Neuropsych Test Iii

Front 1

discuss the incidence of alzheimer’s disease

Back 1

The incidence and prevalence of AD increase exponentially with age. AD is slightly more common in women than men, with a relative risk of 1.5 [2]. This does not appear to be explained by the greater longevity in women. There are inherited forms of AD, all autosomal dominant, that routinely present before age 65, and frequently in the fifth decade or earlier. These account for less than 5 percent of all cases of AD. Patients with Down syndrome develop AD at an earlier age, 10 to 20 years younger than the general population with AD [3].

Front 2

discuss the genetic factors of alzheimer’s disease

Back 2

Autosomal dominant forms of inherited AD have been linked to mutations of the amyloid precursor protein (APP) gene on chromosome 21 and to genes encoding presenilin 1 (PS1) on chromosome 14 and presenilin 2 (PS2) on chromosome 1. In addition, AD pathology occurs in the brains of adults who have trisomy 21 (Down's syndrome).

Front 3

discuss memory impairment in alzheimer’s disease

Back 3

Declarative memory for facts and events, which depend on mesial temporal and neocortical structures are profoundly affected in AD, while subcortical systems supporting procedural memory and motor learning are relatively spared until quite late in the disease. In contrast, immediate memory (encoded in the sensory association and prefrontal cortices) is spared early on, as are memories that are consolidated for long periods of time (years), which can be recalled without hippocampal function.

Front 4

what is Pick disease?

Back 4

(also called sphingomyelin-cholesterol lipidosis) is a group of autosomal recessive disorders associated with splenomegaly, variable neurologic deficits, and the storage of sphingomyelin.

Front 5

what are the clinical features of Pick disease?

Back 5

subdivided into two major categories: 1) type A and type B are allelic disorders caused by mutations in the sphingomyelin phosphodiesterase-1 gene (SMPD1), and characterized by a primary deficiency of acid sphingomyelinase activity 2) type C is caused by mutations of the NPC1 and NPC2 genes that result in impaired cellular processing and transport of low-density lipoprotein (LDL) cholesterol

Front 6

discuss the incidence of vascular dementia

Back 6

the second most common form of dementia after Alzheimer disease

Front 7

discuss the etiology of vascular dementia

Back 7

1) Large artery infarctions, usually cortical, sometimes also or exclusively subcortical in location. 2) Small artery infarctions or lacunes, exclusively subcortical, in the distribution of small penetrating arteries, affecting the basal ganglia, caudate, thalamus, and internal capsule as well as the cerebellum and brainstem.3) Chronic subcortical ischemia occurring in the distribution of small arteries in the periventricular white matter and leading to selective loss of tissue elements in order of their selective vulnerability - neuron, oligodendrocyte, myelinated axon, astrocyte, and endothelial cell

Front 8

discuss the clinical features of vascular dementia

Back 8

two clinical patterns - cortical and subcortical. cortical syndrome has 1) Medial frontal (executive dysfunction, abulia, or apathy) 2) Left parietal (aphasia, apraxia, or agnosia) 3) Right parietal (hemineglect, confusion, agitation, visuospatial and constructional difficulty) 2) Medial temporal (anterograde amnesia). subcortical syndrome has both lacunar infarctions and chronic ischemia affecting the deep cerebral nuclei and white matter pathways leading to Focal motor signs, gait disturbance, urinary symptoms not explained by urologic disease, Personality and mood changes, Cognitive disorder (mild memory deficit, psychomotor retardation, and abnormal executive function).

Front 9

describe Huntington disease (HD)

Back 9

an inherited progressive neurodegenerative disorder characterized by choreiform movements, psychiatric problems, and dementia. It is caused by a trinucleotide (CAG) expansion in the Huntington gene on chromosome 4p and inherited in an autosomal-dominant pattern [1].

Front 10

describe the etiology of Huntington disease

Back 10

caused by a trinucleotide (CAG) expansion in the HD gene (also known as the HTT gene) that encodes the protein huntingtin, resulting in an expanded polyglutamine tract. Huntingtin is present in a large number of tissues throughout the body. However, pathology appears to be limited to the central nervous system, with atrophy of the caudate and putamen (the neostriatum) being most prominent. At the cellular level, protein aggregates are seen both in the cytoplasm and nucleus.

