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At this stage of the debate medications gout probalan 500 mg overnight delivery, it is di cult to medicine youth lyrics cheap probalan 500mg know whether the preceding argu ments are a case of “splitting hairs” or the delineation of a crucial distinction Consciousness 251 with profound consequences for cognitive psychology and neuropsychology symptoms lung cancer order probalan 500 mg mastercard. After all medicine man aurora purchase probalan 500 mg free shipping, almost everyone agrees that the contents of our conscious experience are ordinarily constrained by what we pay attention to. However, one additional piece of evidence garnered by the oldest psychological research method of all, introspection, suggests to us that consciousness is not quite the black–white issue that Dehaene et al. So the debate continues, and both “attention” and “consciousness” still resist clear and unequivocal de nition. However, it is reassuring to note that psycholo gists, neuropsychologists, neuroscientists, and philosophers are collaborating in e orts to clarify these interconnected issues once and for all. Must the global workspace itself always involve frontal activations to cause conscious awareness This should be of interest to neuropsychology because as we have seen, for example in our review of hemineglect, brain damage may lead to a revision of the parameters of self-awareness by rendering patients “indi erent” to half their visual eld or, in the case of anosognosia, one side of their own body. However, in the clinical setting, leaving aside the impoverished self-awareness seen in gross neurological disease (such as late-stage Alzheimer’s), psychiatry has in fact arguably shown more interest in self-awareness. Impairments of this sort are apparent in cases of body-dysmorphic disorder (Albertini & Phillips, 1999), other delusional disorders (Blakemore & Frith, 2003), and, most intriguingly, in certain cases of schizo phrenia (Spence et al. Earlier in this section, we mentioned that their observations of post-recovery split-brain patients initially led both Sperry and Gazzaniga to speculate about the possibility that such individuals experienced a form of dual consciousness. Because of concerns about the authenticity of the early ndings, Gazzaniga has subsequently revised his views, developing an idea earlier mooted by Bever (1983) that the left hemisphere has an enhanced role in high-level self-awareness, as both an “interpreter” of why events (both external and internal) occur, and a selector 252 Chapter 9 Attention and consciousness of appropriate responses (Gazzaniga et al. As Gazzaniga has argued, such a system would o er enormous adaptive bene t, enabling information about di erent events to be woven together into a causal chain to guide future behaviour. Gazzaniga’s evidence is somewhat anecdotal (mostly from split-brain patients), but worthy of review nonetheless. For example, in the small number of patients with both left and right hemisphere language skills, the left hemisphere is better at making associative links between pairs of stimuli. When asked to choose one of six possible words linking two tachistoscopically presented words (“bleed” would, for example, link “pin” and “ nger”; “oven” would link “bread” and “roast”), left hemisphere performance was signi cantly better than right. In another tachistoscopic study, patients were brie y presented with images to the right and left of a xation point: a snowy scene to the left (going to the right hemisphere) and a chicken’s foot to the right (going to the left hemisphere) for example. Then they were asked to choose one cartoon from an array of pictures on the table in front of them to go with each of the tachistoscopically presented images. In this example, one patient chose a picture of a chicken with their right hand and that of a shovel with their left, both ostensibly correct. But when asked why they had made those choices, the patient confabulated (made up part of their answer) by saying the chicken went with the chicken foot (correct) and the shovel was needed to clear out the chicken shed (incorrect). But when asked why they were laughing to themselves or walking out of the room, they generated confabulated answers such as “I just wanted some fresh air”. In each of these examples it appears that the left hemisphere is inter preting actions initiated by the right, which itself is contributing little to the interpretive process. Cooney and Gazzaniga (2003) have extended this logic to explain “anosogno sia for hemiplegia” (unawareness of left-sided paralysis, usually associated with right hemisphere damage): If the area of the brain that normally signals a problem. Second, the ndings themselves rely heavily (though not exclusively) on verbal report, which, for most split-brain patients, means output from the left hemisphere. So the hypothesis could be confounded given the functional isolation of the left from the right hemisphere in this syndrome. Extending the hypothesis to include neurological conditions like anosognosia does not provide a true test of it (although the ndings are certainly consistent with it) because once again most forms of hemineglect are related to right-sided damage. Finally, Chapter summary 253 although some brain-damaged individuals are unaware of their own cognitive impairments and also prone to confabulation (Joseph, 2000), many with pronounced left hemisphere damage are both well aware of their impairments and “enjoy” full consciousness. An “interpreter” function for the left