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The task force recognized that some patients with PCOS may demonstrate regular ovulation at the time of their evaluation, the so-called ovulatory PCOS ( 79 , 80 ). However, it was noted that patients with ovulatory PCOS constituted a minority of the PCOS population and had less severe androgenic and metabolic features than anovulatory women with PCOS. It was also recognized that there exist few data regarding the long-term maintenance of ovulation in women with ovulatory PCOS. Nonetheless, the task force recognized that there were persuasive, albeit limited, data to suggest that hyperandrogenic ovulatory women with polycystic ovaries had some degree of metabolic dysfunction and were amenable to the inclusion of this phenotype as a form of PCOS.

A history of regular predictable vaginal bleeding in a patient without clinical signs of hyperandrogenism can be used as strong evidence of normal ovulation. Alternatively, a history of regular menstrual cycles in patients who demonstrate hyperandrogenic features ( e.g. hirsutism) could not be relied on as evidence of normal ovulation because up to 40% of these women have oligoanovulation when examined more carefully. In these patients, confirmation of ovulatory function by more objective means is required.

Although the task force recognized that specific androgen excess or other endocrine disorders needed to be excluded when establishing the diagnosis of PCOS, it also recognized the validity of tailoring testing to reflect the prevalence of these disorders in the population being studied.

The task force noted that the presence of obesity, insulin resistance, and hyperinsulinism and increased LH levels or an LH to FSH ratio, whereas observed in a significant fraction of patients, should not be used as part of the definition of PCOS.

Notwithstanding the above recommendations, the writing committee acknowledged that two of its members considered the possibility that there are forms of PCOS without overt evidence of hyperandrogenism and that may be associated with metabolic abnormalities and morbidity. However, these investigators also recognized, as did the committee as a whole, that more data are required before validating this supposition. For example, a recent study ( 81 ) noted that women with oligoanovulation and polycystic ovaries but without evidence of hyperandrogenism (n = 66) had basal insulin levels, the principal metabolic parameter assessed, similar to controls and lower than patients with hyperandrogenemia and oligoanovulation, with (n = 246) or without (n = 27) polycystic ovaries, or those with hyperandrogenemia and polycystic ovaries but without oligoanovulation (n = 67).

Based on the above review of the available data, it is the view of the AES Task Force on the Phenotype of PCOS that there should be acceptance of the original NIH/National Institute of Child Health and Human Disease criteria of 1990 with some modifications, taking into consideration the opinion expressed in the proceedings of the 2003 Rotterdam conference ( Fig. 1 ). Considering the four features of ovulatory dysfunction, hirsutism, hyperandrogenemia, and polycystic ovaries, the task force identified nine different phenotypes that could be considered as being PCOS with currently available evidence ( Table 5 ).

The classical SD syndrome rarely forms part of a more widespread disorder (Hodges et al ., 1992 ; Rossor et al ., 2000 ). However, a ‘mixed’ progressive aphasia with features of both PNFA and SD has been described (Grossman and Ash, 2004 ): these patients may be fluent initially but become non-fluent as the disease progresses. Unlike in typical PNFA/progressive AOS, phonetic and motor impairments are not a prominent feature, and unlike in classical SD, parietal lobe features frequently develop (Rohrer et al ., in press). In contrast to logopenic aphasia, word-finding pauses are not salient, and evidence for an association with progranulin mutations (Rohrer et al ., in press) suggests that the spectrum of pathological associations may also be distinct. The nosological status of this progressive mixed aphasia syndrome and its relationship to the other canonical progressive aphasia syndromes remain to be defined.

Speech and language syndromes in degenerative disease are rarely isolated, and in general it is necessary and often helpful to consider associated cognitive and neurological features in localizing the disease process and arriving at a differential diagnosis ( Figs. 1 and 2 ). Clinical judgement is required, first, in deciding whether word-finding difficulty is in fact likely to be secondary to deficits in one of these other domains. In many cases the clue to this lies with the history, and examination can then be directed toward an initial evaluation of other deficits before embarking on a detailed and potentially misleading analysis of word-finding proper (for example, significant visual perceptual impairment may preclude any meaningful assessment of word retrieval based on picture naming tasks). A second key objective is to determine whether the patient has a focal language-based dementia, or whether word-finding difficulty is a leading feature of a more generalized process.

