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Confirming the Diagnosis and Treating Sleep Apnea


 Once you have been given a tentative diagnosis of sleep apnea or a similar sleep/breathing disorder, an all-night sleep test should be arranged. Proper testing for sleep disorders is important because several sleep disorders have superficial similarities and might be confused with sleep apnea or be incorrectly diagnosed if testing is not done properly. An incorrect diagnosis, leading to incorrect treatment, can be a serious error. For example, medications that are often prescribed for narcolepsy or insomnia can actually worsen sleep apnea, so a correct diagnosis is very important.

Narcolepsy is a sleep disorder in which people have irresistible “sleep attacks” at inappropriate times, somewhat as in sleep apnea. However, narcolepsy is a distinct neurologic disorder with its own characteristic symptoms (cataplexy, sleep paralysis, and hypnagogic hallucinations) not found in sleep apnea.

Insomnia is sometimes confused with sleep apnea. Insomnia has numerous causes, and only a few people who have insomnia also have sleep apnea.

Two other sleep disorders sometimes occur alone or along with sleep apnea. These are periodic limb movement in sleep (PLMS, also called periodic leg movement disorder, PLMD, or nocturnal myoclonus) and restless leg syndrome (RLS). Again, appropriate testing by an experienced sleep disorders specialist will avoid confusing one sleep disorder with another.

An overnight sleep test will:

1. Confirm whether you actually have sleep apnea or another form of sleep-disordered breathing
2. Determine the type of sleep/breathing disorder, which must be known in order to select the appropriate treatment
3. Rule out other 
sleep disorders


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Electrophysiological evidence for abnormal preparatory states and inhibitory processing in adult ADHD



Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder that starts in childhood and frequently persists in adults. Several theories postulate deficits in ADHD that have effects across many executive functions or in more narrowly defined aspects, such as response inhibition.


Electrophysiological studies on children, however, indicate that ADHD is not associated with a core deficit of response inhibition, as abnormal inhibitory processing is typically preceded or accompanied by other processing deficits. It is not yet known if this pattern of abnormal processing is evident in adult ADHD. 


Methods: The objective of this paper was to investigate event-related potential indices of preparatory states and subsequent response inhibition processing in adults with ADHD.


Two cued continuous performance tasks were presented to 21 adults meeting current criteria for adult ADHD and combined type ADHD in childhood, and 20 controls. 


Results: The ADHD group exhibited significantly weaker orienting attention to cues, cognitive preparation processes and inhibitory processing. In addition, we observed a strong correlation between the resources allocated to orienting to cues and the strength of the subsequent response strength control processes, suggesting that orienting deficits partly predict and determine response control deficits in ADHD. 


Conclusions: These findings closely resemble those previously found in children with ADHD, which indicate that there is not a core response inhibition deficit in ADHD.


These findings therefore suggest the possibility of developmental stability into adulthood of the underlying abnormal processes in ADHD.


Author: Grainne McLoughlinBjoern AlbrechtTobias BanaschewskiAribert RothenbergerDaniel BrandeisPhilip AshersonJonna Kuntsi

Credits/Source: Behavioral and Brain Functions 2010, 6:66

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POE05 A low creatinine in developmental delay, epilepsy and movement disorders--does it matter?


J Neurol Neurosurg Psychiatry. 2010 Nov;81(11):e47.

POE05 A low creatinine in developmental delay, epilepsy and movement disorders--does it matter?

Hinnell C, Rahman Y, Alkufri F, Samuel M, Turner C, Dalton N, Nashef L.


To highlight creatine deficiency syndromes (CDS) as rare but potentially partially treatable causes of common early neurologic presentations by describing clinical and metabolic characteristics associated with guanidinoacetate methyltransferase (GAMT) deficiency in a family. CDS are inborn errors of creatine metabolism manifesting with developmental delay, epilepsy, movement disorder and behavioural problems. Basic laboratory results, such as low plasma creatinine, can suggest these disorders leading to further metabolic testing, although low-normal "routine" levels may mislead. Oral creatine substitution can improve epilepsy, movement disorder and behaviour, but not intellectual ability, in some patients with GAMT deficiency. A case report suggests presymptomatic treatment may prevent disease manifestations. Two sisters, children of third cousins, were diagnosed in their early twenties after numerous previous negative investigations for other disorders. Both had severely delayed developmental motor and cognitive milestones, symptomatic epilepsy and dystonia, severe and generalised in the older sister. Low plasma creatinine led to further testing and GAMT deficiency was identified. Our case highlights the importance of intermittently re-investigating undiagnosed patients and considering metabolic diagnoses in patients with developmental delay, epilepsy and movement disorder. Early recognition is essential as appropriate therapy may improve certain clinical features.

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Dystonia Medical Research Foundation Fellowships


Dystonia Medical Research Foundation Fellowships


Grantor:Dystonia Medical Research Foundation

Region:All Regions




Dystonia Medical Research Foundation Fellowships

The Dystonia Medical Research Foundation (DMRF) encourages and supports research related to the causes, mechanisms, prevention, and treatment of all forms of dystonia, the third most common movement disorder.

A two-year Fellowship is designed to assist post-doctoral fellows establish careers in research relevant to dystonia.

Funding for fellowships is $50,000 per year for two years.

The deadline for all 2011 applications is December 15, 2010.

Please contact Jody Roosevelt, Grants Manager, at 312-447-5150 or jroosevelt@dystonia-foundation.org if you have any questions.

Dystonia Medical Research FoundationOne East Wacker Drive, Suite 2810
Chicago, Illinois 60601-1905
Phone: 312-755-0198Toll free: 800-377-DYST (3978)
Fax: 312-803-0138
Email: dystonia@dystonia-foundation.org


Categories:Career Development, Chronic Diseases, Clinical Research, Disease-Specific Research, Fellowships, Inheritable Disorders, Motor Disorders, Movement Disorders, Muscle Disorders, Neurology, Neuromuscular, Rare Disorders, Brain, Brain Disorders

Audience:Junior Investigator, Junior Researcher, Junior Scientist, New Investigator, New Researcher, Postdoctoral Fellow, Young Investigator, Young Scientist

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