hemisphere therefore remains, for the time being, an interesting possibility rather than an established fact. As researchers have examined attentional processes it has become clear that “attention” is not a unitary phenomenon, and it probably needs to be partitioned into a series of related but distinct domains. Researchers have made progress in examining the processes involved in selective attention, and an evolving view is that the diverse ndings (relating to early/late and object/space based attention for example) can be best understood if attention is viewed as a resource with a nite capacity. There is continued interest in distinguishing between pre-attentive processes and voluntary orienting in different types of visual search. However, both the cocktail party phenomenon and negative priming remind us that certain non-attended material can also in uence high-level (semantic) processing. Several cortical and subcortical structures appear to be involved in mediating attentional processes. Posner’s and Mesulam’s theories have been further re ned by LaBerge (1995, 2000) into a model that distinguishes between bottom-up (automatic/incidental/pre-attentive) and top-down (deliberate/executive) control. There is a growing consensus that top-down attentional processes overlap signi cantly with the central executive function of working memory. Recent research into the neurological disorders of hemineglect and Balint’s syndrome is reviewed. Particular attention is paid to the underlying pathologies of these conditions in the context of established visual processing streams in the cortex. Corbetta and Shulman’s model of attentional control in the brain is described and reviewed in some detail. Recent developments in our understanding of how the brain might “mediate” consciousness are considered within Pinker’s tripartite taxonomy. Material is drawn both from other parts of this book and from experimental work described else where to illustrate that psychology and neuropsychology are making important 254 Chapter 9 Attention and consciousness contributions to debates about the nature of consciousness. Global workspace theory is introduced as a conceptual model of consciousness, and we offer a avour of ongoing debates about the parameters of such a system, and implicitly of consciousness itself, and its links to/overlap with attention and working memory. Finally, we introduce Gazzaniga’s ideas about the highest level of human conscious control (an interpreter/integrator function of diverse inputs/outputs) which, he has argued, depends on a left hemisphere located (or biased) region of the workspace. Every action we take, every decision we make, has an emotional context and therefore all our cognitive functions are coloured by our emotional state. We do things that will achieve outcomes that we need or want, or to avoid outcomes that would be harmful or unpleasant. The vast majority of our behaviour is aimed at either obtaining rewards (which can be tangible or more abstract—as we will see, social approval, inclusion in a group, altruism, and perceived status can all be extremely rewarding) or avoiding punishments (which can, again, be tangible or more abstract). Emotional responses are crucial to motivated behaviour; if something elicits positive emotions we will seek it out, while if something elicits negative emotions we will avoid it. In the 17th century, the philosopher Descartes used the famous phrase “I think, therefore I am” to suggest that thought is what makes us who we are. Three and a half centuries later, in his in uential book Descartes’ error, Antonio Damasio (1994) argued that it is not only thought that de nes us, but, more fundamentally, feeling. Logical thought does not make us human, rather it is the interaction between what we think and how we feel that is at the core of who we are and what motivates us to behave in the ways we do. Thus to under stand human neuropsychology, we must explore the topics of emotion and motivation. Given that many cognitive neuroscientists now accept the importance of emotion and motivation in the study of behaviour, it is surprising that, until recently, this topic did not have a place in most cognitive neuroscience or neuro psychology textbooks. The study of emotion and motivation has been a huge growth area in the last 5–10 years and this is re ected in the inclusion of chapters in the most up-to date texts. In his recent book, Ward (2006) argued that traditional cognitive psychology theories were derived from computer-based models of information processing. And computers, of course, do not compute emotions and are not motivated to behave. Most signi cantly, the advent of brain-imaging techniques has allowed us to access emotional and motivational function in a way that was not previously possible. People can describe how they feel (or don’t feel) and psychologists can observe behaviour and characterise it as normal or abnormal by reference to expected behaviour. Patients can be given a memory test, or an attention test, and an objective score can be derived from the number of correct and incorrect responses. Similarly, although psychologists can qualitatively assess the extent to which a patient is motivated, objectively measuring that motivation is considerably harder. Some attempts to quantify emotional and motivational function will be discussed below. Functional neuroimaging has revolutionised the study of human emotion and motivation. We can put people in a scanner and measure directly their brain responses to emotional information or to motivational cues.

