CEREBRAL PALSY EXPLAINED
What is CEREBRAL PALSY ?
The term CEREBRAL PALSY refers to any one of a number of neurological disorders that appear in infancy or early childhood and permanently affect body movement and muscle coordination but don’t worsen over time. Even though CEREBRAL PALSY affects muscle movement, it isn’t caused by problems in the muscles or nerves. It is caused by abnormalities in parts of the brain that control muscle movements. The majority of children with CEREBRAL PALSY are born with it, although it may not be detected until months or years later. The early signs of CEREBRAL PALSY usually appear before a child reaches 3 years of age. The most common are a lack of muscle coordination when performing voluntary movements (ataxia); stiff or tight muscles and exaggerated reflexes (spasticity); walking with one foot or leg dragging; walking on the toes, a crouched gait, or a “scissored” gait; and muscle tone that is either too stiff or too floppy. A small number of children have CEREBRAL PALSY as the result of brain damage in the first few months or years of life, brain infections such as bacterial meningitis or viral encephalitis, or head injury from a motor vehicle accident, a fall, or child abuse.
Is there any treatment for CEREBRAL PALSY ?
CEREBRAL PALSY can’t be cured, but treatment will often improve a child's capabilities. Many children go on to enjoy near-normal adult lives if their disabilities are properly managed. In general, the earlier treatment for CEREBRAL PALSY begins the better chance children have of overcoming developmental disabilities or learning new ways to accomplish the tasks that challenge them. Treatment may include physical and occupational therapy, speech therapy, drugs to control seizures, relax muscle spasms, and alleviate pain; surgery to correct anatomical abnormalities or release tight muscles; braces and other orthotic devices; wheelchairs and rolling walkers; and communication aids such as computers with attached voice synthesizers.
What is the prognosis?
CEREBRAL PALSY doesn’t always cause profound disabilities. While one child with severe cerebral palsy might be unable to walk and need extensive, lifelong care, another with mild cerebral palsy might be only slightly awkward and require no special assistance. Supportive treatments, medications, and surgery can help many individuals improve their motor skills and ability to communicate with the world.
What CEREBRAL PALSY research is being done?
Researchers are investigating the roles of mishaps early in brain development, including genetic defects, which are sometimes responsible for the brain malformations and abnormalities that result in CEREBRAL PALSY. Scientists are also looking at traumatic events in newborn babies’ brains, such as bleeding, epileptic seizures, and breathing and circulation problems, which can cause the abnormal release of chemicals that trigger the kind of damage that causes CEREBRAL PALSY. To make sure children are getting the right kinds of therapies, studies are also being done that evaluate both experimental treatments and treatments already in use so that physicians and parents have valid information to help them choose the best therapy.
NIH Patient Recruitment for CEREBRAL PALSY Clinical Trials
At NIH Clinical Center
Throughout the U.S. and Worldwide
Organizations
United CEREBRAL PALSY (UCP)
1660 L Street, NW
Suite 700
Washington, DC 20036
national@ucp.org
http://www.ucp.org
Tel: 202-776-0406 800-USA-5UCP (872-5827)
Fax: 202-776-0414
Pathways Awareness Foundation [For Children With Movement Difficulties]
150 N. Michigan Avenue
Suite 2100
Chicago, IL 60601
friends@pathwaysawareness.org
http://www.pathwaysawareness.org
Tel: 312-893-6620 800-955-CHILD (2445)
Fax: 312-893-6621
March of Dimes Foundation
1275 Mamaroneck Avenue
White Plains, NY 10605
askus@marchofdimes.com
http://www.marchofdimes.com
Tel: 914-428-7100 888-MODIMES (663-4637)
Fax: 914-428-8203
Easter Seals
233 South Wacker Drive
Suite 2400
Chicago, IL 60606
info@easterseals.com
http://www.easterseals.com
Tel: 312-726-6200 800-221-6827
Fax: 312-726-1494
Children's Neurobiological Solutions (CNS) Foundation
1726 Franceschi Road
Santa Barbara, CA 93101
info@cnsfoundation.org
http://www.cnsfoundation.org
Tel: 866-CNS-5580 (267-5580) 805-898-4442
Children's Hemiplegia and Stroke Assocn. (CHASA)
4101 West Green Oaks Blvd., Ste. 305
PMB 149
Arlington, TX 76016
info437@chasa.org
http://www.hemi-kids.org
Tel: 817-492-4325
CEREBRAL PALSY International Research Foundation
1025 Connecticut Avenue
Suite 701
Washington, DC 20036
nmaher@cpirf.org
http://www.cpirf.org
Tel: 202-496-5060
Pedal with Pete [For Research on CEREBRAL PALSY ]
P.O. Box 274
Kent, OH 44240
petezeid@aol.com
http://www.pedalwithpete.com
Tel: 800-304-PETE (7383)
Fax: 330-673-1240
Showing posts with label Neurological. Show all posts
Showing posts with label Neurological. Show all posts
Wednesday, February 25, 2009
Saturday, January 3, 2009
AUTISM and SEIZURES
Definition and Frequency of Epilepsy in Autistic Population.