Front 11

what is essential tremor?

Back 11

the most common neurologic cause of postural or action tremor. ET is referred to as familial tremor when there is a family history (approximately 50 percent of cases have an autosomal dominant pattern of inheritance) and benign essential tremor when it is sporadic. The neuropathology of ET appears to be localized to the brainstem (locus ceruleus) and cerebellum. ET most often affects the hands and arms and can be asymmetric. It can also affect the head, voice, chin, trunk, and legs.

Front 12

what is tardive dyskinesia?

Back 12

a hyperkinetic movement disorder that appears with a delayed onset after prolonged use of dopamine receptor blocking agents, mainly the antipsychotic drugs (also called neuroleptics) and the antiemetic drug, metoclopramide. numerous clinical manifestations include chorea, athetosis, dystonia, akathisia, stereotyped behaviors, and rarely tremor.

Front 13

what are the laboratory features of essential tremor?

Back 13

The routine laboratory evaluation of tremor should include tests of thyroid function, diagnostic studies to exclude Wilson's disease, and screening for heavy metal poisoning such as mercury or arsenic. Wilson's disease should be suspected in anyone under age 40 who has tremor or other involuntary movement or posture. Also helpful are brain imaging and Quantitative computerized analysis

Front 14

describe rigidity.

Back 14

an increased resistance to passive movement about a joint and occurs in approximately 90 percent of patients with PD [15-18]. Rigidityoften begins unilaterally, and typically on the same side as the tremor, if one is present. Rigidity eventually progresses to the contralateral side, and remains asymmetric throughout the disease

Front 15

what is spasticity?

Back 15

believed to result from disruption of descending inhibitory modulation of the alpha motor neurons, producing hyperexcitability, which is manifest as increased muscle tone and spasms

Front 16

what is athetosis?

Back 16

continuous stream of slow, sinuous, writhing movements, typically of the handsand feet.

Front 17

what is the treatment of essential tremor?

Back 17

beta blockers (propanolol), anticonvulsants (primidone, gabapentin), alcohol, benzodiazepines (second line, more for anxiety), botulinum toxin, surgery (thalotomy, deep brain stimulation)

Front 18

what is the treatment of tardive dyskinesia?

Back 18

discontinue dopamine receptor blocking agent, 2nd generation antipsychotic drug, benzodiazepines, botulinum toxin, anticholinergic drugs, vitamin E

Front 19

what are the treatment options for parkinsons?

Back 19

levodopa, MAO B inhibitors, dopamine agonists, COMT inhibitors, anticholinergics, amantadine, estrogen (postmenopausal)

Front 20

what is Dystonia?

Back 20

a movement disorder characterized by involuntary, sustained muscle contractions that result in twisting and repetitive movements or abnormal postures. results from repetitive use

Front 21

what is asterixis?

Back 21

flapping motions of outstretched, dorsiflexed hands

Front 22

what is myoclonus?

Back 22

a clinical sign that is characterized by brief, shock-like, involuntary movements caused by muscular contractions or inhibitions [1]. Muscular contractions produce positive myoclonus, whereas muscular inhibitions produce negative myoclonus (ie, asterixis). Patients will usually describe myoclonus as consisting of "jerks," "shakes," or "spasms."

Front 23

what is multiple sclerosis?

Back 23

most common autoimmune inflammatory demyelinating disease of the central nervous system

Front 24

what are the major pathologic mechanisms that cause the clinical manifestations in multiple sclerosis?

Back 24

Inflammation, demyelination, and axon degeneration. direct proof of an autoimmune cause of MS is lacking, as no specific autoantibody or autoreactive T-cell directed against a self-antigen in the nervous system can passively transfer MS to experimental animals.

Front 25

describe the demographics of MS.

Back 25

affects more women than men. median and mean ages of MS onset are 23.5 and 30 years of age, respectively. patients with MS are more likely than controls to have other autoimmune disorders, such as autoimmune thyroid disease. In addition, patients with other autoimmune disorders are more likely to have MS.

Front 26

describe the innervation of the upper extremity.

Back 26

C1 through C8 spinal cord segments lie between the C1 through C7 vertebral levels. The T1 through T12 cord segments lie between T1 through T8. The five lumbar cord segments are situated at the T9 through T11 vertebral levels, and the S1 through S5 segments lie between T12 to L1. The C1 through C7 nerve roots emerge above their respective vertebrae; the C8 nerve root emerges between the C7 and T1 vertebral bodies.