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Memantine augmentation in treatment resistant obsessive-compulsive disorder: an open-label trial medications related to the blood 500mg probalan visa. N-acetylcysteine add-on treatment in refractory obsessive-compulsive dis order: a randomized medications ending in zole purchase probalan 500mg on-line, double-blind symptoms 2 days after ovulation discount 500mg probalan otc, placebo-controlled trial treatment gastritis probalan 500 mg amex. Animal models of obsessive-compulsive disorder: exploring pharmacology and neural substrates. Cannabinoids elicit antidepressant-like behavior and activate serotonergic neurons through the medial pre frontal cortex. Caudate glucose metabolic rate changes with both drug and behavior ther apy for obsessive-compulsive disorder. Endocannabinoids regulate interneuron migration and morphogenesis by transactivating the TrkB receptor. Effect of long-term administration of antide pressant treatments on serotonin release in brain regions involved in obsessive compulsive disorder. Sequential super stereotypy of an instinctive fixed action pattern in hyper-dopaminergic mutant mice: a model of obsessive compulsive disorder and Tourette’s. Anti-brain autoantibodies and altered excitatory neurotransmitters in obsessive-compulsive disorder. Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psy chiatric disorders. The anxiolytic effect of cannabidiol on chronically stressed mice depends on hippocampal neurogenesis: involvement of the endocannabinoid system. Dissociable aspects of performance on the 5-choice serial reaction time task following lesions of the dorsal anterior cingulate, infralimbic and orbitofrontal cortex in the rat: differ ential effects on selectivity, impulsivity and compulsivity. A switch mechanism between locomo tion and mouthing implicated in sensitization to quinpirole in rats. Effects of glutamate-related drugs on marble-burying behavior in mice: implica tions for obsessive-compulsive disorder. Longlasting consequences of chronic treatment with the dopamine agonist quinpirole for the undrugged behavior of rats. Interactions between the cannabinoid and dopaminergic systems: evidence from animal studies. Mechanisms of action of current and potential pharma cotherapies of obsessive-compulsive disorder. Pharmacotherapy of obsessive-compulsive disorder: evidence-based treatment and beyond. Modulation of effective connectivity during emotional processing by Delta 9-tetrahydrocannabinol and cannabidiol. Efficacy of typical and atypical antipsychotics for primary and comorbid anxiety symptoms or disorders: a review. An open-label trial of riluzole, a glutamate antagonist, in children with treatment-resistant obsessive-compulsive disorder. Serotonergic dissection of obsessive compulsive symptoms: a challenge study with m-chlorophenylpiperazine and sumatriptan. Serotonin and dopamine transporter imaging in patients with obsessive compulsive disorder. The effects of temporary inactivation of the orbital cortex in the signal attenuation rat model of obsessive compulsive disorder. Inhibition of endocannabinoid catabolic enzymes elicits anxiolytic-like effects in the marble burying assay. Animal models of obsessive-compulsive disorder: rationale to understanding psychobiology and pharmacology. Modulation of cognitive and emotional processing by cannabidiol: the role of the ante rior cingulate cortex. N-acetylcysteine augmentation in serotonin reuptake inhibitor refractory obsessive-compulsive disorder. Cerebrospinal fluid biogenic amines in obsessive compulsive dis order, Tourette’s syndrome, and healthy controls. Elevated growth hormone responses to pyridostigmine in obsessive-compulsive disorder: evidence of cholinergic supersensitivity. Summary of the comparative effectiveness review on off-label use of atypical antipsychotics. A case series of aripiprazole augmentation of selective serotonin reuptake inhibitors in treatment-refractory obsessive compulsive disorder. A double blind, placebo-controlled study of risperidone addition in serotonin reuptake inhibitor refractory obsessive-compulsive disorder. Glutamatergic drugs exacerbate symptomatic behavior in a transgenic model of comorbid Tourette’s syn drome and obsessive-compulsive disorder. Integrating evidence from neuroimaging and neuropsychological studies of obsessive-compulsive disorder: the orbitofronto-striatal model revisited. Cannabinoid type 1 receptors and transient receptor potential vanilloid type 1 channels in fear and anxiety—two sides of one coin Clinical fac tors associated with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. Cognitive-behavioral therapy for obsessive-compulsive disorder: a meta-analysis of treatment outcome and modera tors. Glutamate-modulating drugs as novel pharmacother apeutic agents in the treatment of obsessive-compulsive disorder. Glutamate abnormalities in obsessive compul sive disorder: neurobiology, pathophysiology, and treatment. Elevated brain serotonin transporter availability in patients with obsessive-compulsive disorder. Evidence for cortical inhibitory and