Work demonstrating that successful therapeutic strategies in depression may function through neurotrophic and neuroprotective pathways has provided further support for a potential causal relationship between impaired neuroprotection and depression.

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It would appear that a so-called voluntary free act is not so free if neural impulses precede the conscious intention to act prostate cancer xmas cards buy generic proscar canada. There has been much criticism of Libet and his experiments in this arena (see Seifert, 2011). For example, some have criticized him for not considering other brain states that may be occurring before the intention was formed (a kind of deliberating stage). Historically, there have been two views of free will, libertarianism and compatibilism. A libertarian would believe that free will and determinism are incompatible, whereas a compatibilist would believe that they are compatible. In other words, free will is something of which we have more or less, depending on the constraints on us. This is the space within a person can act, a space with constraints or walls around it. A person who has a stroke might experience paralysis and thus might not be able to speak in the way that he or she wants. Other restraint categories include the physical environment, brain anatomy, neurochemistry, physiology, psychology, phenomenology. Spence notes, "It is not the instant of the act but its context that seems to matter" (p. Perhaps it is time to reconsider what we mean by free will and move our attention away from the instant of action to the context of that action. Our job is to work hard in therapy with our patients and try to increase their human response space for communication. The Motor Planning and Programming Levels Motor Planning the second part of planning is motor planning. These blueprints are unrefined when we are babies, but as we grow and learn, they become more refined and precise and need only to be recalled in order to be executed (as opposed to being created anew each time). Proper speech sound production requires that the speech organs move accurately and precisely in terms of articulatory target, timing, muscle tone, and force. Sensory information is also incorporated into the process to give feedback, allowing for midcourse corrections of the articulators. It can occur in the absence of physiologic disturbances associated with the dysarthrias and in the absence of disturbance in any components of language. Ford also has assembly plants with robotic machines that actually follow computer programs to make the car plans come into existence. Motor plans contain the specific, individual movements of the speech organs to produce speech sounds. The Motor Speech System 247 spread throughout the left hemisphere, particularly in the left perisylvian region. It is influenced by numerous other structures, such as the motor control circuits as well as the limbic system and the right hemisphere. These patients know what they want to say, but they cannot "pull up" the appropriate motor plans and programs to execute saying the word. They are like a professional tennis player who suddenly "forgets" how to hit a forehand or backhand but retains his or her muscle strength and range of motion. In addition to searching and groping behavior, patients make more substitution errors than omissions, distortions, or additions. Consonants are more difficult to produce than vowels, and consonant clusters are more difficult than single consonants. These patients are more successful in producing sounds in the front of the mouth as compared to back sounds, probably because frontal sounds are highly visible and easier to mimic. After struggling for many minutes, a patient might suddenly exclaim, "Oh damn it" as clear as a bell. The Basal Ganglia Circuit the basal ganglia are a collection of nuclei including the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. This system is central to the indirect motor system, also known as the extrapyramidal system. The purpose of these loops and neurotransmitters is specifically to regulate muscle tone and posture and to smooth or refine muscle contraction. They also seem to have a dampening effect on the motor signals sent from the cerebral cortex. Damage to the basal ganglia system results in dyskinesias and conditions like Parkinson disease and Huntington disease. In these conditions, we can witness the loss of this dampening effect as we observe tremors and other dyskinesias. The Cerebellar Circuit the cerebellar circuit could also be subsumed under the indirect motor pathway. As discussed previously, the cerebellum rests posterior to the pons and inferior to the temporal lobe. The cerebellum can be divided into two hemispheres, the right cerebellar hemisphere and the left cerebellar hemisphere. Of these three, the posterior lobe plays the most important role in speech production. Specifically, it automatically incorporates feedback "for coordinating skilled, sequential voluntary muscle activity" (Duffy, 2005, p. Afferent tracts greatly outnumber efferent ones, which demonstrates how important sensory feedback. A copy of this message travels the Motor Control Circuits There are two control circuits important to speech, the basal ganglia and the cerebellum. These circuits are