Front 27

describe the innervation of the lower extremety.

Back 27

L2 and L3 mediate hip flexion. L3 and L4 mediate knee extension. L4 and L5 mediate ankle dorsiflexion and hip extension. L5 and S1 mediate knee flexion. S1 and S2 mediate ankle plantar flexion

Front 28

what is the filum terminale?

Back 28

a thin connective tissue filament of the cauda equina that descends from the conus medullaris (terminal end of the spinal cord) with the spinal nerve roots, is connected to the third, fourth, and fifth sacral vertebrae; its terminal part is fused to the periosteum at the base of the coccygeal bone.

Front 29

what is the conus medullaris?

Back 29

the terminal end of the spinal cord. It occurs near lumbar vertebral levels 1 (L1) and 2 (L2)

Front 30

what are three major categories of sensory input that are important to the clinical examination of spinal cord pathology?

Back 30

1) Afferents from muscle spindles 2) Axons mediating sensory modalities of pain and temperature 3) Axons mediating the sensory modalities of proprioception, vibration, and touch discrimination.

Front 31

discuss the clinical importance in the assessment of spinal cord disease of the dorsal columns, the fasciculus gracilis, and the fasciculus cuneatus

Back 31

These contain sensory information regarding joint position and vibration. They are organized anatomically such that cervical sections lie most laterally and sacral segments most medially (figure 7). These pathways will cross in the medulla; hence, in the spinal cord, these tracts contain ipsilateral sensory representation.

Front 32

discuss the clinical importance in the assessment of spinal cord disease of the anterior and lateral spinothalamic tracts

Back 32

contain sensory information regarding pain, temperature, and touch. These axons have crossed in the ventral commissure and therefore contain contralateral sensory representation. This tract is somatotopically organized with cervical inputs located most medially and sacral inputs most laterally

Front 33

discuss the clinical importance in the assessment of spinal cord disease of the corticospinal tracts

Back 33

contain the upper motor neurons that originate in M1 of the primary motor cortex. These axons synapse either directly or indirectly on the anterior horn cells, and as such have distinct sites of anatomic origin within M1 [3]. A single corticomotoneuronal axon synapses with many anterior horn cells of its own motor neuron pool and also with those of agonists and antagonists, allowing for coordination of highly skilled movements.

Front 34

describe the anatomy of sympathetic neurons in the spinal cord

Back 34

lie in the lateral horn of the central gray matter at spinal levels T1-L3. The preganglionic fibers exit via the ventral root, spinal nerve, and ventral ramus to reach the paravertebral ganglion. Many will synapse at the paravertebral ganglion, others pass through it to terminate on postganglionic neurons

Front 35

what are the consequences of spinal cord Lesions above the L2 level?

Back 35

impotence and spastic paralysis of bladder. There is loss of voluntary control of the bladder, which will empty automatically by reflex action.

Front 36

what Dorsal column symptoms?

Back 36

gait ataxia and paresthesias. Corticospinal tract dysfunction produces weakness that, if acute, is accompanied by muscle flaccidity and hyporeflexia and, if chronic, by muscle hypertonia and hyperreflexia. Extensor plantar responses and urinary incontinence may be present.

Front 37

describe Brown-Sequard syndrome

Back 37

A lateral hemisection syndrome involving the dorsal column, corticospinal tract, and spinothalamic tract unilaterally (figure 11). This produces weakness, loss of vibration, and proprioception ipsilateral to the lesion and loss of pain and temperature on the opposite side. The unilateral involvement of descending autonomic fibers does not produce bladder symptoms.

Front 38

describe conus medullaris syndrome

Back 38

Lesions at vertebral level L2 often affect the conus medullaris. There is early and prominent sphincter dysfunction with flaccid paralysis of the bladder and rectum, impotence, and saddle (S3-S5) anesthesia.

Front 39

describe the pathogenesis of multiple sclerosis

Back 39

T cells [CD4+ TH1] react against self myelin antigens and secrete cytokines. Cytokines [IFN-γ] activate macrophages. Activated macrophages and their products caused demyelination

Front 40

describe the gross appearance of the lesions of MS

Back 40

multiple, patchy, depressed, glassy, gray-tan, plaques of demyelination of white matter, firmer consistency (sclerosis)

Front 41

what are the locations for MS lesions?