excitatory dysfunction in obsessive compulsive disorder. Randomized controlled crossover trial of ketamine in obsessive-compulsive dis order: proof-of-concept. Lesions of the medial and lateral striatum in the rat produce differential deficits in attentional performance. Decrease in caudate glutamatergic concentrations in pediatric obsessive-compulsive disorder patients taking paroxetine. Localized orbitofrontal and subcortical metabolic changes and predictors of response to paroxetine treatment in obsessive-compulsive disorder. Aripiprazole improves olanzapine-associated obsessive compulsive symptoms in schizophrenia. Slitrk5 deficiency impairs corticostriatal circuitry and leads to obsessive-compulsive like behaviors in mice. Investigation of cortical glutamate-glutamine and gamma-aminobutyric acid in obsessive-compulsive disorder by proton magnetic resonance spectroscopy. A 1H magnetic resonance spectroscopy study in adults with obsessive compul sive disorder: relationship between metabolite concentrations and symptom severity. Cerebrospinal fluid neurochemistry in children and adolescents with obsessive compulsive disorder. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases. Amygdala volume reductions in pediatric patients with obsessive-compulsive dis order treated with paroxetine: preliminary findings. Marble burying reflects a repetitive and perseverative behavior more than novelty-induced anx iety. Subcellular arrangement of molecules for 2-arachidonoyl-glycerol-mediated retrograde signaling and its physiological contribution to synaptic modulation in the striatum. Involvement of endocannabinoids in antide pressant and anti-compulsive effect of fluoxetine in mice. The endocannabinoid system in the basal ganglia and in the mesolimbic reward system: implications for neurological and psychiatric dis orders. Serotonergic agents restore appropriate decision-making in neonatal rats displaying dopamine D1 receptor mediated vacillatory behavior.

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Clonazepam has had reported modest tic suppressing effects in published case series medications causing dry mouth order 500mg probalan visa. It is usually given two or three times daily medications covered by blue cross blue shield purchase probalan 500 mg overnight delivery, and its most common side effects are sedation and unsteadiness professional english medicine purchase 500mg probalan visa. The drug is marketed in Canada and Europe and is expected to treatment yeast overgrowth safe probalan 500 mg become available soon in the United States. The most common side effects are sedation, depression, insomnia, and parkinsonism. Although tetrabenazine does not cause tardive phenomena, dopamine-depleting agents can cause neuroleptic malignant syndrome even after years of use. When tics have dystonic features, such as holding of a sustained neck posture or sustained eye closure, botulinum toxin may be a preferred treatment. Botulinum may modify sensory feedback (such as from intrafusal muscle fibers) perpetuating processes involved in tic reinforcement. Dopamine agonists pergolide and ropinirole have been reported to improve tic severity in reported trials. Calcium channel antagonists may have activity at dopamine receptors, either through direct blockade or by reducing depolarization of midbrain dopamine neurons. Drugs of interest with activity at glutamate receptors include D-serine, D-cycloserine, sarcosine, modafanil, riluzole, memantine, and talampanel. Increased activity would be expected to reduce motor output and thus might reduce involuntary movements such as tics. Although promising in open-label fashion,[81] it has shown conflicting results in two randomized trials. Further studies using drugs acting on cannabinoid receptors, such as dronabinol or nabilone, may be rational. Behavioral approaches have included operant conditioning models (rewarding tic suppression and discouraging disruptive tics) and massed practice (repeated, voluntarily performance of a tic until fatigue occurs). To date, most reported cases have involved bilateral targeting of the centro-median parafascicular and ventralis oralis complex (central nuclei) of the thalamus. We recommend that children with documented streptococcal infections be treated with an appropriate course of antibiotics, but that treatment with chronic antibiotics or immune-modifying therapies like plasma exchange or intravenous immune globulin are not justified based on existing evidence. Risk of side effects must be weighed carefully against potential benefits in deciding whether to use a drug to treat secondary forms of tics. In patients with tardive phenomena including tics, discontinuation of the offending agent is suggested as first-line treatment, and improvement can be attained with use of clonazepam, an alpha-2 agonist, clozapine, or reintroduction of an antipsychotic. These often include preferential classroom seating, extra time for tests, an opportunity to take tests in a separate quiet room, and assistance with organizing schoolwork. It does seem that upon initiation of therapy stimulants