When Can an Athlete Return to Play After a Concussion?

Patient Presentation
A 15-year-old female comes to clinic with a 2 day history of mild generalized headache. The headache began immediately after she fell while ice skating in the late afternoon. She also had blurry vision and confusion about what had occurred in the early evening, but they resolved. The following day she had mild headache which got better with ibuprofen. She went to basketball practice and the headache returned but did not increase in intensity or change character. Today she continues to have the generalized headache and feels that she has to “think to do things.” The headache is generalized over her entire head.
Her social history shows her to be an active athlete.
The review of systems reveals no fever, nausea/emesis, visual or auditory changes, ataxia or movement problems, dizziness/vertigo, numbness/tingling, difficulty speaking/chewing/swallowing, neck pain or sleep problems.
The pertinent physical exam shows her to be a well developed female with non-specific bruising on her shins and left iliac crest. Her head had a small elevated contusion on the left temporal/parietal area. Her pupils and extraocular movements are normal. Her mental status and neurological examination are also completely normal including short and long term memory.
Because of her history of trauma, continued headache, and new subjective mental status changes, a radiologic evaluation by head CT scan was completed and showed no brain edema, bleeding or mass.
The diagnosis of a Grade 2 Concussion is made and the patient is told to use Ibuprofen more consistently for her headache. She is to refrain from any sports activities or exertion for 1 week. She will have telephone follow-up in 3 days and an office appointment will be made at that time. She is to return sooner if her symptoms worsen.

Discussion
Head injuries in children are very common and thankfully, often are mild. Intracranial pathology is worrisome and includes concussion, contusion, hemorrhage and diffuse axonal injury. Common worrisome symptoms include loss of consciousness, amnesia, persistent emesis, seizures, drowsiness or personality changes.

Concussion is defined as a change in mental status that is caused by trauma and which may or may not involve loss of consciousness. Amnesia and confusion are hallmarks. The confusion and amnesia may occur immediately after the injury or several minutes later.

Early symptoms of concussion (minutes to hours) including headache, dizziness, vertigo, nausea or emesis and lack of situational awareness. Late symptoms (days to weeks) include light headedness, persistent low grade headache, visual or auditory intolerance or changes, easy fatigability, memory problems, poor attention and concentration, irritability and low frustration tolerance, anxiety or depressed mood and sleep problems.

Concussions are graded by confusion, loss of consciousness and time. The American Academy of Neurology recommends management options based on this grading system.

  • Grade 1 – Most common
    • Confusion: Transient

    • Loss of consciousness: None
    • Timing: less than 15 minutes for complete resolution of concussion symptoms or mental status abnormalities on examination
    • Miscellaneous: This is hard to recognize as the momentary confusion is very qualitative and subjective. Athletes sometimes call this “getting their bell rung” or being “dinged.”
    • Treatment:

      • Remove from contest

      • Examine immediately and at 5 minute intervals for the development of mental status abnormalities or postconcussive symptoms at rest and with exertion
      • Return to competition if mental status abnormalities or post-concussive symptoms clear within 15 minutes
      • A second Grade 1 concussion in the same contest eliminates the player from competition that day
      • Return to competition if asymptomatic for one week at rest and with exercise
  • Grade 2
    • Confusion: Transient

    • Loss of consciousness: None
    • Timing: More than 15 minutes for complete resolution of concussion symptoms or mental status abnormalities on examination
    • Miscellaneous: Any symptoms lasting more than one hour should be observed medically.
    • Treatment:
      • Remove from contest and do not allow return that day

      • Frequently examine at the contest site for signs of evolving intracranial pathology
      • A trained person should reexamine the athlete the next day
      • A physician should perform a neurologic examination to clear the athlete for return to play after 1 full asymptomatic week at rest and with exertion
      • If headache or other associated symptoms worsen or persist longer than one week, a CT or MRI scanning is recommended in all instances
      • Following a second Grade 2 concussion, return to play should be deferred until the athlete has had at least two weeks symptom-free at rest and with exertion
      • Any abnormality on CT or MRI scan consistent with brain swelling, contusion, or other intracranial pathology terminates the season for that athlete
  • Grade 3
    • Confusion: Any