Back 41

1) beside the lateral ventricles, they follow the course of paraventricular veins. 2) optic nerves and chiasm 3) brain stem / cerebellum / spinal cord [ascending and descending white fiber tracts]. 4) may extend into the gray matter structures [myelinated fibers running through them]

Front 42

what are the 4 types of demyelinating plaques in MS?

Back 42

active, quiescent, inactive and shadow

Front 43

describe the active demyelinating plaque of MS

Back 43

this is a plaque of ongoing myelin breakdown characterized by macrophages with lipid-rich debris, perivascular cuffs made of inflammatory cells [lymphocytes & monocytes], and preservation of axons & depletion of oligodendrocytes through apoptosis

Front 44

describe the quiescent plaque of MS

Back 44

diminution of the inflammatory cell infiltrate & macrophages; Astrocytes undergo reactive changes in time

Front 45

describe the inactive plaque of MS

Back 45

axons are greatly diminished in number & show severe depletion of myelin. oligodendrocytes show reduction of nuclei number. presence of astrocytic proliferation and gliosis

Front 46

describe the shadow plaque of MS

Back 46

the border between normal and affected white matter is not sharply circumscribed - abnormally thinned-out myelin sheaths = incomplete myelin loss or remyelination

Front 47

describe the 4 patterns of active plaques of MS

Back 47

Pattern I: sharply demarcated & centered on blood vessels. Pattern II: deposition of immunoglobulin and complement. Pattern III: less well demarcated & not centered on vessels; widespread distribution of oligodendrocyte apoptosis. Pattern IV: less well demarcated & not centered on vessels; only central distribution of oligodendrocyte apoptosis. NOTE* Autopsy studies have shown that only one pair of patterns (I/II or III/IV) is present in a given individual, suggesting that these may reflect distinct mechanisms rather than different stages of lesion.

Front 48

what is the significance of optic neuritis and MS?

Back 48

optic neuritis is the most common presenting symptom of MS and up to 50% of patients presenting with optic neuritis go on to develop MS

Front 49

what are the symptoms associated with MS lesions of the spinal cord?

Back 49

motor and sensory impairment of trunk and limbs, spasticity, and difficulties with the voluntary control of bladder function.

Front 50

what are the signs and symptoms of MS involvement in the brainstem?

Back 50

cranial nerve signs, ataxia, nystagmus, and internuclear ophthalmoplegia from interruption of the fibers of the medial longitudinal fasciculus.

Front 51

what does the CSF show in MS?

Back 51

mildly elevated protein level, moderate pleocytosis. Gamma globulin is increased, oligoclonal bands on electrophoresis

Front 52

what are the 2 variants of MS?

Back 52

neuromyelitis optica (Devic disease), acute MS (marburg form)

Front 53

what is neuromyelitis optica?

Back 53

aka devic disease, is a demyelinating disease similar to MS, with presenting symptoms of bilateral optic neuritis and prominent spinal cord involvement; especially in Asians; Progressive or relapsing/remitting course, or manifest as a single episode without subsequent relapses

Front 54

describe Acute disseminated encephalomyelitis (ADEM)

Back 54

demyelinating disease following a viral infection or a viral immunization; after a week or two after infection - headache, lethargy, and coma; rapid progression; Fatal outcome in 20% of cases; in the remaining patients - complete recovery

Front 55

describe Acute necrotizing hemorrhagic encephalomyelitis (ANHE, acute hemorrhagic leukoencephalitis of Weston Hurst).

Back 55

Fulminant syndrome of CNS demyelination; Preceded by a recent episode of upper respiratory infection - Mycoplasma pneumoniae, or indeterminate cause. Fatal in many patients.

Front 56

describe Central pontine myelinolysis.

Back 56

Loss of myelin in basis pontis & pontine tegmentum; sparing periventricular & subpial regions; Extrapontine lesions - supratentorial compartment. results from rapid correction of hyponatremia; extreme serum hyperosmolarity or other metabolic imbalance.

Front 57

describe the symptomatology of central pontine myelinolysis

Back 57

rapidly evolving quadriplegia in alcoholism, severe electrolyte or osmolar imbalance, or orthotopic liver transplantation

Front 58

what is autonomic dysreflexia?

