This document provides information on cerebral palsy (CP), including its definition, causes, classifications, clinical manifestations, diagnosis and treatment. CP is a permanent motor disability caused by brain insult during development. It is classified based on affected motor function and includes spastic diplegia, quadriplegia and hemiplegia. Treatment involves a multidisciplinary team to address motor impairments, prevent complications, and support normal development through therapies and adaptive equipment.
The term ‘cerebral palsy’ includes a group of disorders that result from permanent non-progressive brain damage during early development and are characterized by abnormalities of movement and posture.
The term ‘cerebral palsy’ includes a group of disorders that result from permanent non-progressive brain damage during early development and are characterized by abnormalities of movement and posture.
MOTOR RELEARNING PROGRAM- A physiotherapy approch.pptxSusan Jose
Motor relearning is a frequently used mode of retraining neurologically assaulted patients.lets explore the principles and examples of relearning movement.
Stroke rehabilitation and its aspects to work with patients with hemiplegia and other effects of stroke, other than that you will see some pictures of the used interventions and adaptive equipment used with stroke patients
MOTOR RELEARNING PROGRAM- A physiotherapy approch.pptxSusan Jose
Motor relearning is a frequently used mode of retraining neurologically assaulted patients.lets explore the principles and examples of relearning movement.
Stroke rehabilitation and its aspects to work with patients with hemiplegia and other effects of stroke, other than that you will see some pictures of the used interventions and adaptive equipment used with stroke patients
Outline of presentation
Introduction
Epidemiology
Etiology
Clinical manifestations
Diagnosis
Treatment
INTRODUCTION
Cerebral palsy (CP) refers to a heterogeneous group of conditions involving permanent nonprogressive central motor dysfunction that affect muscle tone, posture, and movement.
These conditions are due to abnormalities of the developing fetal or infantile brain resulting from a variety of causes.
The motor impairment generally results in limitations in functional abilities and activity which can range in severity.
The motor disorders are often accompanied by disturbances of sensation , perception, cognition, communication, and behavior as well as by epilepsy and secondary musculoskeletal problems.
CP has historically been considered a static encephalopathy, but some of the neurologicfeatures of CP, such as movement disorders and orthopedic complications can change or progress over time.
Many children and adults with CP function at a high educational and vocational level,without any sign of cognitive dysfunction
Etiology
CP is caused by a broad group of
Developmental,
Genetic,
Metabolic,
Ischemic,
Infectious, and
Other acquired etiologies
Epidemiology
CP is the most common and costly form of chronic motor disability that begins in childhood
Incidence is 3.6 per 1,000 children with a male: female ratio of 1.4 : 1.
Most children with CP had been born at term with uncomplicated labors anddeliveries
Risk factors
Prematurity and VLBW
Heavy maternal alcohol consumption,
Maternal smoking,
Maternal obesity, and
Infections during pregnancy
In 80% of cases, features were identified pointing to antenatal factors causing abnormal brain development
Fewer than 10% of children with CP had evidence of intrapartum asphyxia
Intrauterine exposure to maternal infection (chorioamnionitis, urinary tract infection) was associated with a significant increase in the risk of CP in normal birthweight infants.
Multiple pregnancy was also associated with a higher incidence of CP
Death of a twin in utero carries an even greater risk of CP
Infertility treatments are also associated with a higher rate of CP
CP is more common and more severe in boys than girls, and this effect is enhanced at the extremes of body weight
Elevated levels of inflammatory cytokines have been reported in heelstick blood collected at birth from children who later were identified with CP.
The prevalence of CP has increased somewhat as a result of the enhanced survival of very premature infants weighing < 1,000 g, who go on to develop CP at a rate of ~ 15 per 100.
However, the GA at birth adjusted prevalence of CP among 2 yr old former premature infants born at 20-27 wk of gestation has decreased over the past decade
The major lesions that contribute to CP in preterm infants are intracerebral hemorrhage and periventricular leukomalacia (PVL).
A group of motor impairment syndromes resulting from disorders of early brain development and often associated with epilepsy and abnormalities of speech, vision and intellect
More than 10 million people suffer from epilepsy in India.Seizures impact the lives of people with epilepsy and their family in many ways including creating barriers to employment and education and facing a sense of discrimination and isolation from their peers who donʼt understand what happens when they see a seizure occur. In India, epilepsy is still thought of as mental illness mainly due to lack of information on the condition among the general public.