    • Loss of consciousness: Any loss of consciousness either brief (seconds) or prolonged (minutes)
    • Timing: Any
    • Miscellaneous: This is usually easily recognized as the athlete is unconscious for any time period.
    • Treatment:
      • If still unconscious or worrisome signs are observed, transport the athlete to the nearest emergency department by ambulance with cervical spine immobilization, if appropriate

      • An emergent, complete neurologic evaluation should be performed and neuroimaging procedures also performed when indicated
      • Hospital admission is indicated if any signs of pathology are detected, or if the mental status of the athlete remains abnormal
      • If findings are normal at the time of the initial medical evaluation, the athlete may be sent home with explicit written instructions to help the family or responsible party observe the athlete
      • Neurologic status should be assessed daily until all symptoms have stabilized or resolved
      • Prolonged unconsciousness, persistent mental status alterations, worsening postconcussive symptoms, or abnormalities on neurologic examination require urgent neurosurgical evaluation or transfer to a trauma center
      • After a brief (seconds) Grade 3 concussion, the athlete should not play until asymptomatic for 1 week at rest and with exertion
      • After a prolonged (minutes) Grade 3 concussion, the athlete should not play until asymptomatic for 2 weeks at rest and with exertion
      • Following a second Grade 3 concussion, the athlete should not play for a minimum of 1 asymptomatic month. The evaluating physician may elect to extend that period beyond 1 month, depending on clinical evaluation and other circumstances
      • CT or MRI scanning is recommended for athletes whose headache or other associated symptoms worsen or persist longer than 1 week
      • Any abnormality on CT or MRI scan consistent with brain swelling, contusion, or other intracranial pathology, terminates the season for that athlete. Future return to play should be seriously discouraged in discussions with the athlete

Learning Point
The time courses for athletes to return to play following concussion, can be summarized as follows:

  
Grade of concussion             Time until return to play
	Grade 1                        15 minutes or less

	Multiple Grade 1               1 week

	Grade 2                        1 week

	Multiple Grade 2               2 weeks

	Grade 3 - brief loss of        1 week
	   consciousness (seconds)

	Grade 3 - prolonged loss of    2 weeks
	   consciousness (minutes)

	Multiple Grade 3               1 month or longer,
	                               based on clinical decision of
	                               evaluating physician

Questions for Further Discussion
1. What should be included in the side-line evaluation of an athlete for possible concussion?
2. When should a head CT or MRI be done for head trauma?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Head Injuries.

American Academy of Neurology Quality Standards Subcommittee. Management of Concussion in Sports. Neurology, 1997;48:581-585,
Available from the Internet at http://www.aan.com/professionals/practice/guideline/index.cfm (rev.Mar 1997 cited 1/6/05).

Woodhead JC. Pediatric Clerkship Guide. Mosby. St. Louis MO, 2003:464-468.

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
January 31, 2005

What are the Different Types of von Willebrand Disease?

Patient Presentation
An 8-year-old male comes to the hematology clinic for his specialty care for von Willebrand Disease.
The past medical history reveals that he was diagnosed with Type 1 von Willebrand Disease as a toddler after abnormal bruising and prolonged bleeding was noted by his family.
The family history has some family members who have heavy menstrual bleeding but no other problems.
The review of systems shows that he has had no significant joint or other bleeding since his last visit. He has desmopressin to be taken at home which has been used twice in the past 6 months after a bike fall and after falling off playground equipment.
The pertinent physical exam shows him to be growing well. He has minor bruising on his legs and arms. There are no problems with his joints.
He is to follow-up in another 6 months.