Back 58

a complication of Spinal cord injuries (SCI) above T6 resulting in the loss of coordinated autonomic responses to demands on heart rate and vascular tone. Uninhibited or exaggerated sympathetic responses to noxious stimuli lead to diffuse vasoconstriction and hypertension

Front 59

what are the renal problems that come from spinal cord injury?

Back 59

SCI produces bladder dysfunction, often referred to as the neurogenic bladder. Othercomplications can result from this, including infections, vesicoureteral reflux, renal failure, and nephrocalculi. Clean intermittent catheterization, supplemented by medications as needed is the usual initial treatment. Some patients require a chronic indwelling catheter. Botulinum toxin and sacral nerve modulators are being investigated alternative treatment options

Front 60

what is cervical spondylotic myelopathy?

Back 60

Degenerative changes in the vertebral bodies, discs, and connecting ligaments encroach on the cervical canal, producing a progressive myelopathy

Front 61

what is syringomyelia?

Back 61

a fluid-filled, gliosis-lined cavity within the spinal cord. Most lesions are between C2 and T9; however, they can descend further down or extend upward into the brainstem (syringobulbia)

Front 62

what is cross tapering?

Back 62

the best technique to assure that the patient's depression is not unmasked from rapid drug withdrawal, while minimizing the risk of drug-drug interactions.

Front 63

discuss the practice of switching from SSRIs to TCAs in the treatment of depression.

Back 63

the most common method used to switch from an SSRI to a tricyclic antidepressant (TCA) is a cross-taper. It is important to remember that fluoxetine and paroxetine are strong inhibitors of the p450 enzyme 2D6. This enzyme is involved in the metabolism of many TCAs and inhibition will cause an increased TCA blood level (in some cases, several-fold higher), which can result in toxicity. Because of this, TCAs should be started at low doses when cross-tapering with an SSRI, particularly with fluoxetine and paroxetine; TCA blood levels can be checked during this period for added safety.

Front 64

discuss the logistics of switch from an SSRI to venlaxafine or duloxetine

Back 64

Since venlafaxine and duloxetine both have strong serotonergic properties, switching immediately from most SSRIs to the equivalent dose of venlafaxine or duloxetine is typically well-tolerated. If starting from a high dose of an SSRI, a cross-taper may be preferable. However, caution is needed in switching from fluoxetine orparoxetine, because venlafaxine and duloxetine are metabolized by p450 2D6 and it is prudent to start them at low doses. Since fluoxetine has a very long half-life, 2D6 inhibition may be present up to five weeks after discontinuation.

Front 65

discuss the logistics of switching from buproprion to or from antedepressants other than MAOIs

Back 65

Bupropion does not have significant serotonergic properties, so would not be expected to mitigate discontinuation symptoms that result from discontinuing medications that are strongly serotonergic. Therefore, when switching from an SSRI, a TCA, venlafaxine, duloxetine, or mirtazapine to bupropion, we recommend cross-tapering off the former medication over a one to two week period (two to three weeks for venlafaxine and duloxetine). Bupropion itself is not frequently associated with discontinuation symptoms. Bupropion can usually be tapered off over the course of one week while initiating a new antidepressant medication at its typical dosing schedule. Bupropion is an inhibitor of the liver enzyme p450 2D6, so may increase the blood levels of medications that rely on this enzyme for their metabolism.

Front 66

discuss the logistics of switching to or from MAOIs

Back 66

Since the combination of MAOIs and other antidepressants can result in severe toxicity (eg, hypertensive crisis, serotonin syndrome), it is recommended that two weeks elapse between discontinuing an MAOI and starting a different antidepressant. Two weeks should also elapse between discontinuing a TCA, SSRI (other than fluoxetine), venlafaxine,duloxetine, or mirtazapine and starting an MAOI. Because of fluoxetine's long half-life, five weeks should elapse between discontinuing fluoxetine and starting an MAOI. When switching between MAOIs we recommend that two weeks elapse between discontinuing the first MAOI and starting the second.