important in motor programming of speech by coordinating, integrating, and refining the movements of the direct and indirect pathways, which will be discussed in a moment. These circuits can be thought of as fine tuners, just as tuning up a car makes it run smoother and more efficiently. Both these circuits could be discussed under the indirect motor pathway, but we will discuss them separately so they receive their due attention. The Motor Speech System 249 to the cerebellum via the corticopontine-cerebellar tract. The cerebellum then compares this information with the proprioception and kinesthetic information it receives from muscles and joints and coordinates muscle activity so that it is smooth and precise. Disruptions in this ability lead to ataxia, a lack of order and coordination between muscles, and adiadochokinesia, an inability to perform rapid, alternating movements. Diadochokinesia can be tested in speech by having a patient say "pa-ta-ka" as rapidly and accurately as possible. Cerebellar damage can lead to a dysarthria called ataxic dysarthria that is characterized by harsh voice, monopitch, loud voice, imprecise consonants, and irregular breakdown in articulation. The Direct Motor Pathway the direct motor pathway is also known as the pyramidal system. The lateral corticobulbar tract will be the focus in this section because it controls the movement of the speech muscles. The cortico portion of this name refers to the cerebral cortex, and the bulbar part refers to the brainstem because it is bulbous. This tract controls the muscles of the neck and face, including those important for speech and swallowing. The pyramidal system receives its name from the primary type of cell in this system, pyramidal neurons. The Betz cell bodies are located in the cerebral cortex, and their axons course down through the lateral corticospinal tract and synapse directly to the ventral horn cells of the spinal cord, which then synapse directly with muscles. The lateral corticobulbar tract follows the same pattern as the lateral corticospinal tract, except it synapses with cranial nerve nuclei in the brainstem rather than the spinal cord. Overall, pyramidal cells are crucial for the modulation of the pyramidal system as well as the nervous system overall (Spruston, 2009). The pyramidal system is a voluntary motor system that controls gross motor movement. Note the directness of this pathway and the decussation at the level of the medulla. The pyramidal tracts then descend through the corona radiata and into the internal capsule. Because tracts like the corticobulbar and corticospinal run through the internal capsule, even small lesions from the Motor Speech System 251 strokes can cause catastrophic motor problems. This decussation is responsible for what is called contralateral innervation, meaning that the right side of the brain controls the left side of the body, and the left side of the brain controls the right side of the body. In the case of the lateral corticobulbar tract, once it has decussated at the medulla, it leaves the brainstem as a cranial nerve that then innervates various muscles in the head and neck.

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In this view androgen hormone nausea buy proscar 5 mg lowest price, a person is merely the sum of his or her parts, essentially a machine like a computer (Rae & Cox, 1999). If the answer to this question is "yes," then a proponent of this view might say that the person is truly a person. If someone has never attained some or all of these capacities, or if a person has lost these abilities, as in the case of Terry, is he or she still a human person Proponents of this view might say "no" and a practice like euthanasia becomes not only possible but in some cases necessary to increase what Princeton philosopher Peter Singer calls the total amount of happiness in the world (Will, 1999). The second way to define a person is to say that his or her substance is a body and a soul, material and immaterial, and that something mysterious. Proponents of this view would argue that Terry, though he has severe disabilities, is still a human person. Singer would say "nothing" and that anyone who argues for humanity being of a different and better essence is committing speciesism, the intentional act of promoting one species over another (Will, 1999). Yet others would argue that there is something unique about humans, something that separates man and woman from beast. These are important and interesting questions because they do affect life decisions, like living wills and end-of-life decisions. Vision can be stimulated through blinking lights, gustatory through applying different tastes, auditory through music or family voices, olfaction through applying different 218 Chapter 9 Consciousness and Disorders of Consciousness smells, and touch through applying different textures or temperatures to the skin. Some coma stimulation programs also add kinesthetic stimulation in the form of posture changes and/or range-of-movement exercises. Studies have been completed examining the effectiveness of this therapy approach; the results of these studies are mixed. Some studies have shown improvement in cognitive status and responsiveness and a decrease in mean length of time in a coma (Karma & Rawat, 2006; Kater, 1989; Mitchell, Bradley, Welch, & Britton, 