Discussion
Bleeding can be caused by problems of platelets, coagulation proteins or the blood vessels. Once the blood vessels are disrupted, platelets are exposed to connective tissue and collagen which causes the platelets to release granules that help other platelets to aggregate to the area. Tissue factors and platelet granules cause circulating prothrombin to converted to thrombin. Thrombin interacts with fibrinogen to form fibrin monomers. Factor VIII causes the fibrin monomers to polymerize. The fibrin polymers and aggregated platelets then form the primary plug that along with blood vessel contraction stops the bleeding.

vonWillebrand Disease was first described in 1926 by Erick Adolph vonWillebrand. (Hemophilia A is the common name for the deficiency in Factor VIII. Hemophilia B is a common name for the deficiency of IX). von Willebrand Factor (vWF) is a multimeric protein which is a carrier for Factor VIII and prevents Factor VIII degredation. vWF also stabilizes the bonds between platelets and endothelial cells. vWF is synthesized and stored in platelets and endothelial cells. VWF is a dimer which binds together to make up multimers of low, intermediate and high molecular weights. The low molecular weight multimers are the Factor VIII carriers. High molecular weight multimers have more sites for platelet binding and therefore are important for normal platelet function.

Many people with von Willebrand Disease are asymptomatic with <3% of the US population affected. The gene is found on chromosome 12p. Acquired forms of vWD can be found also. Menorrhagia is often the only symptom women may have. People are usually diagnosed because of menorrhagia, epistaxis, easy/increased bleeding or bruising, postoperative bleeding, or family history. Physical examination may be normal or have increased bruising or mucosal bleeding.

Screening tests include CBC, template bleeding time, prothrombin time (PT) and activated partical thromboplastin time (aPTT). Generally a normal CBC, normal to prolonged template bleeding time, and aPTT with a normal prothrombin time are seen. Specific tests such as vWF level, Factor VIII activity, Ristocetin activity (i.e. vWF activity), vWF antigen and subtype determination may also be needed or desired. Treatment may include Desmopressin (DDAVP), Factor VIII and Aminocaproic acid (Amicar).

Learning Point
It has 3 main types:

    Type 1 (70-80% of patients)

    • Problem: A quantitative defect with decreased amounts of vWF. The vWF is correctly formed.

    • Genetics: Autosomal dominant with variable penetrance
    • Clinical symptoms: Generally mild
    • Laboratory: May vary in same patient at different times. Generally decreased vWF activity, vWF antigen, and Factor VIII are seen.

    Type 2 (15-20%)

    • Problem: Qualitative defects of the vWF molecule which is present but is made or processed incorrectly

    • Genetics: Autosomal dominant or autosomal recessive
    • Clinical symptoms: Moderate

    Type 2A (most common Type 2 subtype)

    • Problem: There is an increased amount of vWF multimers. The total amount of vWF is decreased.

    • Genetics: Autsomal dominant
    • Laboratory: Normal to decreased Factor VIII and vWF and decreased ristocetin cofactor activity are seen. vWF subtype analysis reveals multimeric abnormalities and decreased amount of intermediate and high molecular weight multimer complexes.

    Type 2B

    • Problem: The vWF molecules are too big and bind platelets too much resulting in an intermittant thrombocytopenia

    • Genetics: Autosomal dominant
    • Laboratory: There are variable amounts of Factor VIII and vWF, and special ristocetin testing shows clumping of normal platelets. Platelet count can fall more during prengnacy, surgical procedures and with taking DDAVP.

    Type 2M

    • Problem: decreased vWF binding to platelets that is not due to a decrease of high molecular weight multimers

    • Laboratory: There is decreased vWF activity. There is also normal vWF antigen, Factor VIII, and subtype analysis

    Type 2 Normandy

    • Problem: vWF doesn’t bind to Factor VIII very well and therefore Factor VIII levels are low

    • Genetics: Autosomal recessive
    • Clinical Symptoms: should be considered when incomplete response to treatment is seen
    • Laboratory: Low Factor VIII levels are seen along with normal vWF antigen and ristocetin cofactor activity.

    Type 3 (rarest)

    • Problem: A quantative and qualitative defect with decreased amounts of vWF and Factor VIII, that also don’t attach to platelets and endothelial cells well.

    • Genetics: Autosomal recessive
    • Clinical symptoms: Most severe symptoms, lack of secondary transfusion response and response to DDAVP
    • Laboratory: Decreased vWF and Factor VIII are seen. vWF multimeric analysis shows variable results.

Questions for Further Discussion
1. What common reasons cause bleeding because of other coagulation pathway protein problems?
2. What is the most common cause of bleeding?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Hemophilia.

Geil, JD. Von Willebrand Disease. eMedicine.
Available from the Internet at http://www.emedicine.com/ped/topic2419.htm (rev. 8/19/2004, cited1/3/2005).