Front 67

discuss the role of serotonin in depression

Back 67

Serotonin (5-HT) is an indoleamine neurotransmitter released in the brain from neurons originating in the brainstem raphe nuclei. Abnormalities in brain serotonergic activity have been implicated in many emotional and behavioral disorders, including mood disorders, obsessive-compulsive disorder, and aggressive behaviors [4]. Although serotonergic neurotransmission in the brain is complex, involving multiple types of pre- and postsynaptic serotonin receptors, it is clear that medications causing increased serotonergic activity are often effective in ameliorating, among others, symptoms of depression, anxiety, and obsessive ruminations.

Front 68

discuss the mechanism of SSRIs in treatment of depression

Back 68

all share the property of blocking the action of the presynaptic serotonin reuptake pump, thereby increasing the amount of serotonin available in the synapse and increasing postsynaptic serotonin receptor occupancy. While this action occurs rather quickly after SSRI therapy is started, the antidepressant effects of SSRIs may not appear for three to six weeks after initiation of treatment. It is proposed that this delay in clinical response is due to a gradual "down regulation" or decrease in some postsynaptic serotonin receptor types in response to the increased amount of synaptic serotonin available

Front 69

discuss the 5 important characteristics of SSRIs in the treatment of depression

Back 69

1) They are all hepatically metabolized 2) They have relatively little affinity for histaminic, dopaminergic, alpha-adrenergic, and cholinergic receptors. 3) They tend to have relatively mild side-effect profiles, although they can be associated with sexual dysfunction 4) They are relatively safe in overdose 5) They all produce changes in sleep architecture (increased REM latency and decreased total REM sleep)

Front 70

what is fluoxetine?

Back 70

the first SSRI to be released in the United States, heralding a new era of antidepressant psychopharmacology. Fluoxetine is indicated for the treatment of major depressive disorder, obsessive-compulsive disorder, and bulimia.

Front 71

what are the adverse effects of SSRIs?

Back 71

suicide risk, sexual dysfunction/infertility, weight change, bleeding

Front 72

name 3 SSRI drugs

Back 72

fluoxetine, sertraline, paroxetine

Front 73

name 3 serotonin-norepinephrine reuptake inhibitors

Back 73

Venlafaxine, Desvenlafaxine, Duloxetine

Front 74

what is venlaxafine?

Back 74

it is a serotonin-norepinephrine reuptake inhibitor. It is a potent inhibitor of serotonin reuptake and, at higher doses, an inhibitor of norepinephrine reuptake. It is also a mild inhibitor of dopamine reuptake.

Front 75

what drugs are used to treat bipolar disorder?

Back 75

lithium, anticonvulsants (valproate, carbamazepine), antipsychotics (haloperidol, aripiprazole), benzos (clonazepam, loazepam)

Front 76

what is allosteric modulation?

Back 76

the regulation of an enzyme or otherprotein by binding an effector molecule at the protein's allosteric site (that is, a site other than the protein's active site). Effectors that enhance the protein's activity are referred to as allosteric activators, whereas those that decrease the protein's activity are called allosteric inhibitors

Front 77

what is the treatment of acute manic episode?

Back 77

Lithium, Anticonvulsants, Antipsychotics, Benzodiazepines

Front 78

what is bipolar disorder?

Back 78

There are two types of bipolar disorder [1]. Bipolar I disorder is diagnosed in patients with a history of at least one episode of mania. Nearly all patients with bipolar I disorder also have episodes of major depression, but these are not required to make the diagnosis. Bipolar II disorder is diagnosed in patients who have had at least one hypomanic episode plus at least one episode of major depression.

Front 79

describe maintanence treatment of bipolar disorder

Back 79

usually consist of the same regimen that successfully treated the acute mood episode. Those who continued divalproex during maintenance therapy were euthymic significantly longer than those who switched to lithium or placebo [16]. Given other studies that suggest lithium is superior to divalproex or valproate, this suggests that maintaining the same regimen rather than switching reduces recurrence of mood episodes. Many patients are unresponsive or intolerant of lithium. For these patients, we suggest lamotrigine,olanzapine, or quetiapine

Front 80

how do stimulants work?

Back 80

affect the dopaminergic and noradrenergic systems, causing the release of catecholamines from storage sites at the central nervous system (CNS) synapses. increased norepinephrine and dopamine concentrations in the brainstem, midbrain, and frontal cortex are thought to be responsible for the increased attention span and concentration that occur in children with ADHD who are treated with stimulants

Front 81

what drugs are used in the treatment of ADHD?