Impairment of episodic memory, the record of events and episodes from the individual's daily life, is a hallmark of AD and is also seen in many other dementias. Pauses in conversation while the patient struggles to recall a name or other detail are commonly described as difficulty in finding words (or names). In particular, patients may lose the thread of a sentence and simply ‘forget’ how the sentence was intended to end: the problem here lies primarily with memory and attentional processes rather than with word-finding per se . The evaluation of memory is particularly important in deciding whether the patient's word-finding difficulty is a manifestation of a progressive aphasia (in which case episodic memory is typically well preserved) or an alternative diagnosis with more widespread cognitive impairment, in particular AD. An impression of this is usually formed from the history: patients with progressive aphasias generally are able to indicate detailed knowledge of current affairs and rarely have significant topographical difficulty, whereas deficits in these aspects of episodic memory typically occur early in the course of Alzheimer's disease. Consensus criteria for the clinical diagnosis of PNFA require the absence of ‘severe amnesia’ (Neary et al ., 1998 ). Available evidence suggests that, while working memory may be deficient in the context of an associated dysexecutive syndrome, episodic memory is generally well preserved in PNFA (Libon et al ., 2007 ). The situation in SD is more complex: amnesia for episodic material is typically not a major clinical issue in these patients, however the use of verbal material on more formal neuropsychological testing (as in tests of recognition memory for words) could in principle confound the assessment of episodic memory per se . Where appropriate indices are used, episodic memory can be shown to be comparable to that of healthy subjects in only a proportion of cases (Nestor et al ., 2006 , Scahill et al ., 2005 ), and this effect is not wholly attributable to disease stage. The clinical message is that episodic memory impairment should not be equated uncritically with AD (just as semantic deficits do not equate to SD): the relative preponderance of deficits in the episodic and semantic domains of memory, and the more qualitative aspects of the clinical history, are likely to be more reliable for differential diagnosis, pending a more sophisticated understanding of the detailed interaction of these different memory systems in different degenerative diseases.

Hi, mostly Vitamin B12 D3 have similar symptoms except those related to neurological (and some which I may not know). I would suggest please check your Vitamin D3 levels and if found deficient or even insufficient get those shots too. Hope to hear to recovering soon.

Cheers Yash


Colleen says

What many people don’t know is that you can have a high level of B12 but it’s not reaching the cells. My serum level of B12 is 1500 (I have taken methy B12 shots for years) but in spite of supplementation of it and folate, my homocysteine level was still high. My doctor ran a micronutrient test that showed in spite of all those shots, I’m deficient in B12 in the cells. I have a c677 methylation defect. So don’t assume your serum levels are accurate.

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Ally says

Collen- were you able to fix this? If so, I’m curious as to how. I’m starting b12 and methylfolate soon myself.


Candace says

I had the same experience- I have very high b12 serum level when blood tested, but neurological b12 defiency symptoms and a nutrient test showed the defiency. I’m homozygous for c677t. I’ve been supplementing with a methyl compound and I’m still deficient according to that nutrient test and symptoms are bad as ever. Has anyone else in this situation found a solution? I’ve been on b12 shots in the past but maybe not enough or consistently enough.

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So you never explained what b12 is? Is it a vitamin or a bacteria? I also could not find any links to studies!! You are not a MD or even a doctor so you can’t advise people without providing evidence to the studies you reference? This is dangerous information Chris and you are misleading the public. I feel sorry for people that take your paleo advice, A diet never proven to be healthy or primal for that matter and in fact the studies show the opposite. Seriously I feel sorry for you that you make money while claiming to help people improve their health. You need to provide peer reviewed studies or it’s just an opinion from a guy who created a website.


Catherine Wessling says

Hi, i’m 32 years old and already 6 years suffering from depression. i’m getting treat by antidepressant drugs “ssri” everyday and b12 injection one a month. every half a year my b12 decreased to 180 and i’m feeling extreme depression. so, usually i’m doing series of injection (about 6 at 2 weeks) and i’m feeling excellent, and so forth.

month ago i did the same series of injections and felt better. but this time only after a month its came back: sadness, depression, no energy. i did blood test and its shows 180 again . how could it be after a series of 6 injection month ago.

something got wrong, what/how its could be? my blood not absorbing b12? or maybe ther are any influence/ correlation between the antidepressant to b12? im feeling very bad, what can i do?

i would appreciate any kind of advise and treatment. thank you

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Diane says

Luba, what form was being injected? I read that the most common type used for injecting was cyanobalamin, the least useful type to our bodies. Maybe you’re not converting it to the active form.

I’ve just been reading a ton of useful information here:


joel says

what type of test will show me my TRUE/REAL b12 status…

there are many tests recommended like total B12, active B12, homocysteine, serum folate, RBC folate etc…?


Judy says

Eleven years ago I found out I have a severe B12 defiency. My level was 41. I’ve been using the B12 oils (methylcibalamin) you can order online for years now. My level has been very good. But my symptoms really haven’t gotten better. My gait is still bad, short-term memory problems, weak very stiff muscles and more. My doctor doesn’t really know what else to do. I use a cane for short distances and a rollater for long distance. I’ve learned to live with this but it does get me down a lot.

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Kate Wader says

Hi, Judy – perhaps you try and read about the Wahl’s Protocol, you can find an article even here, in the section Immunity Autoimmune Disease. It looks from your description like you may benefit from her diet, even if you are not diagnosed with any of autoimmune problems. Her diet increases energy levels providing all essential nutrients needed to produce more energy on a cellular level. She has her website and there are books / ebooks on Amazon as well if you are interested to become familiar with her works.


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