1990; Wilson, Powell, Elliott, & Thwaites, 1991). Other studies have shown that coma stimulation does not appear to make a difference in these patients (Pierce et al. Audiologists may work with these populations in conducting nonbehavioral hearing assessment measures, such as auditory brainstem response. Conclusion Thomas Nagel wrote an article in 1974 titled "What Is It Like to Be a Bat You, the reader, do not know and cannot know anything of my private experience as I write this book unless I decide to reveal something to you. Even then, you will never have a true or complete first-person perspective of my first-person experience. Consciousness is certainly an interesting, complex, and mysterious topic of study. The learner will define consciousness, core consciousness, and extended consciousness. Glutaminergic projections from the classical reticular nuclei travel to the intralaminar nuclei of the thalamus, which the thalamus then projects to much of the cerebral cortex. At the same time, cholinergic projections to the reticular thalamic nuclei hinder sleep. The learner will list and briefly describe at least five specific disorders of consciousness. It is extended consciousness that begins to be assaulted in the early stage of the disease as the autobiographical self begins to deteriorate under the weight of the disease. She was ejected from her truck upon impact with another vehicle and suffered a significant brain injury. Currently, Teresa demonstrates appropriate behavior in response to environmental stimuli. She also attempts to utter sounds during her periods of arousal though her speech is unintelligible. Research the reticular activating system and write a short paper outlining its structure and function. Include a brief summary of the article, and state whether you agree or disagree with Nagle and why. Write a two- to three-page paper on one of the disorders of consciousness presented in this chapter. Explore the literature on coma/sensory stimulation and present the evidence for and against this approach. Coma arousal procedure: A therapeutic intervention in the treatment of head injury. A randomized controlled trial to assess the efficacy 221 of auditory stimulation on selected parameters of comatose patients with traumatic brain injury. This article will discuss the neurology of both hearing and balance as well as survey select disorders that affect these systems. The learner will define the following vestibular disorders: vestibular schwannoma and labyrinthitis. The purpose of this chapter is to survey these two systems, perform an in-depth exploration of the central auditory system, and examine select neurological disorders of hearing. The Neurology of Hearing the Peripheral Auditory System the outer ear includes the pinna (or auricle) and the external auditory meatus. In the outer ear, hearing involves the pinna locating, collecting, and funneling acoustic energy. In the middle ear, acoustic energy is changed, or transduced, into mechanical energy as the tympanic Outer ear membrane begins to vibrate due to sound waves hitting it. At this point, the inner ear has been reached and several other energy changes will occur. Perilymph occupies the scala vestibuli and scala tympani, and endolymph is found in the scala media. As the footplate of the stapes rocks in and out of the cochlea, mechanical energy from the middle ear is changed into hydraulic energy through the creation of waves in these cochlear fluids. As these waves travel through the cochlea, hair cells in the organ of Corti are displaced, causing two more energy changes at these hair cells. First, there is a hydraulic to mechanical energy change at the hair cell cilia as they bend. Second, there is a mechanical to electrochemical energy change at the synapse of the hair cell to the afferent auditory neuron at the base of the hair cell. Resting hair cells in the organ of Corti are in a highly polarized state, just like neurons. The environment outside an individual hair cell is positively charged, whereas the environment in the hair cell is negatively charged. The Neurology of Hearing Outer ear Sound waves are captured by the outer ear and are funnelled through the external auditory canal to the tympanic membrane. The three bones of the middle ear transmit and amplify the vibrations to the oval window of the inner ear. Movements of fluid in the inner ear stimulate the hairs of the auditory hair cells, which result in stimulation of auditory nerve endings. This disruption causes stereocilia at the very end of the hair cells to bend, leading to potassium channels opening at the ends of the stereocilia. A cross-section of the cochlea showing the scalas and organ of Corti in the scala media. Depolarization causes calcium channels at the bottom of the hair cell to open and allow calcium to enter the hair cell. This activity triggers the synaptic vesicles to fuse with the cell membrane and release glutamate across the synaptic cleft to the afferent neuron. In addition to these fibers, vestibular nerve fibers course through the internal auditory canal to the brainstem. As mentioned previously, hydraulic energy is changed into electrochemical energy in the organ of Corti. These energy changes occur at specific places along the organ of Corti, which runs the length of the cochlea.

