Talk:Landau–Kleffner syndrome

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I marked this as a copyvio of this NINDS page, but according to their disclaimer:

All NINDS-prepared information is in the public domain and may be freely copied. Credit to the NINDS or the NIH is appreciated.

So I have added it to the Sources section of the article.

--TheParanoidOne 05:15, 14 July 2005 (UTC)[reply]

This article isn't in terrible shape. Apart from a redirect from

This article is likely to get significantly more traffic and attention going forward since Jenny McCarthys child (famous for being a focal point of the immunization->autism argument) may have been diagnosed with LKS (according to Time mag). Gaijin42 (talk) 16:22, 4 January 2014 (UTC)[reply]

What does "infantile" mean as a medical term? I thought it had to do with before the development of speech (in-fans). --Richardson mcphillips (talk) 19:21, 16 March 2014 (UTC)[reply]

I think it just means 'in or of a child' --2607:FEA8:D5DF:1AF0:AD20:B600:FF9E:4E34 (talk) 13:01, 11 May 2021 (UTC)[reply]

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Given the rarity of this disorder and having a confirmed diagnosis I would like to offer my two cents.

For me, I have a calcified white matter lesion originating in the falx cerebri of my left hemisphere dorsolateral prefrontal cortex. This lesion, at the very least, is in direct contact with the meningitis of the dorsolateral prefrontal cortex in my right hemisphere, and we suspect it has actually fused the two hemispheres together via the cellular fusion wound healing process. It causes conductive coupling of the neural network signaling across the two hemispheres, i.g. dysexecutive syndrome, akin to that seen in a layer 2 broadcast storm within a computer ethernet network after someone accidentally plugs a patch cable into the wrong switch port that causes a bridge loop. Since the white matter bridge is calcified, it responds favorably to treatment with n-type calcium channel blockers. To date, it is best managed by taking a very high dose of levetiracetam prior to bedtime, but it also responds to treatment with lamotrigine, valproate, phenylpiracetam, gapentin, piracetam, aniracetam, et. al. My original diagnosis prior to treatment was ASD with level 3 support needs, with treatment, I'm still disabled, but I'm now able to live by myself semi-independently. Transcranial Magnetic Stimulation was also helpful, ideally both treatments should be done at the same time. Temazepam was instrumental in helping to progressively stop seizure induced nocturnal enuresis. There is also a central apnea component of some type, sleep studies showed high respiratory disturbance index due to periodic and variable breathing, a ResMed AirCurve 10 ASV was prescribed after failing to respond to traditional obstructive apnea protocols, the backup breath that the ASVAuto protocol provides is essential for mitigating oxygen desaturation during episodes of periodic breathing.

Additionally memantine is helpful, we have not yet tried a high dose regimen as described in the GluN2A–L812M study, but response to this medication suggests the possibility of a GRIN gene mutation. Past experimentation with sarcosine and zinc monomethionine supplementation seemed to be mildly help, but at the time I was taking them there were too many other confounders to make any strong conclustions. Low dose prednisone has also been helpful in the past, but I'm not currently on this medication.

Idiopathic hyperprolactinemia was documented on countless occasions after waking up, as well as gynecomastia which eventually had to be surgically removed due to concerns about cancerous growth, biopsy showed the development of glandular tissue, which is suggestive of chronic hyperprolactinemia during the developmental stages of childhood. As a consequence of the hyperprolactinemia, this also caused hypogonadism (low testosterone, high estradiol ratio) and other down stream endocrine problems such as sub-fertility.

Frontal Intermittent Rhythmic Delta Activity was noted on a standard EEG test. I have never had an EEG based polysomnography test performed due to the costs involved with in-patient testing and not having access to physicians who have the appropriate training, but CSWS and/or NFLE are strongly suspected.