Epilepsy is a chronic disorder of the brain characterized by recurrent seizures, as opposed to seizures occurring in association with high fever, drug effects, chemical imbalance (e.g., low blood sugar). Epilepsy can occur without other evidence of neurologic dysfunction, but it is often associated with more global neurologic abnormalities, such as autism, cerebral palsy, or mental retardation.
The majority of autistic persons do not have seizures. However, they are at higher risk for seizures if they have certain specific neurologic conditions, such as tuberous sclerosis, neurofibromatosis, untreated phenylketonuria.
Infantile spasms (sudden generalized muscle contractions, usually beginning between ages 3 and 8 months) do occur in association with autism, often in young children who have tuberous sclerosis or other significant neurologic problems. Other forms of epilepsy--complex partial epilepsy, generalized tonic-clonic epilepsy and, more rarely, absence seizures--also may occur in autistic children. The frequency of epilepsy in autistic children is below 15% (my estimate) and, if seizures do occur, they are more likely to occur in the autistic child who is also mentally retarded.
There is an increased incidence of seizures in otherwise seizure-free autistic persons when they become adolescents. Roughly 25-30% of autistic adolescents have been reported to develop seizures, although such a high incidence has not been noted by me. It is of note that the seizures are usually not serious, are usually controlled by anticonvulsants, and are inclined to diminish in adulthood. The reason for this significant increased frequency of seizures in autistic adolescents is unknown and may represent, at least in part, the general tendency for seizure disorders to become more problematic at puberty.
There are many autistic persons who have behavior and mannerisms, e.g., swaying, sudden repetitive movements, which may raise questions about a seizure disorder. This is a valid concern because seizures can reduce one's awareness of the environment and/or create anxiety and thus enhance autistic behavior and communication problems. How can seizures be distinguished from unusual behaviors?
1. Seizures are sudden and without provoking events. If an autistic person's suspected "seizures" are clearly the consequence of anger, frustration, fear, these episodes are probably not seizures. (On occasion, seizures are provoked by certain light frequencies or sounds. Seizures can also be brought on by prolonged hyperventilation in a person susceptible to seizures.)
2. Seizures generally follow a similar -pattern each time, although some seizures might be more intense and prolonged than others. If the autistic person's "seizures" are varied in movements and mannerisms, these events are probably not seizures.
3. Generalized seizures are often associated with an aura (perhaps a sense of fear or odd sensations) and may be followed by a headache, weakness or exhaustion. If the autistic person has had a major "seizure," it is unlikely he would immediately resume his regular activity.
4. Absence attacks, often suggested by the autistic person's staring mannerisms, involve brief (less than 10 seconds unless frequent episodes) loss of consciousness, often with some eyeblinking or mild facial movements. Complex partial seizures, which can also involve staring, are also often associated with some associated movements, lip-smacking, shuddering. If an autistic person has frequent staring episodes, it is important to determine if there is any response to environmental stimuli and whether there are any associated movements.