can worsen tics in some patients, but this effect is temporary and tic severity usually returns to baseline (or even declines from baseline) within a few weeks. The efficacy and good tolerability of the stimulant methylphenidate in children with tics has been well documented in placebo-controlled trials. Supplemental use of short-acting methylphenidate formulations can be useful, particularly for college students who have unpredictable study hours. The most common stimulant side effects include reduced appetite, weight loss, upset stomach, headache, and insomnia. Selective serotonin reuptake inhibitors Daily Generic dose name How supplied (mg) Clomipramine Capsules: 25, 50, 75 25-250 mg Citalopram Tablets: 20, 40 mg 10-40 Escitalopram Tablets: 5, 10, 20 mg. There are local support groups in many cities that can provide information, guidance, and support. For young patients, major goals of treatment include helping the child to develop self-confidence, personal resilience, and positive psychosocial skills. The ultimate management usually requires a spectrum of interventions that may include education, cognitive-behavioral therapies, counseling, and medications. Contributor roles: Both authors contributed to the conception, design, and writing of the manuscript. Tourette syndrome is only one of several causes of a developmental basal ganglia syndrome. The diverse phenotype and genotype of pantothenate kinase-associated neurodegeneration. Complex tics, stereotypies, and compulsive behavior as clinical presentation of a juvenile progressive dystonia suggestive of Hallervorden-Spatz disease. Neurological consequences of psychotropic drug withdrawal in schizophrenic children. Adult-onset tic disorder, motor stereotypies, and behavioural disturbance associated with antibasal ganglia antibodies. Typical and atypical antipsychotics differentially affect long-term incidence rates of the metabolic syndrome in first episode patients with schizophrenia: a retrospective chart review. Olanzapine in severe Gilles de la Tourette syndrome: a 52-week double-blind cross-over study vs. Aripiprazole: a treatment for severe coprolalia in refractory Gilles de la Tourette syndrome. An open-label study of the efficacy and tolerability of aripiprazole for children and adolescents with tic disorders. A case of tetrabenazine-induced neuroleptic malignant syndrome after prolonged treatment. Vocal tics in Gilles de la Tourette syndrome treated with botulinum toxin injections. Botulinum toxin for simple motor tics: a randomized, double-blind, controlled clinical trial. Cognitive-pharmacologic functional magnetic resonance imaging in tourette syndrome: a pilot study. Excitability of motor cortex inhibitory circuits in Tourette syndrome before and after single dose nicotine. Messing up with traffic: different effects of antipsychotic agents on glutamate receptor complexes in vivo. Nicotinic receptor-mediated regulation of dopamine transporter activity in rat prefrontal cortex. Baclofen treatment in Tourette syndrome: a double-blind, placebo-controlled, crossover trial. Use of levetiracetam to treat tics in children and adolescents with Tourette syndrome. A double blind randomized placebo control trial of levetiracetam in Tourette syndrome. Double-blind placebo randomized study of using levetiracetam to treat tics in children and adolescents with Tourette syndrome. An international perspective on Tourette syndrome: selected findings from 3,500 individuals in 22 countries. Adulthood outcome of tic and obsessive compulsive symptom severity in children with Tourette syndrome. A possible role for hormonal and excitatory neurotransmitter influences in brain development. Repetitive transcranial magnetic stimulation of the supplementary motor area in the treatment of Tourette syndrome: report of two cases. Deep brain stimulation in 18 patients with severe Gilles de la Tourette syndrome refractory to treatment: the surgery and stimulation. Prospective randomized double-blind trial of bilateral thalamic deep brain stimulation in adults with Tourette syndrome. Efficient internal pallidal stimulation in Gilles de la Tourette syndrome: a case report. Therapy-refractory Tourette syndrome: beneficial outcome with globus pallidus internus deep brain stimulation. Deep brain stimulation of the anterior internal capsule for the treatment of Tourette syndrome: technical case report. Neuroleptic-induced tardive Tourette treated with clonazepam: a case report and literature review. Keywords: Gilles de la Tourette syndrome, tics, quality of life, wellbeing, behaviour 1. Prevalence was obtained from each subject prior to enrolment into rates show wide variability, but recent studies suggest the development and validation protocols. Around 90% of patients seen professional translators the authors compared the two in specialist clinics present with co-morbid behavioural translated versions with the original English version, to dif culties, ranging from complex tic-like symptoms yield the linguistic validation of the provisional ques (self-injurious behaviours, non obscene socially inap tionnairein Italian.

