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Let's see if I can do a bigger intro now, and then post for now -- I may lay on the couch as oldest son is quieter now. We lived with his parents for a while after we got married until we got on our feet right after college.
9 months later (what a nice long maternity leave!) I got my wish and we both got jobs within a week of each other.
3 years later Rog was doing great going to college and I also had my home business built by this time, where I was now (by 2000) working almost full time at home doing transcription for different companies. Sometime soon I will finish the history I had started before, about meeting my wonderful hubby, etc.!
Been searching around for different additional friends' diaries to read -- it's fun to see many different people and their interests. Hi COLLEEN - think you're the only reader I have right now -- hope you are feeling good today -- note from 2006 - this is a different Colleen than my daughterA?a‚¬A¦. We just have been so broke for so long that it feels good to be able to pay the bills and having more sounds so good. A little less than a month ago after good old AF was over dh and I had time to get friendly (which is rare!) and here I had all these weird symptoms all month and thought perhaps I was pregnant! Set up live journal for dh too as he was mentioning he wanted to do some blogging about our autistic son, etc. I have such mixed emotions about all this -- I feel proud of myself that I pulled myself together with all our home confusion and WAS able to make a full time job work out for 5 months. Financially it's scary; however, we've been BOTH jobless before, even at the same time, and made it through. So I'm sad I didn't make this company happy, and that they're angry and disappointed in me for missing so much time, but also am relieved in a way to be out of the rat race.
RJ had speech eval today and they want us to closely watch him and work with him a LOT as he may be a little behind. I have accomplished many household tasks -- organized many cabinets and cupboards, rearranged living room, etc. Well, so I'm the busy SAHM and still hope to go back to college, but don't know when that will be. I am trying to lose weight again -- I have been overweight since a child but on and off diets. So, we talked about the book I wrote in high school, that I want to complete but was flabbergasted that I haven't worked on since 1996! He was proud of me that I'm on a daily cleaning schedule now, and that I'm not adding 100 new things to my list.
I've seen this survey several times and wanted to do it since I have NO surveys in my diary, though it's probably written for people much younger than me!
Between 5 & 7 (baby is early riser AND I have to be up early to get oldest ready for bus. I already play guitar -- perhaps I would like to learn the piano with TWO hands instead of one!!
Aldi's bags, a stroller, extra clothes, probably some food, books we were taking to Good Will and kept some in the trunk because they were written in workbooks and we have to throw them out (they don't take those). In '99 I joined a diet system called "Weigh Down" and I followed through my pregnancy and nursing as well. Chris had to have surgery on his ear on Wednesday because he hit it so hard he got cauliflower ear.
17 The righteous cry, and the LORD heareth, and delivereth them out of all their troubles.
18 The LORD is nigh unto them that are of a broken heart; and saveth such as be of a contrite spirit. 19 Many are the afflictions of the righteous: but the LORD delivereth him out of them all. I pray that Chris will be delivered from this ear problem with no damage or further danger. Of children with sensorineural hearing loss of any type, between 11-41% of them have inner abnormalities seen on CT.
Before we start talking about individual syndromes, inherited deafness is usually symmetrical and bilateral, nearly always sensorineural, and usually more severe at high frequencies.
Barakat syndrome, also known as HDR syndrome, is an inherited condition characterized by hypoparathyroidism, sensorineural deafness and renal disease (Barakat et al in 1977). Large Vestibular Aqueduct Syndrome (LVAS) also known as EVA (enlarged vestibular aqueduct).
About 60% of mutations in the SLC26A4 gene known to cause Pendred syndrome can be detected with genetic testing.


Although the SMA's are not generally associated with hearing symptoms, a recent report suggests that the disorder caused by a mutation in TRPV4 can induce a neuropathy as well as hearing loss (Oonk et al, 2014). Waardenburg syndrome (WS) is a largely autosomal dominant disorder characterised by pigmentary anomalies of the skin, hairs, eyes and various defects of other neural crest derived tissues (Read and Newton, 1997). The displacement of the canthus, dystropia cantorum, is the distinguishing feature between WS1 (has it) and WS2 (doesn't have it). Wolfram Syndrome, first described in 1938, is also known as DIDMOAD (diabetes insipidus, diabetes mellitus, optic atrophy, deafness).