Back 81

Stimulant drugs are considered the first-line treatment for ADHD in children based on a long record of safety and efficacy [9-14]. Stimulant drugs include methylphenidate (eg, Ritalin, Methylin, Concerta, Focalin, Metadate), dextroamphetamine (Dexedrine), and mixed amphetamine salts (eg, Adderall).

Front 82

identify conditions treated with stimulants

Back 82

Stimulant medications improve behavior in children with ADHD, children with conditions other than ADHD (eg, learning disabilities, depression), and normal control children

Front 83

what are common side effects of stimulant drugs?

Back 83

Anorexia or appetite disturbance (80 percent), Sleep disturbances (3 to 85 percent), Weight loss (10 to 15 percent)

Front 84

what are the IQ requirements for mental retardation?

Back 84

The lower limit of normal is considered to be two standard deviations below the mean or an IQ of 70. Gradations of severity include IQs in the following ranges: Mild — from between 50 and 55 to approximately 70, Moderate — from between 35 and 40 to between 50 and 55, Severe — from between 20 and 25 to between 35 and 40, Profound — from <20 to 25

Front 85

what are adaptive skills and how are they used to diagnose mental retardation?

Back 85

the skills of daily living that are needed to live, work, and play in the community. They include communication, social and interpersonal skills, self-care, home living, use of community resources, self-direction, functional academic skills (reading, writing, and basic mathematics), work, leisure, and health and safety. Adaptive functioning is considered to be impaired when there is a deficit in at least two of these areas compared to children of the same age and culture.

Front 86

what are the different methods of diagnosing learning disabilities?

Back 86

Standardized psychometric measures (quantitative information), Review of the student's educational history (eg, report cards/grades over time, grade retention), Description of classroom observations (eg, participation behaviors, success in the completion of classroom and home assignments, etc.)

Front 87

what are psychometric tests?

Back 87

tests used to diagnose learning disabilities. Psychometric tests provide standardized procedures for measuring knowledge and abilities in various areas (eg, reading, writing, math, executive functions, language skills, etc.).

Front 88

what are the diagnostic criteria for ADHD?

Back 88

presence of either/or 1) Six (or more) of symptoms of inattention (ie difficulty sustaining attention in tasks or play activities) that have persisted for at least six months to a degree that is maladaptive and inconsistent with developmental level 2) Six (or more) symptoms of hyperactivity-impulsivity (ie Often has difficulty awaiting turn) that have persisted for at least six months to a degree that is maladaptive and inconsistent with developmental level

Front 89

differentiate between diagnosis of autism and aspergers

Back 89

a diagnosis of autistic disorder requires delays or abnormal functioning in at least one of the following areas, with onset before three years of age: Social interaction, Language as used in social communication, Symbolic and imaginative play (ie, behavior). asperber’s includes 1) Qualitative impairment in social interaction (ie Lack of social or emotional reciprocity), 2) Restricted repetitive and stereotyped patterns of behavior, interests, and activities (ie Apparently inflexible adherence to specific, nonfunctional routines or rituals), 3) clinically significant impairment in social, occupational, or other important areas of functioning, and 4) Criteria are not met for another specific pervasive developmental disorder or schizophrenia

Front 90

what is conduct disorder?

Back 90

a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate societal norms or rules are violated. includes Aggression to people and animals, Destruction of property, Deceitfulness or theft, Serious violations of rules

Front 91

what are the diagnostic criteria for Tourette’s syndrome?

Back 91

1) Both multiple motor tics and one or more phonic tics must be present at some time during the illness, although not necessarily concurrently 2) Tics must occur many times a day, nearly every day, or intermittently throughout a period of more than one year 3) Anatomical location, number, frequency, type, complexity, or severity of tics must change over time 4) Onset of tics before the age of 18 years 5) Involuntary movements and noises must not be explained by another medical condition 6) Motor tics, phonic tics, or both must be witnessed by a reliable examiner at some point during the illness or be recorded by videotape or cinematography

Front 92

what is the treatment for selective mutism?

Back 92

the SSRI fluoxetine

Front 93

what classes of drugs are used to treat social anxiety disorder?

Back 93

selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs), beta-blockers, and benzodiazepines.