Monday, September 28, 2015

Specific Language Impairment - Developmental Language Disorder and Abnormal EEG

EEG Abnormalities in Children with Speech and Language Impairment 

Bharati Mehta1 , V. K. Chawla2 , Manish Parakh3 , Poonam Parakh , Bharti Bhandari , Anoop Singh Gurjar 

ABSTRACT Introduction: Epilepsy, a chronic condition of recurrent seizures, affects language, but the extent and nature of the language disturbance varies widely according to the type, severity, and cause of the epilepsy. There is paucity of literature on the electroencephalographic abnormalities in children with speech and language impairment. The present study was therefore planned to find the association of epileptiform EEG abnormalities in children with speech and language impairment and if present, their localization and lateralization to the language areas of the brain that are present predominantly in the left hemisphere. Materials and Methods: The study was conducted on Paediatric patients having speech and language impairment (n=94, age-2 to 8 years) selected on the basis of detailed history and neurologic examination. Video Electroencephalography (EEG) was performed as per American Clinical Neurophysiology Society guidelines using 16 channel RMS computerized EEG machine for a minimum of 40 minutes to capture both wakefulness and sleep along with activation procedures like hyperventilation (if feasible) and photic stimulation. EEG was reviewed for any abnormal EEG background, benign variants, interictal epileptiform discharges and ictal discharges. Results: In our cohort, 19.7% boys and 22.2% girls presented with seizures in their infancy and this gender difference was found to be statistically significant (p<0 .05="" 41.3="" 47.9="" 73.6="" 94="" a="" abnormal="" abnormalities.="" abnormalities="" also="" although="" and="" are="" associated="" background="" brain="" children="" complement="" conclusion:="" current="" definite="" difference.="" discharges="" distinct="" each="" eeg="" epileptiform="" exclusively="" findings="" focal="" frequency="" from="" gender="" generalized="" h2="" hemisphere="" higher="" history="" imaging="" impairment.="" in="" included:="" interictal="" is="" isolation="" it="" language="" left="" multifocal="" no="" occurring="" of="" or="" other="" out="" p="" patients="" pattern="" presence="" recommend="" routine="" seen="" seizures="" significant="" solely="" speech="" study="" such="" that="" the="" them="" there="" to="" was="" we="" with="" without="">

Link here

Language regression is observed both in autistic regression and as part of acquired epileptic aphasia (Landau-Kleffner Syndrome). We prospectively identified 177 children with language regression at four major medical centers, and their clinical characteristics were recorded. Their mean age at regression was 22.8 months. The mean time-to-specialist referral was 38 months of age. Most children (88%) met criteria for autism or manifested autistic features. Males (P = 0.02) and children less than 3 years of age who regressed (P = 0.016) had a higher probability of developing autistic behaviors. Seizures were more common in children who regressed after they reached 3 years of age (P < 0.001), and children with seizures were less likely to have associated autistic regression (P < 0.001). Electroencephalogram abnormalities were reported in 37% of patients and were more common in children with seizures (P < 0.001). At last follow-up, language function was impaired in 88% of the children, although some improvement was noted in 57%. We conclude that the loss of previously acquired language at any age, even if that language only includes a few words or communicative gestures, is often associated with a more global regression in cognition and/or behavior and has serious implications for future function. Early identification and referral of these children is necessary to allow for diagnosis and intervention.

Sunday, September 20, 2015

Drinking energy drinks linked to traumatic brain injuries in teens

Drinking energy drinks is linked to traumatic brain injuries in teenagers.