Delayed onset of hearing loss is common -- infants with CMV and normal hearing at birth should be monitored for 6 years. There are also some deformities of the membranous labyrinth -- as for example the very common Schiebe deformity (pars inferior -- cochlea and saccule).
One would think that the VEMP test would be a good method of detecting the Schiebe deformity, as the VEMP is sensitive to saccule disturbances.
Unusually sized openings between the inner ear and the brain (internal auditory meatus) are usually associated with other bone abnormalities (surprise !). Li Y1, Yang J, Liu J, Wu H.Restudy of malformations of the internal auditory meatus, cochlear nerve canal and cochlear nerve. Oonk AM1, Ekker MS2, Huygen PL3, Kunst HP3, Kremer H4, Schelhaas JJ5, Pennings RJ3.] Intrafamilial Variable Hearing Loss in TRPV4 Induced Spinal Muscular Atrophy.
Email address must have at least 0 and no more than 256 characters.The value of the Email address field is not valid. Two surgical approaches have been used - superior canal resurfacing and superior canal plugging.
Middle fossa craniotomy is a safe surgical procedure and is the most common approach used to repair SCD. If the skull base or tegmen is very low it can be difficult to safely reach the superior canal safely with a transmastoid approach to create two labyrinthotomies (as the SCD is not directly repaired) and then plug these two holes to indirectly repair the defect.
Ideally, the transmastoid approach may be useful for a patient that has SCD and a skull base or tegmen that is NOT low-lying and has no other associated holes or brain herniating into the ear. This patient complained of chronic dysequilibrium and episodic dizziness, worsened with straining and loud noises.
Serial audiograms before surgery showed a progressive severe sensorineural hearing loss on the left ear with a mild to moderate conductive component in the low frequencies, and present stapedial, or acoustic reflexes.
Vestibular Evoked Myogenic Potential Testing (VEMP) revealed markedly decreased thresholds in the left ear (50 to 60dB using tone burst testing), compared with the right (80 to 90 dB). ABOVE: Temporal bone CT scans of the right (A,C) and left (B,D) superior semicircular canals. This patient was followed conservatively for several months with vestibular suppressants but her symptoms worsened. A 4-5mm widely dehiscent SSC was encountered intraoperatively and was plugged with bone wax. Within about one month following her surgery, she noticed a complete resolution of her dizziness with improvement in her conductive hearing loss.
Audiogram, right: Postop hearing test showing closure of her air-bone gap following SCD plugging. Below: 3-D reconstruction, lateral skull CT, showing the approximate size and shape of the middle fossa craniotomy needed to expose and repair a left-sided SCD.
Photo 1: middle fossa craniotomy performed, centered over the external auditory meatus, approximately 4 x 5cm.
Photo 3: bone paste, harvested while turning the middle fossa craniotomy bone flap, is used to resurface the plugged superior semicircular canal. Photo 5: split calverial bone graft followed by a second piece of fascia is used to resurface the remaining skull base floor. Not shown: once the skull base reconstruction is complete, a mini-titanium plate cranioplasty is performed, followed by multiple layer tissue and skin closure. The multi-disciplinary team of pediatric specialists and caregivers stands ready to help achieve the best outcome possible. In children who are deemed likely to have an inner ear abnormality and who are sent for MRI scan, about 40% have abnormalities (McClay et al, 2008). In other words, although there are many many more papers about genetic syndromes than non-syndrome deafness, and lots more text on this page, these conditions that are the subject of so much discussion, are just a little piece to the big genetic hearing loss puzzle. WS1 is mostly caused by PAX3 mutations, while MITF, SNAI2, and SOX10 mutations are associated with WS2.