Rudolph CD, et.al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:1573.

Woodhead JC. Pediatric Clerkship Guide. Mosby. St. Louis MO, 2003:170-179.

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
January 24, 2005

What is the Approach to a Child with Thrombocytopenia?

Patient Presentation
A 4-year-old female comes to clinic because of a rash for 2 days. The rash began on her feet and appeared to go up her body. It is mainly on the trunk currently. Her parents describe small, red, flat dots that haven’t changed in appearance. There is no itching.
The past medical history and family history are negative.
Her review of systems reveals no new soaps, detergents, pets, travel, medications, fever, illnesses or sick contacts, blood in stools or urine, oral lesions, or easy bruising or bleeding.
The pertinent physical exam shows pinpoint, red, non-blanching petechiae over her entire body including the palms and soles, but they are concentrated on the trunk. There are some small bruises on the shins. There are no oral lesions. She has shoddy anterior cervical and inguinal nodes. She has no hepatospleenomegaly.
Her laboratory evaluation revealed a hemoglobin of 12.1 mg/dl, hematocrit of 37%, white blood cell count of 10,500/mm2 with normal differential, and a platelet count of 7,000/mm2. The blood smear was normal as was a coagulation profile and liver function tests.
The diagnosis of idiopathic (immune) thrombocytopenic purpura was made. The patient was admitted for treatment with intravenous immunoglobulin because her platelet count was <10,000/mm2, she had evidence of bleeding with the petechiae and she was a very active child. Her platelet count rose to 36,000/mm2 at discharge and at one week follow-up had increased to 266,000/mm2.

Discussion
Thrombocytopenia is usually defined as platelet counts <150,000/mm2. It can be found because of easy bruising, bleeding or can be an incidental finding on a complete blood count done for other reasons.
The differential diagnosis of thrombocytopenia includes:

  • Increased Platelet Destruction

    • Autoimmune hemolytic anemia – Evan’s syndrome
    • Congenital cyanotic heart disease
    • Disseminated intravascular coagulation
    • Drug – quinine, penicillin, digoxin, anti-epileptics, indomethacin, heparin
    • Idiopathic (immune) thrombocytopenic purpura
    • Neonatal illumine thrombocytopenia
    • Infection
    • Hemolytic-uremic syndrome
    • Hyperplenism
    • Kasabach-Merit syndrome
    • Thrombotic thrombocytopenia purpura
  • Decreased Platelet Production

    • Bone marrow infiltration – e.g. leukemia, storage diseases, myelofibrosis, etc.
    • Bone marrow injury – infection or drugs – usually transient
    • Congenital megakaryocytic thrombocytopenia
    • Congenital bone marrow aphasia – i.e. Fanconi’s anemia
    • Chromosome abnormalities – e.g. Trisomy 13, 18, 21, Turner Syndrome
    • Congenital platelet disorders – Weskit-Aldrich syndrome, May-Hegglin anomaly, Bernard-Soulier syndrome, Alport syndrome
    • Hereditary amegakaryocytopoiesis – usually associated with TAR syndrome (thrombocytopenia-absent radius syndrome)
  • Other

    • Pseudothrombocytopenia – caused by clumped platelets

Idiopathic (immune) thrombocyopenia purpura (ITP) usually occurs in children 2-10 years with a peak between ages 2-5 years. Children usually present with sudden onset of petechiae, ecchymosis, purpura, epistaxis, hematuria or gastrointestinal hemorrhage. They often are otherwise well and have a preceding minor viral illness. Physical examination usually shows only the presenting signs, but evidence of infection or malignancy must be carefully looked for.
Most children (~90%) resolve within 6 months usually without sequelae. If it lasts longer than 6 months it is called chronic ITP. Chronic ITP may resolve but this is less likely. Chronic ITP is more common in children <1 year and >10 years. Mortality from acute ITP fortunately occurs rarely and is usually due to central nervous system hemorrhage.

Laboratory testing usually shows isolated thrombocytopenia. The blood smear shows normal to increased platelet size and normal white and red cell morphology. Bone marrow examinations are often not done in typical cases but would have increased numbers of megakaryocytes.

