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B: Graph illustrating the variation of the magnetic resonance signal as a function of the orientation of the diffusion gradient purchase medrol 16mg amex. The circles (open and closed) correspond to measurements with the diffusion gradients applied in the plane perpendicular to the nerve axis cheap medrol 4mg line. The triangles correspond to diffusion mea- surements obtained by using the gradient parallel to the nerve axis 4mg medrol visa. The anisotropy of the restric- tion to the diffusion of water molecules in the cellular compartments is clearly shown order 16mg medrol with mastercard. In the context of a functional experiment order 4 mg medrol with visa, functional Palo Alto, California) system equipped with an 18-cm connectivity would allow us an array of possible interpreta- horizontal-bore superconducting magnet (Nalorac, tions. The simplest of these solutions that can replicate the Martinez, California) and a set of coils capable of producing observed functional connectivity describes the interactions 120-mT/m field gradients. Proton MR diffusion-weighted and connections that are sufficiently active to be detectable images were obtained by using a spin-echo sequence with at the time of observation. This simplest solution is the an echo time of 50 ms and a repetition time of 1 s. The effective connectivity, which accounts for the interaction that measurements were performed at room temperature (21 C). The b values used for In vivo DTI-based fiber tract analysis is relevant for the diffusion weighting were 0, 200, 400, 800 and 1,600 s • study of structural–functional and anatomic–clinical rela- mm2. The slice thickness was 2 mm, and the field of view tionships. The details of systems neuroanatomy are critical was 7. Damage to specific fiber pathways correlates with the de- The effect of restriction to molecular diffusion within creased cerebral metabolism pattern observed in stroke pa- the nerve is shown in Fig. Functional activation studies in which PET and plied along directions gx (1,0,0) and gz (0,0,1), which fMRI are used contribute to the knowledge of the spatial were perpendicular to the nerve axis gy (0,1,0) in these distribution of cortical and subcortical processing elements. Use of actual indi- Macroscopic Studies vidual information regarding in vivo white matter fiber In a sense, the cerebral white matter can be considered as pathway topography and volumetry may optimize and in- a finite set of discrete and topographically organized fiber crease the predictive power of these models. These anatomic pathways or connections that convey connectivity within and neuroimaging studies of the constituents of the fiber the brain, and the physical connections in their entirety tracts and the connections of the human cerebral cortex will would make up anatomic connectivity. On the other hand, be important in acquiring an understanding of the distrib- the physiologic outcome of activities of neuronal assemblies, uted neural circuits that subserve normal brain function. Applications of the DTI technique in white matter pathway analysis in normal persons and in cases of amyotrophic lateral sclerosis are illustrated. Three normal Integrated Magnetic Resonance tracts—the corticospinal projection, the corpus callosum, Neurologic Examination and the cingulum fiber system—have been selected for the illustration because of their different orientations and also Diffusion tensor imaging can be an important part of a because they represent distinctive classes of connection (i. Quanti- projectional, commissural, and associational, respectively). Specifically, by DTI, of metabolic state by MRS, and of functional state the corpus callosum and the corticospinal tracts were hand- by fMRI provides a highly multidimensional data space for picked, whereas the cingulum fiber system was recon- the elucidation of structural, functional, behavioral, and structed automatically in three dimensions. For instance, the relative contributions shown in Figs. This leads to an optimized, temporally efficient MRI neurologic examination that cap- Amyotrophic Lateral Sclerosis tures the salient features of the structural, metabolic, and In amyotrophic lateral sclerosis (ALS), as degeneration of functional states as they change over time. Monitoring these the upper motor neuron occurs, a progressive damage to the manifestations enables us to elucidate the neurobiological corticospinal tract has been documented in the caudorostral underpinnings of normal brain development and aging in direction (42–45). We used DTI in two patients (cases 1 addition to the endpoints of etiology, natural history, and and 2) to document pronounced bilateral reduction in the therapeutic intervention in disease states (47). The ALS case size of the corticospinal tract at the level of the medulla 1 is an example of this application. Case 1 illustrates an integrated MRI examination this technique to assess the changes in both motor cortical of structure, function, and metabolism. We successfully per- ventional MR images or in the T2-EP images at its ventral formed fMRI in this same patient (Fig. The data indicated larger areas of activa- niques do not allowan accurate definition of the borders tion in the left than in the right hemisphere and reflected of the tract.