This presentation touches every aspect of epilepsy
1. Overview of Epilepsy;
2. Type of Seizures;
3. Diagnosis and Management;
4. Psychological Issues; and
5. Social Perspectives.
Meaning of Cerebral Palsy , Definition of Cerebral Palsy , Areas affected by Cerebral Palsy , Causes of Cerebral Palsy , Types of Cerebral Palsy ( many basis ) , Signs and Symptoms of Cerebral Palsy , Developmental Milestones of Cerebral Palsy child , Associated problems of Cerebral Palsy , Treatment of Cerebral Palsy ,
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
2. Definition
• Cerebral palsy refers to permanent, non progre - ssive and
occasionally evolving, disorders of tone, movement or posture,
caused by an insult to the developing brain.
3. • The motor disorders are often accompanied by
• disturbances of:
• Sensation,
• Perception,
• Cognition,
• Communication, and
• Behavior
• epilepsy and
• Secondary musculoskeletal problems.
4. • CP has been considered a static encephalopathy,but some
features of CP, such as movement disorders and orthopedic
complications,including scoliosis and hip dislocation, can
change or progress over time.
5. Cerebral palsy
• It is the most common chronic motor disability in childhood,
affecting 2-3 infants per 1000 live births.
• While perinatal asphyxia was considered the most common
cause, it accounts for less than 10% of cases.
6. • Etiology of cerebral palsy
• A)Genetic or prenatal:
• Structural malformations of nervous system
• Congenital or intrauterine infections
• Maternal or obstetric complications
• Teratogens
• B)Perinatal:
• Birth asphyxia
• Prematurity; low birth weight
• Birth trauma; intracranial hemorrhage
• Hyperbilirubinemia; hypoglycemia
• Central nervous system (CNS) infection
8. Clinical Manifestations
• The most common presentation is with developmental delay.
• Physical findings are persistence of neonatal reflexes, increased
tone,
• fisting with cortical thumb,
• scissoring of legs, toe-walking,
• abnormal posture and gait
• abnormal movements and/ or hyperreflexia.
9. • Common comorbidities include intellectual disability,
microcephaly, seizures, behaviral problems, difficulty in speech,
language, swallowing or feeding, blindness, deafness,squint,
malnutrition, sleep disturbances and exessive drooling.
• Contractures may develop that are initially dynamic and later
fixed.
10. Classification of Cerebral Palsy and
Major Causes
MOTOR SYNDROME
(APPROX. % OF CP)
NEUROPATHOLOGY/
MRI
MAJOR CAUSES
Spastic diplegia (35%)
Periventricular
leukomalacia
Periventricular cysts
or scars in white matter
enlargement of
ventricles
Prematurity
Ischemia Infection
Endocrine/metabolic (e.g.,
thyroid)
Spastic quadriplegia
(20%)
Periventricular
leukomalacia
Multicystic
encephalomalacia
Ischemia, infection
Endocrine/metabolic/develop
mental
11. MOTOR SYNDROME
NEUROPATHOLOGY MAJOR CAUSES
Hemiplegia (25%)
Stroke: in utero or neonatal
Focal infarct or
cortical
subcortical damage
Cortical malformations
Thrombophilic disorders
Infection
Genetic/developmental
Periventricular hemorrhagic
infarction
Extrapyramial
(athetoid,
dyskinetic) (15%)
Asphyxia: symmetric scars
in
putamen and thalamus
Kernicterus: scars in globus
pallidus, hippocampus
dystonia
Asphyxia
Kernicterus Mitochondrial
Genetic/metabolic
12. Spastic quadriplegia
• Most severe form of CP
• Marked motor impairment of all extremities and
• with intellectual disability and seizures.
• Swallowing difficulties are common as a result of supranuclear
bulbar palsies, often leading to aspiration pneumonia and
growth failure.
• Common lesions seen :severe PVL and multicystic cortical
encephalomalacia.
13. • Neurologic examination
• spasticity in all extremities, decreased spontaneous movements,
• brisk reflexes, and plantar extensor responses.
• Flexion contractures of the knees, elbows, and
• wrists are often present by late childhood.
• Associated developmental disabilities, including speech and
visual abnormalities, are particularly prevalent in this group of
children.
14. Spastic diplegia
• Spastic diplegia is bilateral spasticity of the legs that is greater than in
the arms.
• Strongly associated with damage to the immature white matter.