If there is any question about repeated, unpredictable and similar episodes of unusual behavior and/or movements, an electroencephalogram (EEG) should be done. A sleep EEG is usually the most productive. Obtaining an EEG in the autistic population can require patience, creative scheduling, and sedation. An EEG is done to help localize the origin of the abnormal electrical activity in the brain and can help determine the most appropriate therapy. Other diagnostic studies might be necessary. An MRI or CT would be done to rule out a brain tumor or malformation. Blood studies would be done to rule out metabolic disturbances. In very puzzling cases, EEG telemetry might be used.
Seizure Treatment
If the EEG supports the clinical diagnosis of a seizure disorder or if the clinical history is strongly suggestive but an EEG is unobtainable, anticonvulsant therapy should be considered. Carbamazepine (Tegretol) and valproic acid (Depakene) are the most commonly used anticonvulsants. They have relatively few significant side effects, and often have positive behavioral effects--the improved behaviors may not relate to seizure control. There are a variety of other traditional anticonvulsants, including phenobarbital, diphenylhydantoin (Dilantin), and ethosuximide (Zarontin). Barbiturates often make children more hyperactive and irritable, and diphenylhydantoin has a range of subtle metabolic, endocrinologic, and neurologic side effects. There are also a variety of newer anticonvulsants (vigabatrin, lamotrigine, gabapentin) which hold promise.
It is important to note that all anticonvulsants may have behavioral and cognitive side effects. Therefore, anticonvulsant therapy needs to be carefully monitored and probably not considered in a person with rare, brief and/or questionable seizures.
Epilepsy is a chronic disorder of the brain characterized by recurrent seizures, as opposed to seizures occurring in association with high fever, drug effects, chemical imbalance (e.g., low blood sugar). Epilepsy can occur without other evidence of neurologic dysfunction, but it is often associated with more global neurologic abnormalities, such as autism, cerebral palsy, or mental retardation.
The majority of autistic persons do not have seizures. However, they are at higher risk for seizures if they have certain specific neurologic conditions, such as tuberous sclerosis, neurofibromatosis, untreated phenylketonuria.
Infantile spasms (sudden generalized muscle contractions, usually beginning between ages 3 and 8 months) do occur in association with autism, often in young children who have tuberous sclerosis or other significant neurologic problems. Other forms of epilepsy--complex partial epilepsy, generalized tonic-clonic epilepsy and, more rarely, absence seizures--also may occur in autistic children. The frequency of epilepsy in autistic children is below 15% (my estimate) and, if seizures do occur, they are more likely to occur in the autistic child who is also mentally retarded.
There is an increased incidence of seizures in otherwise seizure-free autistic persons when they become adolescents. Roughly 25-30% of autistic adolescents have been reported to develop seizures, although such a high incidence has not been noted by me. It is of note that the seizures are usually not serious, are usually controlled by anticonvulsants, and are inclined to diminish in adulthood. The reason for this significant increased frequency of seizures in autistic adolescents is unknown and may represent, at least in part, the general tendency for seizure disorders to become more problematic at puberty.
There are many autistic persons who have behavior and mannerisms, e.g., swaying, sudden repetitive movements, which may raise questions about a seizure disorder. This is a valid concern because seizures can reduce one's awareness of the environment and/or create anxiety and thus enhance autistic behavior and communication problems. How can seizures be distinguished from unusual behaviors?
1. Seizures are sudden and without provoking events. If an autistic person's suspected "seizures" are clearly the consequence of anger, frustration, fear, these episodes are probably not seizures. (On occasion, seizures are provoked by certain light frequencies or sounds. Seizures can also be brought on by prolonged hyperventilation in a person susceptible to seizures.)
2. Seizures generally follow a similar -pattern each time, although some seizures might be more intense and prolonged than others. If the autistic person's "seizures" are varied in movements and mannerisms, these events are probably not seizures.
3. Generalized seizures are often associated with an aura (perhaps a sense of fear or odd sensations) and may be followed by a headache, weakness or exhaustion. If the autistic person has had a major "seizure," it is unlikely he would immediately resume his regular activity.
