Male Nude Photography- Classic Fetal 2008

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People with psychogenic movement disorders often have experienced a major life event eg, failure to attain an expected promotion, death of a loved one. Malingering disorders may occur when an individual seeks disability and other compensation. Specifically, malingering occurs when the patient seeks a tangible reward for being sick. A person who malingers may seek to be excused from work or school because of the feigned illness.

A malingerer may seek compensation in the form of disability payments for the alleged illness. Factitious disorder occurs when an individual feigns illness in order to assume the sick role. People with factitious disorders appear to seek the attention accorded to a patient.

Like conversion disorders, factitious disorders are not well understood.

An extremely severe form of factitious disorder is manifested as Munchausen syndrome. Munchausen syndrome is characterized by the apparently deliberate feigning of symptoms and signs. People with Munchausen syndrome may fabricate elaborate and bizarre stories. They may agree to multiple operations in an attempt to diagnose and treat the fabricated illnesses. Munchausen syndrome by proxy occurs when a parent seeks treatment for a child, typically an infant who cannot speak. The parent fabricates a history of false symptoms for the healthy child, which leads to unnecessary diagnostic and therapeutic interventions.

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Munchausen syndrome by proxy is a form of child abuse. Suspected cases of Munchausen syndrome by proxy merit report to child protective services. Although people with psychogenic movement disorders may seek and demand medication and surgery, they are likely to experience severe adverse effects.

Therefore, pharmacologic and surgical interventions should be avoided in patients with psychogenic movement disorders. These disorders must be differentiated from voluntary expressions of emotion characteristic of cultural and ethnic groups, such as zaghrouta.

A genetic basis for TD has not been identified. The prevalence of TD is higher in cigarette smokers. The various subtypes of TD vary markedly in frequency. Orofacial TDs differ from peripheral TDs with regard to the occurrence of comorbid acute movement disorders. Acute tremor, acute akathisia, and acute Parkinsonism are more common in people with peripheral TD. Distinguishing acute and TDs in an individual patient can represent a serious diagnostic challenge. TD occurs in all ages. Connor et al found that 5. Elderly female patients appear to be particularly susceptible to the development of TD.

TD occurs in persons of every race. Africans and African Americans appear to be especially vulnerable to TD after exposure to low doses of neuroleptics for short durations. However, it is difficult to draw any firm conclusions from these findings, because the investigators conducted their studies in different settings.

A number of other variables, such as therapeutic approaches, methodologic inconsistencies, diet, weather, and varied assessments, may also contribute to the differences reported in various racial groups. Fully inform the patient or the legal surrogate if the patient is incompetent of the possible courses of action. Discuss with the patient the advantages and disadvantages of dopamine antagonist treatment. A written treatment plan that documents agreement with the treatment course between the clinician and patient is helpful. Regularly review and revise the treatment plan as needed.

If a patient exhibits a movement disorder when taking a drug, then gradual discontinuance of the causative drug generally is a wise course if the patient can tolerate a reduction in dose.

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Advise the patient to obtain a medical alert bracelet to warn against the administration of dopamine-receptor blocking drugs. Patients often have movement disorders that may actually represent a mixture or overlap of several dyskinesia disorders. Individuals treated with neuroleptics may demonstrate both acute and chronic effects, manifested by acute dyskinesias and tardive dyskinesia TD. Akathisia and tics may be manifested simultaneously after long-term treatment with neuroleptics. When a patient is seen for the first time, diagnosis of acute and chronic dyskinesias may be difficult without a careful history.

Therefore, a full neurologic and pharmacologic history may provide the basis for distinguishing idiopathic Tourette disorder from acute medication-induced tardive tics. Patients and families often cannot provide accurate histories; thus, firm diagnoses may be impossible. Because acute and tardive medication effects may occur simultaneously, the distinction may be challenging in a clinical setting. Observing patients carefully on a regular basis and precisely documenting through the use of structured rating instruments the phenomenology and topography of movements and the pharmacologic treatments at each visit will help provide a basis for accurate future diagnosis of acute dyskinesia and TD.


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Although TD has been observed after exposure to various substances eg, levodopa, amphetamine, and metoclopramide , the prototypical TD is the orofacial ie, buccolingual, masticatory hyperkinesia induced by neuroleptics antipsychotic dopamine D 2 -receptor blockers. People with other movement disorders and those with diabetes mellitus are at increased risk of TD. Neuroleptic-induced TD is characterized by choreiform, athetoid, and rhythmic movements of the tongue, jaw, trunk, and extremities that have persisted for at least 4 weeks and that began during treatment with neuroleptics or within 4 weeks of discontinuing neuroleptics.