Teens who reported a traumatic brain injury in the past year were seven times more likely to have consumed at least five energy drinks in the past week than those without a history of TBI, according to a study published in PLOS ONE.
Researchers also found that teens who reported sustaining a TBI within the past year were at least twice as likely to have consumed energy drinks mixed with alcohol than teens who reported sustaining a TBI more than a year previously.
"We've found a link between increased brain injuries and the consumption of energy drinks or energy drinks mixed with alcohol," said Dr. Michael Cusimano, a neurosurgeon at St. Michael's Hospital. "This is significant because energy drinks have previously been associated with general injuries, but not specifically with TBI."
Dr. Cusimano said energy drink consumption could interfere with recovery efforts for teens who have sustained a TBI. "Energy drinks, such a Red Bull and Rockstar, contain high levels of caffeine and change the chemical state of the body, which can prevent people from getting back on track after a TBI," said Dr. Cusimano. "Brain injuries among adolescents are particularly concerning because their brains are still developing."
At a time when energy drink consumption is rising among teens in Canada and the United States, the study also suggests that the caffeinated drinks are particularly linked with those who play sports.
"I think that energy drinks appeal to teens, especially athletes, because the drinks provide temporary benefits such as increased alertness, improved mood and enhanced mental and physical states," said Dr. Cusimano. "Advertisements for the drinks also often feature prominent athletes."
Teens who reported suffering a TBI in the past year while playing sports were twice as likely to consume energy drinks as teens who reported a TBI from other injuries in the same time period.
Data for the study was collected by the Centre for Addiction and Mental Health's 2013 Ontario Student Drug Use and Health Survey. Approximately 10,000 students ages 11 to 20 participated in the self-administered, in-classroom survey. TBI was defined as an injury resulting in the loss of consciousness for at least five minutes, or being hospitalized for at least one night.
"It is particularly concerning to see that teens who report a recent TBI are also twice as likely to report consuming energy drinks mixed with alcohol," said Dr. Robert Mann, senior scientist at the Centre for Addiction and Mental Health in Toronto and director of the OSDUHS. "While we cannot say this link is causal, it's a behaviour that could cause further injury and so we should be looking at this relationship closely in future research."
About 22 per cent of all students surveyed reported they'd experienced a TBI, with sports injuries accounting for almost half of TBI cases experienced in the past year.
Previous research at St. Michael's Hospital found that TBI is associated with poor academic performance, mental health issues, violence, substance abuse and aggression in both teens and adults -- factors that can interfere with rehabilitation, said Dr. Cusimano.
According to the new study, a better understanding of the link between TBI and energy drinks could help medical professionals, parents, teachers and coaches understand how to better prevent, diagnose and treat brain injuries.
Read more here

Children with issues in classroom may have sleep disorder

Children who show ADD or ADHD symptoms in the classroom may be experiencing a sleep disorder.

More parents are waking up to the fact that sleep disorders are more common than most of us think. Now the American Academy of Pediatrics and doctors continue to warn parents that sleep disorders can trick you into thinking you’re dealing with something else all together.
Dr. Akinyemi Ajayi, the Medical Director of Children’s Sleep Lab, says that when a child is tired and can’t focus in the classroom or they’re fidgeting to stay awake, a teacher sees that and may presume the child has ADD and ADHD.
Parents Garrett and Joey Myers had the same problem with their twin daughters Monica and Megan. The girls were never diagnosed with a learning disorder, and it was a journey of many doctor visits to figure out why there girls where having behavioral problems.
“It’s a never ending battle of what looks like eating disorder or anxiety or OCD,” said Garret Myers, the girls’ father.
As the parents visited one medical expert after the next, mom Joey Myers, tried to ask doctors if the twins could possibly have narcolepsy, like she was diagnosed with in adulthood. So finally, the Myers met Dr. Ajayi, who after a series of test, determined the twins did have narcolepsy.
The girls are now being treated at separate therapeutic boarding schools out of state. “They basically have to finish growing up,” said Garrett Myers. “They stopped and at 10-years old, they regressed.”
Now the parents are trying to educate others moms and dad to be vigilant if they feel their child might be experiencing problems because of a sleep disorder.
Read more here

Drinking caffeine in the evenings can cause a 40-minute delay in the circadian clock phase

A study shows that drinking caffeine in the evenings can have effects in a person's circadian clock such as a 40-minute phase delay.