4. Absence attacks, often suggested by the autistic person's staring mannerisms, involve brief (less than 10 seconds unless frequent episodes) loss of consciousness, often with some eyeblinking or mild facial movements. Complex partial seizures, which can also involve staring, are also often associated with some associated movements, lip-smacking, shuddering. If an autistic person has frequent staring episodes, it is important to determine if there is any response to environmental stimuli and whether there are any associated movements.
If there is any question about repeated, unpredictable and similar episodes of unusual behavior and/or movements, an electroencephalogram (EEG) should be done. A sleep EEG is usually the most productive. Obtaining an EEG in the autistic population can require patience, creative scheduling, and sedation. An EEG is done to help localize the origin of the abnormal electrical activity in the brain and can help determine the most appropriate therapy. Other diagnostic studies might be necessary. An MRI or CT would be done to rule out a brain tumor or malformation. Blood studies would be done to rule out metabolic disturbances. In very puzzling cases, EEG telemetry might be used.
Seizure Treatment
If the EEG supports the clinical diagnosis of a seizure disorder or if the clinical history is strongly suggestive but an EEG is unobtainable, anticonvulsant therapy should be considered. Carbamazepine (Tegretol) and valproic acid (Depakene) are the most commonly used anticonvulsants. They have relatively few significant side effects, and often have positive behavioral effects--the improved behaviors may not relate to seizure control. There are a variety of other traditional anticonvulsants, including phenobarbital, diphenylhydantoin (Dilantin), and ethosuximide (Zarontin). Barbiturates often make children more hyperactive and irritable, and diphenylhydantoin has a range of subtle metabolic, endocrinologic, and neurologic side effects. There are also a variety of newer anticonvulsants (vigabatrin, lamotrigine, gabapentin) which hold promise.
It is important to note that all anticonvulsants may have behavioral and cognitive side effects. Therefore, anticonvulsant therapy needs to be carefully monitored and probably not considered in a person with rare, brief and/or questionable seizures.
Sunday, August 17, 2008
TOURETTE SYNDROME (TS)
Tourette Syndrome (TS) is a neurological or "neurochemical" disorder characterized by tics -- involuntary, rapid, sudden movements or vocalizations that occur repeatedly in the same way.
The cause has not been established, although current research presents considerable evidence that the disorder stems from the abnormal metabolism of at least one brain chemical (neurotransmitter) called dopamine. Very likely other neurotransmitters, such as serotonin, are also involved.
In 1825 the first case of TS was reported in medical literature by Dr. Itard. It was a description of the Marquise de Dampierre, a noblewoman whose symptoms included involuntary tics of many parts of her body and various vocalizations including echolalia [repetition or echoing of verbal utterances] and coprolalia [involuntary swearing or the involuntary utterance of obscene words or socially inappropriate & derogatory remarks]. She lived to the age of 86 and was again described in 1883 by Dr. Georges Gilles de la Tourette, the French neurologist for whom the disorder was named. Samuel Johnson, the lexicographer and André Malraux, the French author, are among the famous people who are thought to have had TS.
SYMPTOMS OF TOURETTES
The most common first symptom is a facial tic, such as rapidly blinking eyes or twitches of the mouth. However, involuntary sounds, such as throat clearing and sniffing, or tics of the limbs may be the initial signs. For some, the disorder begins abruptly with multiple symptoms of movements and sounds.
The symptoms include;
Both multiple motor and one or more vocal tics present at some time during the illness although not necessarily in the same way;
The occurrence of ticks many times a day (usually in bouts) nearly every day or intermittently throughout a span of more than one year;
The periodic change in the number, frequency, type and location of the tics, disappear for weeks or months at a time; and
Onset before the age of 18.
The term "involuntary" used to describe TS tics is a source of confusion since it is known that most people with TS do have some control over the symptoms. What is recognized is that the control which can be exerted from seconds to hours at a time, may merely postpone more severe outbursts of symptoms. Tics are experienced as irresistible as the urge to sneeze and must eventually be expressed. People with TS often seek a secluded spot to release their symptoms after delaying them in school or at work. Typically, tics increase as a result of tension or stress (but are not caused by stress) and decrease with relaxation or concentration on an absorbing task.