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True or False: Muscle spindles would be considered interoceptors because they are embedded within muscle androgen hormone zyklus order proscar online from canada. In the map of this image, the notation "C1" refers to the nerve. Depolarization of causes the hair cell to shorten, producing an impulse on the basilar membrane. The is responsible for sensing changes in movement of the head. Delta opioid receptors presynaptically regulate cutaneous mechanoreceptory neuron input to the spinal cord dorsal horn. Targeted disruption of the Kcnq1 gene produces a mouse model of Jervell and LangeNielsen Syndrome. Conscious neurosensory mapping of the internal structures of the human knee without intraarticular anesthesia. Perceptual responses to microstimulation of single afferents innervating joints, muscles and skin of the human hand. The fine structure of spiral ligament cells relates to ion return to the stria and varies with place-frequency. Reflex circuitry originating from the muscle spindles to the tibialis anterior muscle. The central nervous system is very hierarchical, and you can see the evolution within that hierarchy. The spinal reflex arc is the basic sensorimotor communication system between the outside world and our bodies. Expand that to pain sensation, and painful stimulus causes a muscle to contract to protect the body. We have fancier reflexes that cover multiple spinal cord segments, providing an even more complex response system. The thalamus is the major structure of the diencephalon (to be discussed in Chapter 5), and it is the last stop before the cerebral cortex for information that has come through senses from the spinal cord and brainstem sensory nerves. Put another way, the thalamus is the highest evolutionary sensory system that remains unconscious. In the same vein, the basal ganglia are a set of nuclei (to be discussed in Chapter 5) that are part of the highest non-conscious motor control system. These nuclei are close to consciousness and are capable of some very organized motor activity. The cerebral cortex is the place where consciousness arises and where voluntary action is initiated. Realize that there are several other "cortices" (plural for cortex), since cortex simply means "bark," as in "bark of a tree. This is where our sense of self arises as a result of the interaction of some 17 billion neurons (Azevedo et al. If you were to count 1 synapse per second without stopping, you would be over 2,850 years old before you finished! In the same vein, the cerebral cortex is where we are able to voluntarily respond or act on the environment. We are consciously aware at the level of the cortex, and we make conscious decisions to act from there, and this is critically important to us as therapists. The ability to reflect on our actions and make change is essential for success in any endeavor. We are conscious because of the complexity of the cerebral cortex, and we can make sense of our sensory universe and make decisions about how to respond to it. This is not the same as lying, which is a deliberate attempt to misrepresent yourself or other information. You can think of reality as a "connect the dots" picture: the dots are our sensations and our memory of how those sensations connect with other information. I smell bread cooking, see sunlight coming in the window, and hear birds singing: my cognitive processes connect these sensory perceptions with memories of their occurrence in the past, so that I have a percept that binds them together and very likely elicits a strong positive emotional response. We weave the fabric of reality from these perceptions and memory of them having occurred in the past, either together or separately (for instance, I have smelled bread baking in a bakery, and have heard birds at the park). Because we have amazingly powerful memories and multiple, multiple sensory inputs at any instant, this reality we weave looks and feels "solid" and immutable. A client of ours had suffered brain damage from a cardiac event that left her anoxic for several minutes. As she emerged from her coma it was apparent that she had numerous deficits and yet had a very intact language and speech system, as well as an excellent sense of humor. Essentially, she had lost a great deal of her memory and her "gnosis," or knowledge, of objects (tactile agnosia is the inability to "know" what something is when perceived through the touch modality). She had tactile agnosia, some auditory agnosia, visual agnosia, and cortical blindness (cortical blindness occurs when the pathways for vision are intact but a lesion to the cerebral cortex causes one to be unable to see). Our client had all the components necessary to demonstrate exquisite confabulation. Her memory, sensation, and cognitive processes had significant holes, so the "dots" in her connect-the-dots picture were much farther spaced apart than ours. With her intact language and speech system, she simply wove the parts she did have into a fabric that made sense to her. Her mind "wanted" an intact reality, and she wove that reality out of the content she had available. She had the memory of flying in a small plane, and one of spending a fun weekend in Reno, and wove that into a story of piloting a small plane to Reno for a weekend at the blackjack tables. All of that neural density and complexity leads to a level of self-organization that we are only just now dreaming of in the computer science and artificial intelligence