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The three key components of functioning and disability are inter-related and may interact with the health condition treatment dynamics 500mg probalan with mastercard. The reported prevalence of intellectual disability re ects consideration of the de nition used medicine naproxen 500mg cheap probalan 500 mg otc, method of ascertainment of the data medicine 95a probalan 500mg lowest price, and the characteristics of the population studied medications xarelto cheap 500mg probalan with amex. Based on the typical bell-shaped distribution of intel ligence in the general population and 2 standard deviations below the mean as a cutoff point, approximately 2. The prevalence and causes of vision impairment vary in different parts of the world depending on multiple factors. Acknowledgments this chapter is adapted with permission from authors’ previous works [56, 57]. The sections on hearing loss and vision impairment are adapted from (public domain) United States Centers for Disease Control. The international classi cation of functioning Disability and Health: its development process and content validity. Reported biomedical causes and associated medical conditions for mental retardation among 10-year-old children, metropolitan Atlanta, 1985 to 1987. Learning disabilities: de nitions, epidemiology, diagnosis, and intervention strate gies. Reading disability in adjudicated youth: prevalence rates, current models, traditional and innovative treatments. Prevalence of autism spectrum disorders – autism and developmental disabilities monitoring network, United States, 2006. Prevalence of pervasive developmental disorders in children and adolescents with mental retardation. Speci c genetic disorders and autism: clinical contribution towards their identi cation. Academy of neurology practice parameter: diagnostic assessment of the child with cerebral palsy. Mental health disorders among individu als with mental retardation: challenges to accurate prevalence estimates. Prevalence of psychiatric disorders in children and adolescents with and without intellectual disability. Intellectual disability co-occurring with schizophrenia and other psychiatric illness: population-based study. Psychiatric disorders in children with autism spectrum disorders: prevalence, comorbidity, and associated factors in a population-derived sample. Multi-informant reports of psychiatric symptoms among high-functioning adolescents with Asperger syn drome or autism. Psychiatric and psychosocial problems in adults with normal-intelligence autism spectrum disorders. Patel Abstract Development generally follows four domains, namely motor, speech and language, social–emotional, and cognitive. The predominant signs and symptoms of atypical development vary depending on the age of the infant or the child. For example, a delay in achieving motor milestones as expected is generally recognized early in infancy, atypical language development is more often recognized in early child hood, and academic dif culties are recognized in late childhood and adolescence. This chapter reviews the basic concepts and de nitions applied in the study of developmental problems, the main features of common conditions considered in the differential diagnoses of developmental disorders, and describes signs that should prompt further developmental evaluation. Introduction Development generally follows four domains and has a typical progression when it is proceeding as expected: (1) motor development consists of ne motor and gross motor domains; (2) speech and language development has both receptive and expressive domains; (3) social–emotional development is a re ection of or a combi nation of development in other domains that includes ne motor adaptive abilities, overall communication abilities, and cognitive abilities; and (4) cognitive develop ment generally refers to visual–perceptual, visual–motor, and problem-solving skills and abilities [1–6]. The typical development is based on certain key principles [1–5, 7, 8]: (1) gross motor development progresses in a cephalo-caudal sequence whereas ne motor D. These key concepts are useful when applied in developmental screening, surveillance, and evaluation (see Table 2. Atypical development can be described as a delay, deviation, dissociation, or regression (see Table 2. For example, when there is delayed motor development relative to other domains in cerebral palsy Regression Loss of previously acquired developmental milestones or skills or failure to acquire new skills error of measurement of 5 on an individually administered standardized intelligence test) with limitations in adaptive behavior as expressed in conceptual, social, and practical adaptive skills [10–15]. Clinical Features Infants Predominant Delay in Motor Milestones Generally, in infants, delayed or atypical motor development manifests earlier than other domains of development. Because there is a range of periods during which infants attain typical milestones, the most common cause of