Individuals not only struggle with the condition itself, they must bear the double burden of the stigma attached.
TREATMENT of TOURETTES
The majority of people with TS are not significantly disabled by their tics or behavioural symptoms and therefore do not require medication. However, there are medications to help control symptoms when they interfere with functioning. The drugs include haloperidol (Haldol®), pimozide (Orap®), clonidine (Catapres®), clonazepam (Rivotril®) and nitrazepam (Mogadon®). Stimulants such as methylphenidate (Ritalin®) and dextroamphetamine (Dexedrine®), that are prescribed for hyperactivity may temporarily increase tics and should be used cautiously. Obsessive compulsive symptoms may be controlled with fluoxetine (Prozax®), clomipramine (Anafranil®) and other similar medications.
The dosage necessary to achieve maximum control of symptoms varies for each patient and must be gauged carefully by a doctor. The medicine is administered in small doses with gradual increases to the point where there is a maximum alleviation of symptoms with minimal side effects. Some of the undesirable reactions to medications are fatigue, motor restlessness, weight gain and social withdrawal, most of which can be reduced with specific medications. Side effects such as depression and cognitive impairment can sometimes be alleviated with dosage reduction or a change of medication.
Other types of therapy may also be helpful. Sometimes psychotherapy can assist a person with TS and help his/her family cope with the psycho-social problems associated with TS. Some behavioural therapies can teach the substitution of one tic with another that is more acceptable. The use of relaxation techniques and/or biofeedback may help during prolonged periods of high stress.
GENES and TOURETTES
The majority of people with TS are not significantly disabled by their tics or behavioural symptoms and therefore do not require medication. However, there are medications to help control symptoms when they interfere with functioning. The drugs include haloperidol (Haldol®), pimozide (Orap®), clonidine (Catapres®), clonazepam (Rivotril®) and nitrazepam (Mogadon®). Stimulants such as methylphenidate (Ritalin®) and dextroamphetamine (Dexedrine®), that are prescribed for hyperactivity may temporarily increase tics and should be used cautiously. Obsessive compulsive symptoms may be controlled with fluoxetine (Prozax®), clomipramine (Anafranil®) and other similar medications.
The dosage necessary to achieve maximum control of symptoms varies for each patient and must be gauged carefully by a doctor. The medicine is administered in small doses with gradual increases to the point where there is a maximum alleviation of symptoms with minimal side effects. Some of the undesirable reactions to medications are fatigue, motor restlessness, weight gain and social withdrawal, most of which can be reduced with specific medications. Side effects such as depression and cognitive impairment can sometimes be alleviated with dosage reduction or a change of medication.
Other types of therapy may also be helpful. Sometimes psychotherapy can assist a person with TS and help his/her family cope with the psycho-social problems associated with TS. Some behavioural therapies can teach the substitution of one tic with another that is more acceptable. The use of relaxation techniques and/or biofeedback may help during prolonged periods of high stress.
The cause has not been established, although current research presents considerable evidence that the disorder stems from the abnormal metabolism of at least one brain chemical (neurotransmitter) called dopamine. Very likely other neurotransmitters, such as serotonin, are also involved.
In 1825 the first case of TS was reported in medical literature by Dr. Itard. It was a description of the Marquise de Dampierre, a noblewoman whose symptoms included involuntary tics of many parts of her body and various vocalizations including echolalia [repetition or echoing of verbal utterances] and coprolalia [involuntary swearing or the involuntary utterance of obscene words or socially inappropriate & derogatory remarks]. She lived to the age of 86 and was again described in 1883 by Dr. Georges Gilles de la Tourette, the French neurologist for whom the disorder was named. Samuel Johnson, the lexicographer and André Malraux, the French author, are among the famous people who are thought to have had TS.