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Clusters 2 The authors acknowledge the support of the PBO Founda- and 3 are dealt with elsewhere in the volume 16 mg medrol overnight delivery. There is often poor insight or delusional convic- 1 discount medrol 16 mg free shipping. Psychosocial function tion quality medrol 16 mg, and secondary depression and social phobia medrol 16mg low cost. A recent double-blind crossover trial compared the SRI 2 buy discount medrol 4mg. Diagnostic and Statistical Manual of Mental Disorders, fourth clomipramine to the noradrenergic reuptake inhibitor desi- ed. Washington, DC: American Psychiatric Association, 1994. Desipramine, the active control, was chosen to con- of obsessive-compulsive disorder in five US communities. Arch trol for nonspecific antidepressant and antidepressants, and Gen Psychiatry 1988;45:1094–1099. The epidemiology and differential because it has a similar side-effect profile to CMI, enhancing diagnosis of obsessive-compulsive disorder. The SRI CMI resulted in significantly greater 1994;55(Suppl):5–14. The prognostic significance of severity than did DMI, and also improved measures of func- obsessive-compulsive symptoms in schizophrenia. Subjects with delusional conviction regarding body der in patients with schizophrenia or schizoaffective disorder. Obsessive and like OCD, but in contrast to other mood or anxiety disor- compulsive symptoms in chronic schizophrenia. The delusional conviction in BDD appears disorder in patients with first-episode schizophrenia. Am J Psy- secondary to obsessive preoccupation, and also responds to chiatry 1999;156:1998–2000. Clozapine and obsession in patients with recent-onset schizophrenia and other psychotic disorders. Treatment of obsessive- compulsive syndromes in schizophrenia. Comorbidity of obses- In summary, SSRIs and the tricyclic antidepressant clomi- sive-compulsive disorder in bipolar disorder. J Affect Disord pramine are currently the first-line treatment for OCD, 1995;34:117–120. Furthermore, not all patients tolerate SSRIs, and comorbidity in patients with mood spectrum disorder with psy- there is often a time delay in seeing a full therapeutic re- chotic features. Thus, other pharmacologic approaches to treating bipolar and unipolar affective comorbidity in obsessive-compul- OCD have been investigated, and certainly combinations sive disorder. Fluoxetine-induce mania in a patient with obsessive- considered the treatment of choice. Am J Psychiatry 1992;148(10): novel monotherapy strategies have been explored in refrac- 1403–1404. Antidepressant-induced mania in obses- tory patients, with serotonergic enhancers, dopamine/sero- sive-compulsive disorder. Am J Psychiatry 1992;149(9): tonin antagonists, enhancers of second messenger systems, 1282–1283. Antidepressant induced hypo- 1660 Neuropsychopharmacology: The Fifth Generation of Progress mania in obsessive-compulsive disorder. Serotonin and drug-induced therapeu- pulsive disorder. J Child Adoles Psychopharmacol 1998;8(1): tic responses in major depression, obsessive-compulsive and 73–80. In: Jenike MA, Baer L, Mini- addition in fluvoxamine-refractory obsessive-compulsive disor- chiello WE, eds. Obsessive-compulsive disorders: theory and man- der. The Gilles de la Tourette syndrome: the cur- resistant obsessive-compulsive disorder. Neurological soft-signs HT2A receptor genes polymorphisms in obsessive-compulsive in obsessive-compulsive disorder.