Diagnosis of neuroleptic-induced TD generally requires exposure to neuroleptics for at least 3 months. At least 1 month of exposure is typically required if the patient is aged 60 years or older. Oral and genital pain can be prominent manifestations of TD. Neuroleptic-induced TD is excluded if symptoms and signs result from another neurologic or medical disorder, ill-fitted dentures, or other medications. For example, hyperthyroidism may manifest with choreiform movements of the limbs.

Furthermore, neuroleptic-induced TD cannot be diagnosed if symptoms and signs result from an acute neuroleptic-induced movement disorder. Antiparkinsonism agents usually do not improve neuroleptic-induced dyskinesias.

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Decreasing the dose of the neuroleptic may increase the movements temporarily. In some patients, increasing the dose of the neuroleptic diminishes movements, thereby masking the TD. Although the neuroleptic dose may temporarily diminish the disorder, regular increments are needed to achieve apparent beneficial effects. Over the long term, maintaining and increasing doses of neuroleptics to mask TD may be ineffective.

However, situations may exist in which masking of TD by continuing and escalating neuroleptic doses may be justified. Benefits and risks must be weighed. Neuroleptic-induced TDs are absent during sleep. On initial examination, obtain a history of neurologic disorders that may involve the basal ganglia eg, cerebrovascular disease, encephalitis, head trauma, and neoplasms. Obtain a family history for hereditary dyskinesias associated with Huntington disease, Wilson disease, and torsion dystonia.

Inquire about medications, including amphetamines, levodopa, and substances that may result in dyskinesias see Etiology. Specifically note whether antiemetic medications especially metoclopramide, prochlorperazine, and related compounds are being administered. Unlike TD, Sydenham chorea is a disorder associated with a history of group A streptococcal infection and rheumatic fever in children. It typically affects children and adolescents 6 months or more after an infection with group A streptococci.

Prompt administration of antibiotic therapy for infections with group A streptococci dramatically reduces the incidence of Sydenham chorea. The female-to-male ratio is approximately Sydenham chorea is characterized by the rapid onset of chorea, muscular weakness, hypotonia, dysarthria, obsessions, compulsions, and other behavioral and emotional disturbances. After an abrupt or insidious onset, Sydenham chorea worsens over weeks and then resolves over 3—6 months.

Chorea may persist after the episode has ended. One fifth of patients with Sydenham chorea experience a recurrence, typically within 2 years of the initial episode. Pantothenate kinase-associated neurodegeneration PKAN Hallervorden-Spatz disease occurs in patients aged 10—15 years, a different age group than that of persons with TD. PKAN is an extremely rare, progressive neurogenetic disorder with autosomal recessive inheritance associated with dementia and death approximately 20 y after onset.

It is characterized by rigidity, dystonia, choreoathetosis, spasticity, foot deformity, and intellectual deterioration. It is associated with excessive iron deposition in the basal ganglia that can be observed on MRI. Differentiate neuroleptic-induced TD from spontaneous dyskinesias and mannerisms of psychosis and other mental disorders. Administer the AIMS at baseline before the institution of pharmacotherapy to document any movements present, then at least every 3 months thereafter during the course of treatment.

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Part of the AIMS assessment includes observation of the patient when he or she is distracted by other activities. Patients may suppress movements while concentrating intensely. Therefore, administration of the AIMS can be supplemented by requesting that the patient perform additional tasks during the assessment. Movements may then be demonstrated when the patient is concentrating on the additional tasks. For example, during the administration of item 5 of the AIMS assessment, have the patient sit in a chair with hands on knees, legs slightly apart, and feet flat on the floor.

Examine the entire body for movements while the patient is in this position, then ask the patient to count backwards from In addition, during item 5 of the AIMS, ask the patient to sit with hands hanging unsupported between the legs if male, or hanging over the knees if female and wearing a dress.

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Observe the hands and other body areas, then request that the patient describe in detail the path traveled that day. Ask the patient where the trip started, what streets were traveled, where turns were made, where the trip terminated, and what floor and room were entered. These procedures stimulate the patient and may provoke the appearance of movement disorders. The AIMS may be modified to allow repeated brief assessments during the course of a single patient examination to check for possible effects of interventions.

In other words, by administering the modified AIMS regularly after the administration of a treatment, the time course of abnormal movements may be regularly recorded and plotted. To assess the appropriateness of treatment with antipsychotic medication, [ 33 , 34 , 41 ] the Psychoactive Medication Quality Assurance Rating Survey PQRS see the first image below can be used at initial assessment and then repeated annually, [ 42 ] and the PQRS Screening Criteria see the second image below can be repeated monthly [ 43 ].

Specific TDs resulting from long-term use of dopamine antagonists eg, orofacial dyskinesia, tardive akathisia, tardive blepharospasm, tardive dystonia, tardive myoclonus, and tardive tics may occur concurrently. Tardive akathisia is manifested by repetitive tapping, squirming, and marching movements.

It occurs as the dose of the dopamine antagonist is decreased after long-term treatment.