It's no secret that slugging down caffeinated drinks in the evening can disrupt sleep.
But a new study led by the University of Colorado Boulder and the Medical Research Council's Laboratory of Molecular Biology in Cambridge, England shows for the first time that evening caffeine delays the internal circadian clock that tells us when to get ready for sleep and when to prepare to wake up. The research team showed the amount of caffeine in a double espresso or its equivalent three hours before bedtime induced a 40-minute phase delay in the roughly 24-hour human biological clock.
The study also showed for the first time how caffeine affects "cellular timekeeping" in the human body, said CU-Boulder Professor Kenneth Wright, who co-led the study with John O'Neill of the Medical Research Council's Laboratory of Molecular Biology (LMB) in Cambridge. While it has been known that caffeine influences circadian clocks of even primitive creatures like algae and fruit flies, the new study shows that the internal clocks in human cells can be impacted by caffeine intake.
"This is the first study to show that caffeine, the mostly widely used psychoactive drug in the world, has an influence on the human circadian clock," said Wright, a professor in CU-Boulder's Department of Integrative Physiology. "It also provides new and exciting insights into the effects of caffeine on human physiology."
A paper on the subject led by Wright and O'Neill is being published online in the Sept 16 issue of Science Translational Medicine.
For the study the team recruited five human subjects, three females and two males, who went though a double-blind, placebo-controlled 49-day protocol through CU-Boulder's Sleep and Chronobiology Laboratory, which is directed by Wright. The subjects were tested under four conditions: low light and a placebo pill; low light and the equivalent of a 200-milligram caffeine pill dependent on the subject's weight; bright light and a placebo pill; and bright light and the caffeine pill.
Saliva samples of each participant were tested periodically during the study for levels of the hormone melatonin, which is produced naturally by the pineal gland when directed to do so by the brain's "master clock." The master clock is re-set by exposure to light and coordinates cellular clocks throughout the human body. Melatonin levels in the blood increase to signal the onset of biological nighttime during each 24-hour period and decrease at the start of biological daytime, said Wright.
Those who took the caffeine pill under low-light conditions were found to have a roughly 40-minute delay in their nightly circadian rhythm compared to those who took the placebo pill under low light conditions, said Wright. The magnitude of delay from the caffeine dose was about half that of the delay induced in test subjects by a three-hour exposure to bright, overhead light that began at each person's normal bedtime.
The study also showed that bright light alone and bright light combined with caffeine induced circadian phase delays in the test subjects of about 85 minutes and 105 minutes respectively. There were no significant differences between the dim light/caffeine combination and the bright light/placebo combination. Nor were there significant differences between the bright light/placebo and bright light/caffeine combinations. The results may indicate a "ceiling" was reached in the phase delay of the human circadian clock due to the external factors, Wright said.
In addition, researchers at O'Neill's lab at the LMB in Cambridge used "reporter" genes that made cells glow when the clock genes were expressed to measure changes caused by caffeine. O'Neill's group showed that caffeine can block cell receptors of the neurotransmitter adenosine, which normally promotes sleep and suppresses arousal.
The results may help to explain why caffeine-drinking "night owls" go to bed later and wake up later and may have implications for the treatment of some circadian sleep-wake disorders, said Wright.
The new results could benefit travelers. Properly timed caffeine use could help shift the circadian clocks of those flying west over multiple time zones, said Wright.
In a 2013 study, Wright and his research team showed one week of camping in the Rocky Mountains with no artificial light, not even flashlights, synchronized the circadian clocks of the eight study subjects with the timing of sunrise and sunset.
Read more here

Six ways electronics disrupt neurophysiology and cause mood disturbance...

A really excellent piece sent to me by Ari Rotenberg. Late at night.....
Dr. Josh Rotenberg

Screentime Is Making Kids Moody, Crazy and Lazy

Computers at night upset physiology and cause sleep disorders...Dr Rotenberg
Children or teens who are “revved up” and prone to rages or—alternatively—who are depressed and apathetic have become disturbingly commonplace. Chronically irritable children are often in a state of abnormally high arousal, and may seem “wired and tired.” That is, they’re agitated but exhausted. Because chronically high arousal levels impact memory and the ability to relate, these kids are also likely to struggle academically and socially.
At some point, a child with these symptoms may be given a mental-health diagnosis such as major depressionbipolar disorder, or ADHD, and offered corresponding treatments, including therapy and medication. But often these treatments don’t work very well, and the downward spiral continues.

Wednesday, September 16, 2015

Forecast - A Chance of Protests at Memorial Hermann over woman arrested at OBGYN's office!

We are an independent practice and not owned by Memorial Hermann.

Yet, our main office is at Memorial City.

 If the forecast is "sunny with a chance of protests",  please leave early and use the covered parking lots to bypass any congestion.

Dr. Rotenberg

A Message from President & CEO Dan Wolterman

Dear Memorial Hermann Medical Staff Physician,

You may be aware of a recent incident regarding a patient being arrested at one of the Memorial Hermann Medical Group (MHMG) clinics. As a result, there has been some news coverage and online conversation that has inadvertently and unfortunately thrust Memorial Hermann into the immigration discussion in this country. As an affiliated physician of Memorial Hermann you should know the facts and truth about this situation: The patient's arrest was not about immigration or residency status.