apparent motor delay is a normal variation or maturational lag [2, 4]. The most signi cant cause of motor delay in infancy is cerebral palsy which consists of motor delay, abnormal tone, and posture [2, 3, 7, 8, 16, 17]. Clinical presentation and features of infants and children with cerebral palsy may vary depending on its type and severity [16, 17]. A child over 2 months of age with cerebral palsy may have poor head control, stiff legs, and scissoring. A child over 6 months of age may still not have head control, may not sit unsupported, and might preferentially use only one extremity. A child over 10 months of age might crawl by pushing off with one hand and leg while dragging the opposite hand and leg and may not sit without support. A child over 12 months of age might not be crawling and may not stand with support. A child over 24 months of age may not be yet walking or able to push a toy with wheels. Other causes of predominant motor delay include traumatic insults to the central nervous system damage (kernicterus, birth injury, stroke, metabolic insults, and con genital infections); spinal cord disorders (myelomeningocele, Werdnig–Hoffmann disease); myopathies; muscular dystrophies; and benign congenital hypotonia [4, 7, 8, 11, 12]. Patel Atypical Development Affecting Social, Cognitive, and Language Milestones A full evaluation for autism, signi cant cognitive delay, or language impairment is mandatory in infants with the following: no babbling, pointing, or other gestures by 12 months of age, no single words by 16 months, no two word spontaneous phrases by 24 months of age, and any loss of previously acquired language or social skills [5–8]. A de ciency in joint attention, that is, the ability to attend both an object and a person at the same time. Other conditions to consider in infants with predominant language, cognitive, and social delays include hearing impairment, severe cognitive de cits, genetic disor ders, inborn errors of metabolism including hypothyroidism, and severe nutritional or environmental deprivation. Some of the less common conditions associated with progressive encephalopa thy with onset before age 2 years include metabolic conditions such as disorders of amino acid metabolism, lysosomal storage disease, hypothyroidism, mitochon drial diseases, tuberous sclerosis, Lesch–Nyhan syndrome, Rett syndrome, Canavan disease, and Pelizaeus–Merzbacher disease [4]. Children Atypical Language Development Speech and language problems may present as any number of symptoms including poor intelligibility (normal 25% by age 2, 50% by age 2, 75% by age 3, and 100% by age 4), persistent baby talk, mispronunciations of words, or lack of spontaneous speech [18–24]. Speech is the production of sounds for words, prosody is the pat tern of rhythm, stress, and intonation of the speech, and language is a system of symbolic knowledge represented in the brain used for meaningful communication [18–20]. Air ow obstruction accompanies the production of consonant sounds, whereas it does not in the case of vowel sounds. Main causes of atypical development in preschool-age children are autism spec trum disorders, intellectual disability, and developmental language disorders [3, 5–8, 12, 14]. Children with autism have qualitative impairment in communication skills, qualitative impairment in social relatedness, and a range of atypical stereo typical behaviors [6, 26]. Autism spectrum disorders typically are recognized by age 3 years, some as early as 18 months or earlier [6]. Parents usually rst notice unusual behaviors and language dif culties in the child. They may describe the child as not socially responsive to others or who may intensely focus on one item for a long period of time. A child with autism spectrum disorder may not play pretend games, want others to leave him alone, have trouble understanding other people’s feelings, and demonstrate echolalia [6, 27, 32]. Asperger syndrome demonstrates normal cognitive and language abilities and predominant de cits in social development [23–35]. Children with intellectual disability have predominant de cits in cognitive and language abilities. Their social development is consistent with their mental age, and they have no motor de cits. Some of the signs of intellectual disability that the par ent may observe include – that the child is late to sit, crawl, or walk; learn to talk; have trouble speaking; nd it hard to remember things; have trouble understanding social roles; have trouble seeing the results of their actions; or have trouble solving problems [12–14]. There is no identi able speci c cause in most children with mild intellectual disabilities. The likelihood of identifying a speci c etiology increases as the severity of intellectual disability increases. Some of the known causes of intel lectual disability include fragile X syndrome, fetal alcohol syndrome, other genetic syndromes, lead toxicity, iron de ciency, brain malformations or dysgenesis, and tuberous sclerosis [9, 11–15].

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