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Mental Retardation Updated 3/2011

Adam Barta, MD, Jennifer L. Ayres, PhD
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BASICS

  • Description
  • Epidemiology
  • Risk Factors
  • General Prevention
  • Etiology
  • Associated Conditions

DIAGNOSIS

  • Signs and Symptoms
  • Tests
  • Differential Diagnosis

TREATMENT

  • Medication (Drugs)

Ongoing Care

  • Follow-Up Recommendations
  • Diet
  • Patient Education
  • Prognosis
The following is an excerpt....
BASICS
  • Mental retardation (MR) is a global deficit in cognitive functioning, as evidenced by a significant difference between one's mental and chronological ages (AKA "intelligence quotient" or "IQ") and significantly impaired adaptive functioning (1).
  • Although these cognitive issues typically have a pervasive impact, patients with MR will display highly variable levels of functioning and subsequent service needs.
  • Patients must be evaluated individually. Treatment plans must be tailored to specific needs.
  • The current DSM-IV-TR diagnosis is "Mental Retardation." However, since that term is deemed to be somewhat pejorative, the new DSM-V diagnosis will be "Intellectual Disability."
Description
  • MR is defined as an IQ <70 and a significant impairment in an area of adaptive functioning such as communication ...

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FIGURE 30.26. Fluorescence in situ hybridization in A employed a chromosome 5 painting probe on a cell from a patient with severe mental retardation and self-abusive behavior. On G-banded analysis, an abnormal dark staining band was seen in the p arm of chromosome 1. Using a 24-chromosome painting probe device (Cytocell, Ltd., Oxfordshire, UK), the abnormal segment was identified to be derived from chromosome 5 and confirmed using another chromosome 5 painting probe (Vysis, Inc, Downer's Grove, IL.). A hybridization signal is seen on both normal 5 homologs as well as an inserted segment in the p arm of chromosome 1. His karyotype is 46,XY,ins(1;5). In B, a locus-specific probe cocktail (Vysis, Inc., Downer's Grove, IL) used in the identification of patients with Williams syndrome was applied to a cells from a patient with clinical features of the syndrome. The orange-pink signal identifies the hybridization of a probe containing DNA sequences (including the elastin gene) known to be deleted in Williams syndrome (7q11.23). The green hybridization signal identifies control probes for 7q31. The absence of a signal with the critical region probe on one chromosome 7 identifies a deletion of the elastin gene. Credit: McClatchey KD M.D., D.D.S. Clinical Laboratory Medicine, 2nd Edition. Philadelphia: Lippincott Williams & Wilkins, 2002.
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