All the foregoing observa- ously with the formation and release of A 4 mg medrol mastercard. A secre- tion could be totally prevented by brefeldin A (24 medrol 16mg on-line,62) order medrol 4mg visa, and Localization of APP Processing by monensin (24) generic 16mg medrol fast delivery, two agents that potently block intracellu- By using a mixture of protease inhibitors and by approaches lar trafficking cheap medrol 4 mg overnight delivery. This finding suggests that A may be gener- such as metabolic labeling, pulse chase experiments, and ated during the transport of APP through the Golgi appara- cell treatments with various agents known to affect a charac- tus en route to the plasma membrane. APP polypeptide compartment of the constitutional secretory pathway (50, undergoes complex post-translational modifications, in- 51). These data were supported by Sambamurti and co- cluding sulfation, phosphorylation, and both N- and O- workers (52), who demonstrated using [35S] labeling and linked glycosylation (44,63). These modifications occur temperature block that -secretase activity occurs in the during the trafficking of the protein through the secretory trans-Golgi network or in a late trans-Golgi compartment pathway. Thus, APP is cotranslationally translocated into just after sulfate incorporation (53). At this stage, some of evidenced by labeling of APP after biotinylation (54) or the APP may have already been processed by - and - radioiodination (55) of cell-surface membranes. Then, a percentage of mature molecules is trans- approach allows recovering secreted biotinylated or iodi- ported to the plasma membrane by secretory vesicles (64). This finding indi- At or near the cell surface, some APP molecules undergo cates that -secretase activity can also occur at the plasma proteolysis by the protease designated -secretase. Alter- membrane level in several cell systems (see also ref. The cellular sites of A production have been thor- trafficked to late endosomes and lysosomes for apparent 1202 Neuropsychopharmacology: The Fifth Generation of Progress degradation (56,59), or it is rapidly recycled within early however, mutations in tau are associated with frontotem- endosomes to the cell surface (66). It appears that, at MUTATIONS IN APP IN EARLY-ONSET AD least in cultured cells, only a few of all biosynthesized APP molecules undergo either the -secretase or the -secretase Genes may be related to disease in two ways: through muta- fate; many full-length precursor molecules remain inserted tions that by themselves are sufficient to cause the disease into internal membranes, particularly in the Golgi. This latter group is referred to as Neurofibrillary tangles are another important histologic fea- susceptibility genes. They consist of PHFs in a double helix (diame- most cases of AD occur sporadically, autosomal dominant ter, 20 nm) found in the cytoplasm of neurons, particularly transmission has been identified in families with early-onset of the pyramidal cells of the cerebral cortex and hippocam- AD, defined as beginning before the age of 65 years. PHFs are composed principally of phosphorylated cases are relatively rare; worldwide, only several hundred tau, a low-molecular-weight microtubule-associated protein families are currently known to carry deterministic muta- (68). Extensive research carried out since the early Tau is a family of six proteins derived by alternative 1980s has isolated certain genes that, when mutated, cause mRNA splicing from a single gene located on chromosome AD, notably APP on chromosome 21 (79,80), the PS1 gene 17. These molecular isoforms of tau differ in whether they on chromosome 14 (81), and the PS2 gene on chromosome contain three or four tubulin-binding domains of 31 or 32 1 (81). Mutations in these genes lead to early-onset AD and amino acids each near the C-terminal end and no, one, or explain only a small proportion of total AD cases. Further- two inserts of 29 amino acids each at N-terminal end of more, trisomy 21 (Down syndrome or DS) increases the the molecule. In addition, some susceptibility genes are currently Tau in AD brain, especially in PHFs, is abnormally hy- being studied, of which polymorphisms of the APOE gene perphosphorylated and glycosylated. At the later stages of have received the most attention. The presence of the tangle formation, the tau is increasingly ubiquinated. In a APOE-4 allele has been identified as a genetic risk factor normal neuron, biological function depends on an intact for sporadic AD and familial AD (FAD) of late onset. All microtubule network through which much of the axoplas- these genetic causes of AD are discussed in detail later. The AD abnormally phosphory- lated tau (AD P-tau) competes with tubulin in binding to normal tau, MAP1, and MAP2 and inhibits their microtu- AD in Down Syndrome bule assembly-promoting activities. The disruption of the In considering the molecular pathology of DS, a matter of microtubule network probably compromises the axonal critical interest is that virtually all patients with DS who transport and starts retrograde degeneration of the affected survive beyond 35 years of age develop neuropathologic neurons. The neuronal cytoskeleton in AD is progressively changes that closely resemble AD (82). Thus, there is the disrupted and is replaced by bundles of PHFs, leading to abnormal accumulation of A in the brains of both patients the formation of neurofibrillary tangles (67). To date, 21 phosphorylation sites in the AD abnormally Patients with DS are thought to express high levels of APP phosphorylated tau have been identified (69). Among the because of an extra copy of chromosome 21. The most several protein kinases that have been implicated in the straightforward explanation for dementia in DS is the pres- phosphorylation are glycogen synthase kinase-3 (70), neu- ence of three instead of two copies of APP in patients with ronal Cdc-like protein kinase (71), mitogen-activated pro- DS (83). Other genes that are potentially overexpressed in tein kinase (72), Ca2 /calmodulin-dependent protein ki- DS are located within a segment of chromosome 21, termed nase II (73), casein kinase I (74), and cyclic adenosine the Down locus.