• The first clinical indication of spastic diplegia is often noted is
commando crawl
• Addctor spasticity leading to difficulty in application of a diaper
• If there is paraspinal muscle involvement, the child may be unable to sit.
• Examination of the child reveals spasticity in the legs with brisk
reflexes, ankle clonus, and a bilateral Babinski sign.
15. • When the child is suspended by the axillae, a scissoring
posture of the lower extremities is maintained.
• Tiptoe walking
• Intellectual development of patients is often normal. and
seizures are minimal.
• Learning disabilities and deficits in other abilities, such as
vision, because of disruption of white matter pathways.
• The most common neuropathologic finding in children with
spastic diplegia is periventricular leukomalacia (PVL),
which is visualized on MRI brain.
16. Spastic hemiplegia
• Decreased spontaneous movements on affected side.
• Hand preference at a very early age.
• The arm is often more involved than the leg and difficulty in
• hand manipulation is obvious by 1 yr of age.
• Walking is usually delayed until 18-24 mo,
• circumductive gait is apparent.
• Extremities may show growth arrest.
• Spasticity is greatest in antigravity muscles.
17. • Equinovarus deformity of the foot.
• Tiptoe walking.
• Ankle clonus and Babinski sign may be present.
• the deep tendon reflexes are increased, and weakness of the
hand and foot dorsiflexors present
• About one third of patients have a seizure disorder
• Approximately 25% have cognitive abnormalities including
mental retardation.
• MRI is far more sensitive than cranial CT scan .
18. Athetoid CP/choreoathetoid /dyskinetic
CP
• Less common than spastic CP (15–20% of patients with CP )
• hypotonic with poor head control and marked head lag and develop
variably increased tone with rigidity and dystonia over years.
• Upper extremities more affected than the lower extremities.
• Feeding may be difficult, and tongue thrust and drooling maybe prominent
• Speech is affected because the oropharyngeal muscles are involved.
• seizures are uncommon, and intellect is preserved in many patients.
19. • Causes
• Birth asphyxia: Lesions in mostly the basal ganglia and
thalamus.
• Kernicterus:Lesions in the globus pallidus bilaterally.
• Metabolic genetic disorders such as mitochondrial disorders and
glutaric aciduria. MRI scanning and possibly metabolic testing
are important.
• (DOPA)-responsive dystonia (Segawa disease): have diurnal
variation in their signs with worsening dystonia in the legs
during the day; respond to small doses of L-dopa and/or
cerebrospinal fluid can be sent for neurotransmitter analysis.
20. Associated comorbidities are common and include
1. Pain (in 75%),
2. Cognitive disability (50%),
3. Hip displacement (30%),
4. Seizures (25%),
5. Behavioral disorders (25%),
6. Sleep disturbances (20%),
7. Visual impairment (19%)
8. Hearing impairment (4%).
21. • Ataxic CP: is caused by cerebellar malformations and is
associated with other cerebellar signs.
• Mixed CP: refers to a presentation including both spastic and
extrapyramidal features.
22. Diagnosis
• History and physical examination should be done to rule out a
progressive disorder of the CNS, including degenerative
diseases, metabolic disorders, spinal cord tumor, or muscular
dystrophy.
• The possibility of anomalies at the base of the skull or other
disorders affecting the cervical spinal cord needs to be
considered in patients with little involvement of the arms or
cranial nerves.
23. • An MRI brain is indicated to determine the
• location and extent of structural lesions or associated congenital
malformations;
• MRI spinal cord is indicated if there is any question about
spinal cord pathology.
• Tests of hearing and visual function.
• Genetic evaluation should be considered in patients with
congenital malformations (chromosomes) or evidence of
metabolic disorders (e.g., amino acids, organic acids, MR
spectroscopy)
24. • In addition urea cycle disorder arginase deficiency is a rare
cause of spastic diplegia and a deficiency of sulfite oxidase or
molybdenum cofactor can present as CP caused by perinatal
asphyxia
• Tests to detect inherited thrombophilic disorders may be
indicated in patients in whom an in utero or neonatal stroke is
suspected as the cause of CP.
• Because CP is usually associated with a wide spectrum of
developmental disorders, a multidisciplinary approach is most
helpful in the assessment and treatment of such children.
25. • The differential diagnosis must include disorders that may mimic the
various types of CP.