SYMPTOMS OF TOURETTES
The most common first symptom is a facial tic, such as rapidly blinking eyes or twitches of the mouth. However, involuntary sounds, such as throat clearing and sniffing, or tics of the limbs may be the initial signs. For some, the disorder begins abruptly with multiple symptoms of movements and sounds.
The symptoms include;
Both multiple motor and one or more vocal tics present at some time during the illness although not necessarily in the same way;
The occurrence of ticks many times a day (usually in bouts) nearly every day or intermittently throughout a span of more than one year;
The periodic change in the number, frequency, type and location of the tics, disappear for weeks or months at a time; and
Onset before the age of 18.
The term "involuntary" used to describe TS tics is a source of confusion since it is known that most people with TS do have some control over the symptoms. What is recognized is that the control which can be exerted from seconds to hours at a time, may merely postpone more severe outbursts of symptoms. Tics are experienced as irresistible as the urge to sneeze and must eventually be expressed. People with TS often seek a secluded spot to release their symptoms after delaying them in school or at work. Typically, tics increase as a result of tension or stress (but are not caused by stress) and decrease with relaxation or concentration on an absorbing task.
Individuals not only struggle with the condition itself, they must bear the double burden of the stigma attached.
TREATMENT of TOURETTES
The majority of people with TS are not significantly disabled by their tics or behavioural symptoms and therefore do not require medication. However, there are medications to help control symptoms when they interfere with functioning. The drugs include haloperidol (Haldol®), pimozide (Orap®), clonidine (Catapres®), clonazepam (Rivotril®) and nitrazepam (Mogadon®). Stimulants such as methylphenidate (Ritalin®) and dextroamphetamine (Dexedrine®), that are prescribed for hyperactivity may temporarily increase tics and should be used cautiously. Obsessive compulsive symptoms may be controlled with fluoxetine (Prozax®), clomipramine (Anafranil®) and other similar medications.
The dosage necessary to achieve maximum control of symptoms varies for each patient and must be gauged carefully by a doctor. The medicine is administered in small doses with gradual increases to the point where there is a maximum alleviation of symptoms with minimal side effects. Some of the undesirable reactions to medications are fatigue, motor restlessness, weight gain and social withdrawal, most of which can be reduced with specific medications. Side effects such as depression and cognitive impairment can sometimes be alleviated with dosage reduction or a change of medication.
Other types of therapy may also be helpful. Sometimes psychotherapy can assist a person with TS and help his/her family cope with the psycho-social problems associated with TS. Some behavioural therapies can teach the substitution of one tic with another that is more acceptable. The use of relaxation techniques and/or biofeedback may help during prolonged periods of high stress.
GENES and TOURETTES
The majority of people with TS are not significantly disabled by their tics or behavioural symptoms and therefore do not require medication. However, there are medications to help control symptoms when they interfere with functioning. The drugs include haloperidol (Haldol®), pimozide (Orap®), clonidine (Catapres®), clonazepam (Rivotril®) and nitrazepam (Mogadon®). Stimulants such as methylphenidate (Ritalin®) and dextroamphetamine (Dexedrine®), that are prescribed for hyperactivity may temporarily increase tics and should be used cautiously. Obsessive compulsive symptoms may be controlled with fluoxetine (Prozax®), clomipramine (Anafranil®) and other similar medications.
The dosage necessary to achieve maximum control of symptoms varies for each patient and must be gauged carefully by a doctor. The medicine is administered in small doses with gradual increases to the point where there is a maximum alleviation of symptoms with minimal side effects. Some of the undesirable reactions to medications are fatigue, motor restlessness, weight gain and social withdrawal, most of which can be reduced with specific medications. Side effects such as depression and cognitive impairment can sometimes be alleviated with dosage reduction or a change of medication.
Other types of therapy may also be helpful. Sometimes psychotherapy can assist a person with TS and help his/her family cope with the psycho-social problems associated with TS. Some behavioural therapies can teach the substitution of one tic with another that is more acceptable. The use of relaxation techniques and/or biofeedback may help during prolonged periods of high stress.
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