worlds. The brain is the most complex and highly evolved structure in the known universe, and the very nature of that complexity and that neural density gives it the possibility for creating this most complex of the cognitive processes, consciousness. We need to acknowledge, as we lay out a framework of structures and their functions, that the whole is very much greater than the sum of the parts! Ischemia refers to loss or reduction of blood flow due to some blockage, such as a clot or a narrowing of an artery, while hemorrhage is blood being released out of the blood vessel into the surrounding area. Arteriosclerosis is a category of diseases in which there is a thickening of an artery wall that results in stenosis (narrowing) of the artery. The artery wall loses elasticity, which contributes to increased blood pressure (hypertension). Atherosclerosis is a form of arteriosclerosis in which the white blood cells and smooth muscle cells combine to occlude the artery. Because many of the white blood cells are still functional, inflammation occurs at the site. Other cells, including cholesterol and triglycerides, contribute to the occlusion. The accumulated cells crystallize on the inner surface, and if they break loose from the blockage, they enter the bloodstream as a floating clot known as an embolus. A common site of occlusion is the bifurcation of the common carotid artery into the internal and external carotid arteries. If an embolus is sufficiently large to block the internal carotid artery, all of the speech and language areas will be affected due to ischemia involving the middle cerebral artery. The cerebral cortex is a voluminous structure that, on gross examination, has two mirror-image halves (cerebral hemispheres), a number of outfoldings and infoldings, and large separations or fissures. The larger components of the central nervous system are separated by three meningeal linings that protect and support the structure of the brain. The cortex itself is a 4-mm thick layer of gray matter (neuron cell bodies) that overlies a mass of white matter fibers. This layer folds in on itself in many locations, forming gyri (plural of gyrus) as outfoldings, and sulci (plural of sulcus), which are infoldings. The cerebral cortex is divided into left and right hemispheres, separated by the superior longitudinal fissure. Each hemisphere has a significant precentral gyrus, which is the boundary between the frontal and parietal lobes (to be discussed later). On each side is the temporal lobe, separated from the frontal and parietal lobes by the lateral fissure (or lateral sulcus or Sylvian fissure). The dura mater (dura = tough; mater = mother) is the outermost layer of the meninges and is composed of two layers of tough connective tissue that are tightly bound together. The outer layer is more inelastic than the inner layer, and the space between them is termed the epidural space. The arachnoid mater is a spider-like covering (arachnoid = spider; mater = mother) that lies beneath the dura mater and through which many blood vessels of the brain pass.

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Neuron Form and Function Now that we have surveyed different nervous system cells mens health idris purchase proscar 5mg line, we will focus on neurons because they are important in neural transmission. We will first learn the form or structure of neurons and then turn our attention to how they work. Neuron Form Discussing neuron form involves two structures, the neuron itself and something called a synapse. We will look at the structure and types of neurons first and then explore the structure of a synapse. This will prepare us to consider neuron function since both structures are crucial to the sending of neural messages. Neurons contain two basic parts-a cell body or soma (Greek for "body") and projections called neurites. Neurites can be further divided into two main types-dendrites (Greek for "tree"), which receive signals and pass them toward the cell body, and axons (Greek for "axis"), which 68 Chapter 4 the Cells of the Nervous System Spine head Spine neck Dendrite Thin Mushroom Stubby Ramified (branching) devoted to special senses, like hearing, smell, and vision. Lastly, multipolar neurons are motor in nature and have multiple projections coming off the cell body, most of which are dendrites along with a single axon. In contrast, motor neurons connect to body structures involved with movement, like muscles. Other classification schemes include classifying neurons based on dendrite shape, axon length, and neurotransmitter chemistry (Bear, Connors, & Paradiso, 2007). Within these buttons are vesicles or sacs that hold chemicals called neurotransmitters; when stimulated, the presynaptic membrane vesicles release the neurotransmitters, which pass through the synaptic space or cleft and connect to receptor sites on the postsynaptic membrane. The result is that the signal is passed from one neuron to the other neuron through this chemical process. After the signal is passed from one neuron to another, some of the neurotransmitters are reabsorbed by the presynaptic membrane (or a neighboring glial cell) and returned to the vesicles. An axodendritic synapse involves the axon of one neuron connecting and sending a chemical signal to the dendrite of another neuron. These connections are called axosomatic synapses, and they are usually inhibitory. This is called an axoaxonic synapse, and it is typically modulatory, meaning it regulates a