The patient arrived at our clinic for routine care where she presented potentially false identification. For quality and safety reasons, our staff requests and verifies proper identification to ensure appropriate treatment. The patient was unable to provide another valid form of identification and in an effort to verify the authenticity of the suspicious driver's license, the office then called the licensing bureau of the Texas Department of Public Safety (DPS). DPS instructed our staff to contact local law enforcement to validate the driver's license number. This inquiry confirmed a false identification. Local law enforcement took this information and made the decision to arrest the patient. To our knowledge, this is a unique event in Memorial Hermann's history.

We did not ask for this individual to be arrested. This is a decision that was made by law enforcement, including the District Attorney's office. We did not press charges. We simply called DPS to question a potentially false identification.

At Memorial Hermann, our responsibility and commitment is to care for all patients - regardless of their race, ethnicity, color, religion, immigration or residency status. As you know, we do not ask our patients about residency or immigration status nor do we report an undocumented patient to law enforcement.

Nevertheless, in the coming days, we anticipate more attention to this issue, including a planned protest at our corporate offices at Memorial City on Thursday. Due to the anticipated protest, additional media attention, and heightened emotion around the immigration issue, we are asking our employees to be alert and vigilant about suspicious activity at their facility. Our concern is for the safety of our patients and staff. Please immediately contact security if you have a concern.

If approached by the news media or if you receive inquiries from the public, do not respond and immediately email the Corporate Communications team Please be mindful of our social media policy, as well.

We appreciate the great care and compassion you demonstrate daily to our patients and their families. You should be proud of our 108-year history of providing exceptional care to all patients in the region we serve. Annually, we treat approximately 2 million patients - many of whom are uninsured and/or potentially undocumented. Indeed, this past year, we provided more than $430 million towards improving access to health care for thousands of families in our region. We are a System that cares for all people.

What happened to the patient is unfortunate. We also appreciate the sensitivity of this matter. As such, we consider this an opportunity to evaluate our processes and if necessary, improve them. Thank you for all that you do. You are the reason our System is nationally recognized for providing the highest quality and safest care in the country.


Tuesday, September 08, 2015

Chromosomal Microarray Analysis for Intellectual Disabilities. What is a Microarray?

Chromosomal Microarray Analysis for Intellectual Disabilities

What is the need to strive for a genetic diagnosis?
A diagnostic chromosomal microarray will provide the medical care team, family, and patient with a firm diagnosis.

  • In several instances, ineffective or contraindicated therapies need not be initiated or stopped if they are already underway. The focus could then shift to appropriate medical care. 
  • In some children educational planning may be changed based on the test results. 
  • Some families might choose to limit medical care to palliative measures based on a diagnosis associated with a poor prognosis. 
  • The results of family testing to determine risk for future children can strongly influence reproductive choices, both positively when the risk appears low and negatively when the risk appears high. 
  • Establishing a specific genetic diagnosis by microarray can render moot extensive testing that most patients otherwise undergo for the diagnostic evaluation of ID: blood and urine tests for metabolic disorders, multiple brain MRIs requiring sedation, electroencephalograms, lumbar punctures for metabolic tests of spinal fluid, and skin and muscle biopsies. 
  • A positive microarray, especially when obtained early in the workup of a patient, could reduce both individual and societal costs associated with testing and medical care. (Michelson 2011; Tirosh & Jaffe 2011; Van Karnebeek & Stockler 2012) 

Microarray testing is widely available and its cost has been steadily declining. It is foreseeable that, as the cost of full exome sequencing comes down, whole exome testing may be the best way to perform the primary sequencing of the chromosomes, with the microarray remaining the best way to detect CNVs. The full interpretation of genomic testing would consist of an abnormal microarray, or a normal microarray in conjunction with whole exome sequencing. As technology moves forward, this prediction will require refinement.

Neurologists and geneticists tend to order CMA testing more frequently than other specialists. (Coulter et al. 2011) Of 49 respondents to a 2012 questionnaire-based survey sent to members of the AAN Child Neurology Section, all but one ordered microarray testing on a routine basis. 4 commented that they would refer the patient to colleagues in genetic medicine also to decide if the test should be ordered. Their reasons for referral were that either the approval process was easier for the medical geneticist or that their institution required a geneticist’s prior approval. Clinical utility, comfort with ordering and interpreting the test and ease of obtaining insurance coverage were the detriments for ordering the test. Unfamiliarity with the test, its interpretation, and difficulty of obtaining insurance coverage in some regions were the reasons for not ordering the tests. In one medical center, where more than a dozen health care providers evaluated patients with ID and dysmorphism, uninfluenced by insurance coverage, microarray ordering and testing frequencies varied from “almost always” to “never.” (Unpublished AAN survey 2012) This survey result, although limited by a 15% response rate, accords with the general experience indicating that the application of this technology still varies much. Large longitudinal studies of test ordering practices have not yet been done. This is one reason for the unavailability of data associated with utilization, costs and benefits. However, small sample studies have shown that positive test findings result in significant changes in medical care. (Coulter et al. 2011; Saam et al. 2008)