Treatment may include careful observation, intravenous immunoglobulin, steroids and spleenectomy, and avoidance of precipitating medications. Children with atypical presentations, chronic thrombocytopenia, or children who will be treated with steroids, should have a bone marrow biopsy to rule out underlying malignancy or other causes of thrombocytopenia.

Learning Point
The approach to thrombocytopenia includes three major categories – history, physical examination and laboratory evaluation.

  • History should include questions about:

    • Type of bleeding
      • Deep bleeding such as joints or bone is usually due to a clotting factor deficiency such as hemophilia A or B
      • Epistaxis, oral, or excessive menstrual bleeding is usually due to a platelet disorder or fibrinogen abnormality
    • Drug history e.g. aspirin or non-steroidal anti-inflammatory medications
    • Recent infections or immunizations
    • Family history of bleeding

  • Physical examination should be carefully performed looking for:

    • Spleenomegaly with or without hepatomegaly
    • Lymphadenopathy
    • Skeletal abnormalities – these may be subtle and need radiographs to detect
    • Skin – e.g.hemangiomas, purpura

  • Laboratory evaluation generally includes:

    • Complete blood count with white blood cell differential and platelet count
    • Peripheral blood smear for morphology
    • Coagulation profile
    • May also include Coombs test, liver function tests, and bone marrow examination

Questions for Further Discussion
1. When should a hematologist/oncologist be consulted?
2. What are the advantages/disadvantages and indications for using immunoglobulin or steroid treatment?

Related Cases

To Learn More

To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Bruises.

Rudolph CD, et.al. Rudolph’s Pediatrics. 21st edit. McGraw-Hill, New York, NY. 2003:1555–1559.

Woodhead JC. Pediatric Clerkship Guide. Mosby. St. Louis MO, 2003:170-179.

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
Janaury 18, 2005

What Are the Facial Characteristics of Fetal Alcohol Syndrome?

Patient Presentation
A 15-year-old female comes to the developmental pediatric clinic for a second opinion about fetal alcohol syndrome, attention deficit disorder and school problems. Her academic difficulties began in the Head Start program and continue today with global academic problems. She also suffers from severe inattention in multiple settings.
Previously she received special education help in a separate classroom with similar children. This academic year, she receives extra help in a regular classroom. She was recently suspended for refusing to do any work at school and is more non-compliant at home also.
Her past medical history reveals that her mother drank alcohol before and during pregnancy, and is a recovering alcoholic currently. She has been treated with short-acting methylphenidate (RitalinTM) for her inattention with some symptom relief.
The family history is positive for alcoholism, attention deficit disorder and learning disabilities.
During the physical exam she is fidgety, impulsive and easily distracted. Her growth parameters are at the 25%. Her face has an thin upper lip, flat philtrum and is somewhat ‘fish-mouthed.” Her ears are flat with a enlarged helix. She has abnormal palmar creases and short fifth metacarpals. She is slightly hypotonic.
Her neurodevelopmental evaluation shows her with impulsivity and distractability. She had weaknesses in fine motor function, receptive and expressive language, temporal sequential organization and visual processing. Her strength is in gross motor skills.
Her educational evaluation reveals global learning problems including attention, language, visual spatial orientation and temporal sequential organization. She is behind 1-2 grade levels academically in all subjects.
Her psychologic screening shows no depression and she readily acknowledges her problems. She is frustrated by the lack of help at school.

The diagnosis of fetal alcohol syndrome, attention deficit disorder, and global learning disabilities was confirmed. Recommendations for improved medical management of attention deficit disorder, academic intervention and psychosocial supports were given and were being put into place at follow-up.

Discussion
Fetal alcohol syndrome (FAS) is a group of behavioral, neurological and physical birth defects associated with maternal alcohol abuse during pregnancy. In general, the amount of alcohol and the timing during gestation are associated with the severity of the syndrome.

Neurological abnormalities vary from severe to minimal and include microcephaly, developmental delays, neurobehavioral disorder, memory loss, hyperactivity, and diminished cognition.
Other problems include sleep disorders, information processing problems, and sensory integration problems. These problems can be life-long.