signal (Seikel, King, & Drumright, 2010). Some dendrites have spines on them that are involved in chemical transmission of signals (Bear, Connors, & Paradiso, 2007). Their shape also appears to isolate connections from each other, so there is no interference (Araya, Eisenthal, & Yuste, 2006; Araya, Jiang, Eisenthal, & Yuste, 2006). Functionally, myelin not only keeps electrical signals in the axon but also speeds up the transmission of signals. Myelin is essential to a properly working nervous system; demyelinating diseases, like multiple sclerosis, can result in severe neurological deficits. In humans, this process begins during the 14th week of development and continues into adolescence. Neurons can be classified in several different ways; one of the most common ways is by the number of neurites the neuron has. Unipolar (or pseudopolar) neurons have a single projection that functions as an axon and comes off the cell body. These neurons are located in structures Neurotransmitters As mentioned earlier, neurotransmitters are chemical messengers that transmit messages from a presynaptic membrane to a postsynaptic membrane through the synaptic cleft. In order to be a neurotransmitter, Purves (2004) states three conditions must be met: It must be present in the presynaptic membrane. In terms of structure, there are two basic categories of neurotransmitters: large molecule and small molecule. Large molecule neurotransmitters (neuropeptides) are considered large because they consist of 3 to 36 amino acids. Small molecule neurotransmitters (amines and amino acids) consist of single amino acids and are short lasting. It was once thought that each neuron held only one specific neurotransmitter, but now we know that a neuron can hold multiple types. Small molecules are held in synaptic vesicles on the presynaptic membrane, and large molecules are stored in secretory granules on the axon terminals. Axon Axodendritic synapse Axosomatic synapse Axoaxonic synapse Axon neurons (neuromodulation). Functionally, neurotransmitters mediate transmission between neurons by exciting (starting), inhibiting (stopping), or modulating (regulating a signal) postsynaptic action potentials. It is also released at the neuromuscular junction between the vagus nerve and cardiac tissue. There is some evidence that imbalances in glutamate play a role in schizophrenia (Kandel et al. It acts by binding to postsynaptic receptor sites, blocking the action of other neurotransmitters. The first is the mesostriatal pathway that begins in the substantia nigra and projects to the basal ganglia. The second pathway is the mesolimbic pathway that originates from an area in the brainstem called the tegmentum and projects to the limbic system, which is our emotional system. Dysfunction in this pathway can lead to positive schizophrenic symptoms such as delusions or hallucinations. The third pathway is the mesocortical pathway, which also arises from the tegmentum (area of the brainstem), but projects to the prefrontal cortex. Impairment to this pathway leads to the negative symptoms of schizophrenia, like flat affect and emotion, lack of speech, and lack of motivation (Blumenfeld, 2010). Epinephrine: Also known as adrenaline, epinephrine is involved in regulating heart rate, blood pressure, and breathing and in the fight-or-flight response. Epinephrine-containing neurons originate in the brainstem and project to the thalamus and hypothalamus (Purves, 2004). High levels are associated with anxiety; low levels are associated with fatigue and poor concentration. Neurons containing this neurotransmitter arise out of the brainstem and project to the entire forebrain. They have both excitatory and inhibitory effects on the nervous system and regulate functions such as mood, sleep, and appetite. Low levels of this neurotransmitter relate to depression, anxiety, obsessive-compulsive disorders, and eating disorders. Substance P: the perception of pain is an important protective biological mechanism. For example, imagine how much damage we could do to our hand around a hot burner if we did not perceive pain. Substance P sensitizes us to pain and also causes inflammation at an injury site, which leads to healing (Kandel et al. Chronically increased levels of substance P can lead to inflammatory skin disorders, such as eczema, whereas low levels have been associated with Alzheimer disease and type 1 diabetes. In this process, that part of the axon that is distal from the soma and anterograde from the injury degenerates and the axon terminal pulls away from the synapse. Why is there a difference in regeneration properties between the two parts of the nervous system Important Aspects of Neuron Function As stated earlier, neurons and glial cells are the primary cells of the nervous system, but we will be considering only neurons here. The main job of neurons is communication, which they do through tracts, or neural pathways. A neural pathway consists of a series of neurons connected together to make communication between the brain and the body possible. We will discuss specific neural pathways when we discuss the internal organization of the spinal cord as well as the motor speech system. This damage can occur through cutting or crushing an axon, a phenomenon known as an axotomy. Axons in the central nervous system are more likely to undergo Wallerian degeneration. Second there is afferent communication, which is bottom-up or ascending communication through neural pathways from the body to the brain.