Nature Clinical Practice Neurology (2006) 2, 147-158
Received 13 July 2005 | Accepted 9 January 2006

Technology Insight: querying the genome with microarrays—progress and hope for neurological disease

Thursday, September 03, 2015

Management of Degenerative Cerebellar Disorders & Ataxia - Consensus Paper!

Here is a great summary of medical treatments for ataxia and cerebellar disorders. There is a lot of work to be done. JR

Consensus Paper: Management of Degenerative Cerebellar Disorders


Treatment of motor symptoms of degenerative cerebellar ataxia remains difficult. Yet there are recent developments that are likely to lead to significant improvements in the future. Most desirable would be a causative treatment of the underlying cerebellar disease. This is currently available only for a very small subset of cerebellar ataxias with known metabolic dysfunction. However, increasing knowledge of the pathophysiology of hereditary ataxia should lead to an increasing number of medically sensible drug trials. In this paper, data from recent drug trials in patients with recessive and dominant cerebellar ataxias will be summarized. 
There is consensus that up to date, no medication has been proven effective. 
Aminopyridines and acetazolamide are the only exception, which are beneficial in patients with episodic ataxia type 2. Aminopyridines are also effective in a subset of patients presenting with downbeat nystagmus. As such, all authors agreed that the mainstays of treatment of degenerative cerebellar ataxia are currently physiotherapy, occupational therapy, and speech therapy. 
For many years, well-controlled rehabilitation studies in patients with cerebellar ataxia were lacking. Data of recently published studies show that coordinative training improves motor function in both adult and juvenile patients with cerebellar degeneration. Given the well-known contribution of the cerebellum to motor learning, possible mechanisms underlying improvement will be outlined. There is consensus that evidence-based guidelines for the physiotherapy of degenerative cerebellar ataxia need to be developed. Future developments in physiotherapeutical interventions will be discussed including application of non-invasive brain stimulation.
Keywords: Cerebellum, Cerebellar ataxia, Motor rehabilitation, Physiotherapy, Drug therapy