The differential diagnosis includes Cornelia de Lange syndrome, Noonan Syndrome, maternal phenylketonuria, and fetal hydantoin syndrome.

There is no specific test for FAS. Treatment includes neuropsychological and educational assessments to imnprove educational, behavioral, and social skills.

Attention Deficit Disorder with and without Hyperactivity (ADHD) is a common behavioral problem in childhood. It is a group of behaviors that appear early in life and typically persist. The general categories include hyperactivity, inattentiveness and impulsivity. The Diagnostic and Statistical Manual of Mental Disorders 4th Edition has specific criteria for its diagnosis, but each child has a different symptom constellation.
The cause of ADHD is not known but genetic, central nervous system, and environmental factors may all play a part. Often other problems are associated with ADHD including developmental disorders (e.g. speech and language problems or academic problems), mental retardation, oppositional defiant disorder, conduct disorder, and anxiety disorder.
Treatment is a multimodal approach specifically tailored to the individual and may include behavioral and psychosocial supports, appropriate educational placement and medications such as stimulants.

People with learning disorders (LD) have normal cognitive abilities but specific problems with types of learning or information processing. LD can occur alone but often are found as co-morbid conditions. They affect ~5% of children enrolled in United States schools. Each child’s problem constellation is unique.

LD include:

  • Dyslexia – language processing
  • Dyscalculia – math skills
  • Dysgraphia – written expression
  • Dyspraxia – fine motor skills
  • Spelling problems
  • Auditory processing disorder – interpreting auditory information
  • Visual processing disorder – interpreting visual information
  • Verbal processing disorder – interpreting and using verbal information
  • ADHD (some people include this as an LD or categorize it as a related problem)

Learning Point
Characteristic facial features of FAS includes microophthalmia, short palpebral fissures, flat philtrum, thin upper lip, scooped nose, wide nasal bridge, and wide set ears. Some of these features are very subtle and maybe only apparent with age (2-3 years) but may be decreased by adolescence.

Figure 7 – 01-10-05 – Diagram showing the craniofacial features associated with fetal alcohol syndrome from the National Institute on Alcohol Abuse and Alcoholism.

All growth parameters are decreased with weight more affected than height in childhood. Expected adult height is often not obtained. Other physical stigmata include: abnormal position or function of joints, altered palmar creases, small fifth fingers and nails, cardiac anomalies especially ventricular septal defects, ptosis, cleft lip and/or palate, micrognathia, large ears, short or webbed neck, vertebral and rib anomalies, meningomyelocoele, hydrocephalus, and hypoplastic labia majora.

Questions for Further Discussion
1. What educational interventions can be implemented in the classroom for children with ADHD?
2. What is Public Law 504 and how does it relate to children with disabilities?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Information prescriptions for patients can be found at Pediatric Common Questions, Quick Answers for this topic: Fetal Alcohol Syndrome.

Jones KL. Smith’s Recognizable Patterns of Human Malformation. 4th Edit. W.B. Saunders. 1988:491-494.

Morse BA, Weiner L. Fetal Alcohol Syndrome in Behavioral and Developmental Pediatrics: A Handbook for Primary Care. Parker S, Zuckerman B. eds. Little, Brown and Company, Boston, MA. 1995:149-152.

LD At a Glance. National Center for Learning Disorders.
Available from the Internet at <a href="http://www.merck.com/mrkshared/mmanual/section19/chapter262/262c.jsphttp://www.merck.com/mrkshared/mmanual/section19/chapter262/262c.jsp (cited 12/16/04).

Learning Disorders. Merck Manual
Available from the Internet at <a href="http://www.ld.org/LDInfoZone/InfoZone_FactSheetIndex.cfmhttp://www.ld.org/LDInfoZone/InfoZone_FactSheetIndex.cfm (cited 12/16/04).

DSM-IV-TR: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. BehaveNet.
Available from the Internet at <a href="http://www.behavenet.com/capsules/disorders/dsm4tr.htmhttp://www.behavenet.com/capsules/disorders/dsm4tr.htm (cited 12/16/04).

Author
Donna M. D’Alessandro, MD
Associate Professor of Pediatrics, Children’s Hospital of Iowa

Date
January 10, 2005