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Milk thistle is a native of the Mediterranean region and has also spread to East Asia prostate 94 buy proscar online from canada, Europe, Australia, and the Americas. Its flowers, leaves, and roots have been used in the European diet as vegetable, and its achene is used as a coffee. In 1968, a flavonolignan complex in milk thistle fruit was identified and isolated. The major bioactive substituent present in the plant is the flavonoid complex silymarin, which is about 80% of the extract. Role of nanocarriers and their surface modification in targeting delivery of bioactive compounds G. The plants from the family of Gnetaceae have been used as traditional medicines for many years. Gnetin C has been explored for more than 10 years, principally by Japanese scientists. Welldocumented clinical data is already available and even more studies are continuing to emerge [21e24]. Various phytochemicals including flavonoids, alkaloids, and plant steroids known as physalins (A and B), with anolides and secosteroids, which have never been reported before, are present in this plant [27e30]. Complexity of bioactive compounds Most bioactive substances isolated from plants are either in the form of crude extract, fraction, and single compound show poor bioavailability, hence have low-therapeutic outcome, resulting from the challenging physicochemical properties, instability issues, or extensive in vivo response. Bioavailability and solubility are key issues that have emerged as top technical concerns in drug formulation and delivery even for bioactive compounds. Biological barriers 21 In addition, stability of the active agents both physically and chemically also contribute significantly during formulation development. The main challenges faced by pharmaceutical companies in drug formulation as described in many reports [31e36] are safety (c. In oral solid dosage forms, the top three formulation challenges are bioavailability (41%), stability (37%), and solubility (35%). The fact that bioactive compounds are challenging during formulation and delivery has been described in several reports [31e36]. As discussed in the first part of introduction, several potential bioactive compounds exhibit a lack of pharmaceutical properties like low solubility and permeability, sensitivity toward external factors (humidity, light, and temperature), as well as presystemic degradation upon entering the body. All these challenges have led to unsuccessful therapy in the clinic using bioactive components. Different types of biological barriers are described next to present the critical parameters on the therapeutic failures as well as to find the appropriate strategies or solutions by which a bioactive can be delivered successfully in vivo to exert desired clinical effects. The design of strategies to control the transport of therapeutic compounds through these physiological barriers has become an imperative and a challenging need in the quest for better therapeutics. The physical barriers for drugs entering systemic circulation are the membrane, a biological architecture of a membrane border, like a single-layer or multilayer cell lining. Biological barriers A major challenge in the drug delivery area is how to transport the active agents across the biological system entering the blood circulation and reaching the target of action to demonstrate the biological effects. Biological barriers are designed naturally with the aim to protect the organism from foreign materials that can damage homeostasis and physiologic function and eventually can threaten the 3. Drug-metabolizing enzymes are present in almost all parts of the body where the drug is passing through, such as gastrointestinal tract, respiratory system, ocular mucosa, in the blood circulation, and other entry points of drugs to the systemic compartment. Role of nanocarriers and their surface modification in targeting delivery of bioactive compounds Drug transporters are the proteins that are present in many organs (liver, lung, kidney, intestine, brain, skin, blood vessels, and others). Naturally, the proteins play important roles for traffic between organs and elimination of drugs and foreign compounds. Their function somehow is beneficial, but they may also display deleterious effects that do not allow drugs to enter the target organ to show their effects. Efflux pumps demonstrate resistance to cytotoxic drugs, hence also act as a barrier for drug delivery. By their nature, efflux pumps are transport proteins involved in the extrusion of toxic substrates from cells into the external environment. These membrane proteins function as a pump that can decrease the intracellular accumulation of drug, leading to the ineffective drug therapy. For better drug delivery, the key to understanding how these pumps operate involves the determination of the structures of representative pumps and the elucidation of the conformational changes that accompany drug translocation. The successful outcome of the nanocarrier to help the bioactive compounds show their effect upon reaching the target site of action is also determined by the in