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Farone: Pediatric Psychopharmacology Unit discount medrol 16 mg line, Child Psychia- try Service 16 mg medrol with visa, Massachusetts General Hospital; Harvard Medical School; Massa- to improve with stimulant treatment 4mg medrol otc. There is little evidence chusetts Mental Health Center; Harvard Institute of Psychiatric Epidemiology of a differential response to methylphenidate medrol 4mg mastercard, pemoline cheap 16 mg medrol mastercard, and and Genetics, Boston, Massachusetts. The average response rate for each is Joseph Biederman: Pediatric Psychopharmacology Unit, Child Psychia- try Service, Massachusetts General Hospital; Harvard Medical School, Boston, 70%. Stimulants enhance social skills at home and in school. Solanto suggested that stimulants may also activate uational cues and to modulate the intensity of their behav- presynaptic inhibitory autoreceptors and may lead to re- ior. They also show improved communication, greater duced dopaminergic and noradrenergic activity (21). The responsiveness, and fewer negative interactions. Neuro- maximal therapeutic effects of stimulants occur during the psychological studies show that stimulants improve vigi- absorption phase of the kinetic curve, within 2 hours after lance, cognitive impulsivity, reaction time, short-term ingestion. The absorption phase parallels the acute release memory, and learning of verbal and nonverbal material in of neurotransmitters into synaptic clefts, a finding providing children with ADHD. A plausible model for the effective anti-ADHD agents. TCAs include secondary and effects of stimulants in ADHD is that, through dopami- tertiary amines with a wide range of receptor actions, effi- nergic or noradrenergic pathways, these drugs increase the cacy, and side effects. Secondary amines are more selective inhibitory influences of frontal cortical activity on subcorti- (noradrenergic) with fewer side effects. TCAs have found either a moderate or robust response rate Human studies of the catecholamine hypothesis of of ADHD symptoms (8–10). These studies show anti- ADHD that focused on catecholamine metabolites and en- ADHD efficacy for imipramine, desipramine, amitriptyline, zymes in serum and cerebrospinal fluid produced conflict- nortriptyline, and clomipramine. Perhaps the best summary of this litera- studies show that TCAs produce moderate to strong effects ture is that aberrations in no single neurotransmitter system on ADHD symptoms. In contrast, neurocognitive symp- can account for the available data. Of course, because studies toms are do not respond well to TCA treatment. Because of neurotransmitter systems rely on peripheral measures, of rare reports of sudden death among TCA-treated chil- which may not reflect brain concentrations, we cannot ex- dren, these drugs are not a first-line treatment for ADHD pect such studies to be completely informative. Neverthe- and are only used after carefully weighing the risks and less, although such studies do not provide a clear profile of benefits of treating or not treating a child who does not neurotransmitter dysfunction in ADHD, on balance, they respond to other agents. One approach has been the are rarely used because of their potential for hypertensive use of 6-hydroxydopamine to create lesions in dopamine crisis, several studies suggested that monoamine oxidase in- pathways in developing rats. Because these lesions created hibitors may be effective in juvenile and adult ADHD (14). Disruption of catecholaminergic showed efficacy in a controlled study of adults with ADHD transmission with chronic low-dose N-methyl-4-phenyl- (15) and in an open study of children with ADHD (16). In this latter work, TCAs, there is only weak evidence that either 2-noradren- MPTP administration to monkeys caused cognitive impair- ergic agonists or serotonin reuptake inhibitors effectively ments on tasks thought to require efficient frontal-striatal combat ADHD (17). A controlled clinical trial showed that neural networks. These cognitive impairments mirrored transdermal nicotine improved ADHD symptoms and those seen in monkeys with frontal lesions (26,27). Like neuropsychological functioning in adults with ADHD (18). Methylphenidate and experimental compound ABT-418 to treat adult ADHD the dopamine D2 receptor agonist LY-171555 reversed the effectively (19). ABT-418 is a potent and selective agonist behavioral deficits but not the cognitive dysfunction (28, for 4 2-subtype central nervous system neuronal nicotinic 29). Studies using the SHR have implicated As the foregoing review shows, effective medications for dopaminergic and noradrenergic systems. For example, the ADHD act in noradrenergic and dopaminergic systems.

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