Mutations of EDNRB, EDN3 and SOX10 genes are responsible for Waardenburg syndrome type IV (Otreba et al, 2013) .
According to Plantinga et al (2008), all patients had similar sensorineural hearing loss with a gently downsloping pattern.


The organ of Corti, particularly the basal turn of the cochlea and adjacent ganglion cells, is affected most prominently.
Ther reason is that these deformities cannot be diagnosed on CT scan, as CT scans are not able to define abnormalities of the membranous labyrinth. Screening of SLC26A4, FOXI1, KCNJ10, and GJB2 in Bilateral Deafness Patients with Inner Ear Malformation. Although theoretically less traumatic to the membraneous labyrinth, resurfacing techniques have led to recurrent symptoms secondary to shifting or resorption of the bone and fascia reconstruction. In some cases, the SCD may be located along the SIDE of the canal (Case #4) and not on the TOP, as seen in most classic cases of SCDS. These were high resolution CT scans reformatted to the planes of Stenver (A,B) and Poschel (C,D).
A big concern was that she was deaf in the right ear since birth, and so there was great reluctance to offer a left sided SCD repair. Because the surrounding tegmen (skull base) is often very thin or also dehiscence, a bone graft was used to reconstruct the floor around and on top of the plugged canal.
The tegmen represents the floor of the middle fossa, which is exposed using an extradural dissection to reveal the dehiscent left superior semicircular canal.
Marker analysis enables identification of the region of the genome where the disease gene lies. Of course, this does not mean that 40% of all deaf children will have MRI abnormalties, but rather 40% of those who are thought by their doctors to have an MRI abnormality, and who are sent for an MRI, have MRI abnormalities. It is associated with congenital anomalies of all three parts of the ear (external, middle and inner ear) as well as the IAC and vestibular aqueduct (see below). Roughly two thirds of the Turner's population has hearing loss, about evenly split between sensorineural and conductive types (Ingeborg et al, 2005). More than 100 different disease-causing mutations have been reported in many ethnic groups(Chen et al, 2010). Hearing loss is most notable with higher frequencies, while low-frequency hearing is relatively preserved. Plugging with bone wax, bone paste, or fascia has been more commonly used to create a stable seal of the dehiscent superior semicircular canal. The craniotomy approach is ideal to 1) visual the SCD directly and 2) repair the tegmen defect(s) directly using bone and fascia.
If the defect is located on the side of the canal away from the surgeon (posterior-medial), the SCD may be more difficult to visualize using a craniotomy approach.
She notes an extremely violent episode of vertigo, in the vertical plane, during child birth. A very thin, but intact bony covering is see over the right superior semicircular canal (A,C) compared with a dehiscent left superior semicircular canal (B,D). However she could no longer care for her young children and was unable to function normally, and so after careful counseling, she elected to proceed with a surgical repair of her left SCD via a middle fossa craniotomy approach. I'm just not sure I'm now going to send back him to day care at all right now - may just work with him at home intensely for awhile.
In other words, it means that the abnormal rate for clinicians at the location where this study was done (Dallas), is about 40%.
It seems likely that outside of academic settings, cookie-bite hearing patterns are even more likely to be associated with inherited hearing loss. Renal disease includes nephrotic syndrome, renal dysplasia, hypoplasia or aplasia, chronic renal failure, hematuria, proteinuria and others. Pendred is associated with large vestibular aqueduct syndrome (see above) as well as Mondini (see below). The SOX10 mutation is also involved in the Kallman syndrome with deafness (Pingault et al, 2015). She has since had hearing loss, autophony, and sensitivity to loud noises and pressure on this left ear. Note that many persons with thyroid problems have Meniere's disease (Brenner et al, 2004), and thus LVAS, Meniere's and Pendred syndrome may all be interconnected. The MITF (microphthalmia transcription factor) is related to the melanogenesis process (i.e. Mom." But I don't really see how we can both work full time right now - I really think once he finds the job he really wants to go for, and gets it, that I will (at least eventually) have to quit working, or the balance will fail.



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