Ampyra for ataxia?  Literature references

11. Strupp M, Kalla R, Dichgans M, Freilinger T, Glasauer S, Brandt T. Treatment of episodic ataxia type 2 with the potassium channel blocker 4-aminopyridine. Neurology. 2004;62:1623–5. [PubMed]
12. Alvina K, Khodakhah K. The therapeutic mode of action of 4-aminopyridine in cerebellar ataxia. J Neurosci. 2010;30:7258–68. [PMC free article] [PubMed]
13. Weisz CJ, Raike RS, Soria-Jasso LE, Hess EJ. Potassium channel blockers inhibit the triggers of attacks in the calcium channel mouse mutant tottering. J Neurosci. 2005;25:4141–5. [PubMed]
14. Claassen J, Teufel J, Kalla R, Spiegel R, Strupp M. Effects of dalfampridine on attacks in patients with episodic ataxia type 2: an observational study. J Neurol. 2013;260:668–9. [PubMed]
15. Hufner K, Stephan T, Kalla R, Deutschlander A, Wagner J, Holtmannspotter M, et al. Structural and functional MRIs disclose cerebellar pathologies in idiopathic downbeat nystagmus. Neurology.2007;69:1128–35. [PubMed]
16. Wagner JN, Glaser M, Brandt T, Strupp M. Downbeat nystagmus: aetiology and comorbidity in 117 patients. J Neurol Neurosurg Psychiatry. 2008;79:672–7. [PubMed]
17. Kalla R, Deutschlander A, Hufner K, Stephan T, Jahn K, Glasauer S, et al. Detection of floccular hypometabolism in downbeat nystagmus by fMRI. Neurology. 2006;66:281–3. [PubMed]
18. Kalla R, Glasauer S, Buttner U, Brandt T, Strupp M. 4-Aminopyridine restores vertical and horizontal neural integrator function in downbeat nystagmus. Brain. 2007;130:2441–51. [PubMed]
19. Tsunemi T, Ishikawa K, Tsukui K, Sumi T, Kitamura K, Mizusawa H. The effect of 3,4-diaminopyridine on the patients with hereditary pure cerebellar ataxia. J Neurol Sci. 2010;292:81–4.[PubMed]
20. Kalla R, Spiegel R, Claassen J, Bardins S, Hahn A, Schneider E, et al. Comparison of 10-mg doses of 4-aminopyridine and 3,4-diaminopyridine for the treatment of downbeat nystagmus. J Neuroophthalmol.2011;31:320–5. [PubMed]
21. Judge SI, Bever CT., Jr Potassium channel blockers in multiple sclerosis: neuronal Kv channels and effects of symptomatic treatment. Pharmcol Ther. 2006;111:224–59. [PubMed]
22. Claassen J, Spiegel R, Kalla R, Faldon M, Kennard C, Danchaivijitr C, et al. A randomised double-blind, cross-over trial of 4-aminopyridine for downbeat nystagmus—effects on slowphase eye velocity, postural stability, locomotion and symptoms. J Neurol Neurosurg Psychiatry. 2013 doi: 10.1136/jnnp-2012-304736. [PubMed] [Cross Ref]
23. Feil K, Claaβen J, Bardins S, Teufel J, Krafczyk S, Schneider E, et al. Effect of chlorzoxazone in patients with downbeat nystagmus: a pilot trial. Neurology. 2013;81:1152–8. [PubMed]
24. Averbuch-Heller L, Tusa RJ, Fuhry L, Rottach KG, Ganser GL, Heide W, et al. A double-blind controlled study of gabapentin and baclofen as treatment for acquired nystagmus. Ann Neurol.1997;41:818–25. [PubMed]
25. Schniepp R, Jakl V, Wuehr M, Havla J, Kumpfel T, Dieterich M, et al. Treatment with 4-aminopyridine improves upper limb tremor of a patient with multiple sclerosis: a video case report. Mult Scler. 2013;19:506–8. [PubMed]
26. Schniepp R, Wuehr M, Ackl N, Danek A, Brandt T, Strupp M, et al. 4-Aminopyridine improves gait variability in cerebellar ataxia due to CACNA 1A mutation. J Neurol. 2011;258:1708–11. [PubMed]
27. Schniepp R, Wuehr M, Neuhaeusser M, Benecke AK, Adrion C, Brandt T, et al. 4-Aminopyridine and cerebellar gait: a retrospective case series. J Neurol. 2012;259:2491–3. [PubMed]
28. Giordano I, Bogdanow M, Jacobi H, Jahn K, Minnerop M, Schoels L, et al. Experience in a short-term trial with 4-aminopyridine in cerebellar ataxia. J Neurol. 2013;260:2175–6. [PubMed]
29. Etzion Y, Grossman Y. Highly 4-aminopyridine sensitive delayed rectifier current modulates the excitability of guinea pig cerebellar Purkinje cells. Exp Brain Res. 2001;139:419–25. [PubMed]
30. Hourez R, Servais L, Orduz D, Gall D, Millard I, de Kerchove d'Exaerde A, et al. Aminopyridines correct early dysfunction and delay neurodegeneration in a mouse model of spinocerebellar ataxia type 1. J Neurosci. 2011;31:11795–807. [PubMed]

Must listen for anyone who works with or knows anyone with autism!

Great quotes:

"Not everything that steps out of line or is unusual is inferior."  - Hans Asperger

When you have met one person with autism, you have met one person with autism.

- JR

'NeuroTribes' Examines The History — And Myths — Of The Autism Spectrum

In 1938, an Austrian pediatrician named Hans Asperger gave the first public talk on autism in history. Asperger was speaking to an audience of Nazis, and he feared that his patients — children who fell onto what we now call the autism spectrum — were in danger of being sent to Nazi extermination camps.
As Asperger spoke, he highlighted his "most promising" patients, a notion that would stick with the autistic spectrum for decades to come.
"That is where the idea of so-called high-functioning versus low-functioning autistic people comes from really — it comes from Asperger's attempt to save the lives of the children in his clinic," science writer Steve Silberman tells Fresh Air's Terry Gross.
Silberman chronicles the history of autism and examines some of the myths surrounding our current understanding of the condition in his new book,NeuroTribes. Along the way, he revisits Asperger's calculated efforts to save his patients.
Link to story here