vivo behavior of the nanocarrier, in particular in the phase of biological membrane passage to reach the systemic circulation, during traveling in the circulation to reach the target site and after reaching the target. Various nanoparticles are being studied for delivery of synthetic as well as bioactive drugs. In this section, different drug delivery systems explored for bioactive drug delivery are discussed (Table 2. Different types of nanocarrier systems are developed based on the characteristic of the bioactive compounds as well as the aim of their delivery target. The former focuses more on the use of the excipients, the composition, and the manufacturing process, while the later emphasizes the drug-carrier constructs. The following discussion reviews the typically used drug delivery systems in bioactive delivery that are effective in overcoming the biological barriers, thereby improving the drug therapeutic index. In this category, we selected liposomes, nanoemulsions, and lipid nanoparticles; other forms of nanoparticles are still under research and have not yet reached the market like the above ones, hence we decided to discuss only the relevant ones. Nanocarrier: a strategy to overcome biological barriers A primary reason for drug failing to demonstrate its effect is the biology underlying the molecular-, cellular-, and tissue-level barriers, which makes the delivery process extremely complex. Therefore, to bypass the limitations regarding the biology of conventional drug delivery, it might be best to improve on the concepts and approaches that are efficient and effective [37,38]. One way to overcome barrier challenges could be formation of effective drug delivery. Partition in the lipophilic core is improved by adding 1-dodecanol Flavonols the scarce solubility of most flavonols in oil phase requires the addition of amphiphilic molecules in the lipophilic core Improved thermo- and photostability Enhanced delivery Flavones Apigenin, luteolin, rutin, tangeretin Supersaturated flavones in oil phases easily form crystals, requiring the addition of compounds, such as soy protein isolates, to slow down the crystallization process Flavanones exhibit poor water solubility. Oil and emulsifier are added to ensure maximum loading and stability in the nanoemulsion Incorporation in oil droplets should be promoted by suitable emulsifiers. Role of nanocarriers and their surface modification in targeting delivery of bioactive compounds Bioactive-loaded nanocarrier systems and the potential medical promise. In the case of lipid nanoparticles, a majority of lipids excipients are derived from dietary oils/ fats, which offers advantages in terms of biodegradability and the ability to penetrate the biological membrane barriers. The selection of lipid by considering the chemical structure and properties determines the type of nanocarriers. Therefore, types of lipid are very important for successful delivery of the bioactive compounds loaded in the nanocarrier systems. The type of lipids composing liposomes determine the surface charge, size, and the method of liposome preparation. The surface rigidity and fluidity of liposomes are influenced using additional agents like cholesterol. The choice of liposome preparation method is dependent on a variety of factors like lipid composition and size for in vivo drug delivery, etc. Liposomes have demonstrated the potential benefit to improve the bioactivity of various natural compounds with lack in pharmaceutical properties [74]. As the natural compounds are appreciated for their broad spectrum activities, this makes them more appropriate to interfere in multifactorial diseases, such as cancer. Role of nanocarriers and their surface modification in targeting delivery of bioactive compounds generally have better safety profiles, and are well accepted by the public. Despite these factors, the use of bioactive compounds poses a number of challenges that need to be overcome for better establishment as clinically effective therapeutic agents. Currently, there is a huge lack of human clinical trials that address their absorption, distribution, metabolism, and excretion in relation to efficacy. As reported, various compounds that indicated poor bioavailability as well as being unstable and prone to degradation or oxidation, such as resveratrol (logP 3. These molecules exhibit proven antimicrobial activity, however, show low water solubility and high toxicity. This finding confirms the promise of liposomal approach to encapsulate a potential natural anticancer compound with high cell selectivity [77]. This is because of its easy preparation at both laboratory and industry production scale, and the unique emulsion characteristics compared to other nanocarrier systems. The flexibilities of nanoemulsions are promising to create novel carrier systems with advanced potential benefits as drug transporters. Nanoemulsions can also be used as building blocks for other types of structures, such as filled hydrogels. Filled hydrogels are designed to encapsulate, protect, and control the release of bioactive components by changing their dimensions, internal composition, or structure.