• These may include the hereditary spastic diplegias , monoamine
transmitter disorders , and many treatable inborn errors of metabolism,
including disorders of amino acids, creatine, fatty acid oxidation,
lysosomes, mitochondria, organic acids, and vitamin cofactors.
26. Treatment
• For children with CP, a team of physicians, including
neurodevelopmental pediatricians, pediatric neurologists, and
physical medicine, rehabilitation specialists, as well as
occupational and physical therapists, speech pathologists, social
workers, educators, and developmental psychologists, is
important to reduce abnormalities of movement and tone and to
optimize normal psychomotor development.
27. • Parents should be educated how to work with their
• child in daily activities such as feeding, carrying, dressing,
bathing, and playing in ways that limit the effects of abnormal
muscle tone.
• Families &children also taught series of exercises designed to
prevent the development of contractures, esp. tight Achilles
tendon.
28. Physiotherapy and Occupational
Therapy
• Physical and occupational therapires are useful for promoting
mobility and the use of the upper extremities for activities of
daily living.
29. Speech Therapy
• Speech therapist promote acquisition of a functional means of
communication and work on swallowing issues.
• These therapists help children to achieve their potential and
often recommend further evaluations and adaptive equipment.
30. Spastic diplegia
• Children with spastic diplegia are treated initially with the
assistance of adaptive equipment, such as orthoses, walkers,
poles, and standing frames.
• If a patient has marked spasticity of the lower extremities or
evidence of hip dislocation, consideration should be given to
performing surgical soft-tissue procedures that reduce muscle
spasm around the hip girdle, including an adductor tenotomy or
psoas transfer and release.
• A rhizotomy procedure in which the roots of the spinal nerves
are divided produces considerable improvement in selected
patients with severe spastic diplegia.
31. Spastic hemiplegia
• A tight heel cord in a child with spastic hemiplegia may be
treated surgically by tenotomy of the Achilles tendon or
• Spastic hemiplegia may be treated sometimes with serial
botulinum toxin injections.
32. Quadriplegia
• Quadriplegia is managed with motorized wheelchairs, special
feeding devices, modified typewriters, and customized seating
arrangements.
33. Hemiplegic CP
• The function of the affected extremities in children with
hemiplegic CP can often be improved by therapy in which
movement of the good side is constrained with casts while the
impaired extremities perform exercises that induce improved
hand and arm functioning.
• This constraint-induced movement therapy is effective in
patients of all ages.
34. Pharmacotherapy
Several drugs can be used to treat spasticity, including
1) oral diazepam (0.01-0.3 mg/kg/day,divided qid),
2) baclofen (0.2-2mg/kg/day, divided bid or tid),
3) dantrolene (0.5-10 mg/kg/day, bid).
Side effects
Sedation for benzodiazepines and Lowered seizure threshold for
baclofen.
35. Pharmacotherapy
1) Small doses of levodopa (0.5-2 mg/kg/day) can be used to
treat dystonia or DOPA responsive dystonia.
2) Artane (trihexyphenidyl, 0.25 mg/day, divided bid or tid and
titrated upward) is sometimes useful for treating dystonia and can
increase the use of the upper extremities and vocalizations.
3) Reserpine (0.01-0.02 mg/kg/day, divided bid to a maximum of
0.25 mg daily) tetrabenazine (12.5-25.0 mg, divided bid or tid) can
be useful for hyperkinetic movement disorders,including athetosis
or chorea.
36. • Intrathecal baclofen delivered with an implanted pump has been
used successfully in many children with severe spasticity.
• Botulinum toxin injected into specific muscle groups for the
management of spasticity shows a very positive response in
many patients
• Deep brain stimulation has been used in selected refractory
patients.
• Hyperbaric oxygen has not been shown to improve the
condition of children with CP.
37. • Communication skills may be enhanced by the use of
• Bliss symbols, talking typewriters, electronic speech–
generating devices, and specially adapted computers, including
artificial intelligence computers to augment motor and language
function.
• Significant behavior problems may substantially interfere with
the development of a child with CP; their early identification
and management are important, and the assistance of a
psychologist or psychiatrist may be necessary.
38. • Learning and attention deficit disorders and
• mental retardation are assessed and managed by a psychologist
and educator.
• Strabismus, nystagmus, and optic atrophy are common in
children with CP; an ophthalmologist should be included in the
initial assessment and ongoing treatment.
• Lower urinary tract dysfunction should receive prompt
assessment and treatment.