Posts tagged as:

cognitive changes

Lyme Update: New Neuroscience Evidence

by Dr Charles Parker on July 5, 2010 · 1 comment

If you're new here, you may want to subscribe to my RSS feed. Thanks for visiting!

The blacklegged tick (Ixodes scapularis), the ...

Black-legged Tick - Image via Wikipedia

Lyme Testing Details Are Changing: MyLyme ID, The New Standard
Why should we become very interested in Lyme? Why should those with psychiatric concerns even think about this odd presentation often relegated to infectious disease docs? Simple: Lyme Disease is the Great Imitator, and regularly shows clinically with significant psychiatric presentations from dementia, to depression, to our old friend here at CorePsych Blog: ADHD.

Lyme and Psychiatric Diagnosis
Lyme, in fact, again confirms my underlying proposition that ADHD symptoms often imply more than simple appearances. See the emotional and behavioral implications in this NPLDA Lyme Assessment Form from Robert C. Bransfield, M.D. [Information from patients with late stage neuropsychiatric Lyme disease (NPLD) was entered into a database to serve as a reference point for diagnosis and tracking the patient's status after diagnosis. - Also see this excellent Psychiatric Times article on Lyme and Neuropsychiatric Disorders]

And Dr Bransfield [see his article here on cognitive impairments with Lyme] goes on to say:

All involved with late state Lyme disease agree there is a large amount
of inaccurate information on this subject. This disagreement exists at every
level – journals, scientific meetings, clinical practice, media outlets,
etc. (17,18,19) Some of this disagreement can best be viewed as the normal
difference of opinion seen when scientists approach a very complex problem
from a very different perspective. To fuel the intensity of these disputes,
some approach these issues with a significant bias. The full recognition of
this illness has implications, which could effect tourism, real estate
values, disability, insurance company/managed care liability, workman’s
compensation cases, motor vehicle issues, some criminal cases, and political
issues. Bias issues can adversely effect patient care, research funding, and
medical regulatory issues. Some of those previously impacted by bias now
have difficulty approaching this disease with full-unhampered objectivity.

Lyme disease is clearly a very complex disease. When considering a
similar spirochete disease, syphilis, it has been said, “To know syphilis is
to know medicine.” However, to know Lyme disease is not only to know
medicine but also neurology, psychiatry, politics, economics, and law
.

And from Wikipedia:

Diffuse white matter pathology can disrupt these ubiquitous gray matter connections and could account for deficits in attention, memory, visuospatial ability, complex cognition, and emotional status. (Did I leave anything out? – And see this Wiki link also for SPECT imaging implications diagnostically.)

Other Excellent Lyme Resources:
Dr Kenneth Singleton: the Lyme Disease Solution – see page 58 for psychiatric conditions.
Check out this website for the Lyme Disease Association.
International Lyme and Associated Diseases Society website.

New NeuroScience testing with MyLyme ID The first comprehensive laboratory assessment tool.
Now we have to get more serious, for those already deeply into the long-term implications of less comprehensive testing.

The combination of B. burgdorferi (Lyme) specific memory T cell response and cytokine analysis, in conjunction with standard western blot, provides both cellular and humoral [blood] immune response, as well as patient inflammatory response assessment.  This comprehensive assessment provides the most complete clinical analysis of infection status and immune response that can be utilized to guide therapeutic intervention protocols. Review this relevant reference on LLT-MELISA Lyme from ScienceDirect June ’06.

MY Lyme Immune I.D.™ Comprehensive Assessment (#5652) Includes:
1. —- Immune Tolerance Test® (ITT®)
Identifies memory T cell response specific for B. burgdorferi (Lyme) antigens, even “hidden” or low levels.
Includes a panel of B. burgdorferi (Lyme) specific antigens that offer early and late stage identification.

The specific antigens:
OspC     – Early antigen appears shortly after tick bite or transfer of the spirochete
p41        – Early and late antigen that provides mobility to the spirochete
VlsE-1   – Late antigen appears after spirochete infection
p100     – Late stage antigen
DbpA    – Essential protein needed for overall virulence

2. —- Cytokine Analysis
Analysis of B. burgdorferi (Lyme) antigen specific inflammatory immune response in patients.
Provides guidance for effective intervention protocols.
Assessment includes cytokines, chemokines, and immune growth factors:
IL-1β        IL-6        IL-8        IL-10        G-CSF        IFN-g        TNF-α

3. —- Western Blot Analysis (IgG and IgM)
Western Blot is the industry standard methodology – already frequently used.

It appears that this new level of testing will bring more clear evidence to the diagnostic table. Interestingly, the opportunity for application of even more comprehensive neurotransmitter and hormonal testing will add more interventions to the clinical treatment process.

Do drop a comment and share the details of your take on this new MyLyme testing – or your take on testing in general!

Do take a look at this video on the problem of missed Lyme and the Lyme movie Under Our Skin here on You Tube.
cp

Make sure you take a look at these pages!
ADHD Medication Rules Purchase
“Rules” Affiliate Link
Neuroscience Details

If you found this article interesting please SHARE it:
Bookmark and Share

{ 1 comment }

Hard Evidence: Gluten Sensitivity and Neurologic Impairment

by Dr Charles Parker on August 18, 2007 · 3 comments

Brain and Immunity

Brain and Immunity

Gluten Sensitivity: A neurological problem with gait, peripheral neuropathy and cognitive disturbances.- Comments on testing with IgG Antigliadin Antibodies: Some facts for the medical readers and those interested in more information.

The brain and the bowel really are connected: check out this evidence. Please do share this with your medical provider if they doubt the celiac material [copied all the refs here, and link below to the article itself]. Directly from this article:

Gluten sensitivity as a neurological illness
M Hadjivassiliou, R A Grünewald and G A B Davies-Jones [Department of Neurology, The Royal Hallamshire Hospital, Glossop Road, Sheffield, S10 2JF, UK]
Journal of Neurology Neurosurgery and Psychiatry
2002;72:560-563

AT: http://jnnp.bmj.com/cgi/content/full/72/5/560
[Italics my own emphasis- these are only portions of the full text]

RECENT ADVANCES: PREVALENCE, SMALL BOWEL
HISTOLOGY, AND GENETIC SUSCEPTIBILITY

Some studies looking at normal populations have
shown that the prevalence of CD [celiac disease]
is much higher than previously thought
(approximating to 1 in 100). Most of such
patients have no gastrointestinal symptoms. In
addition, experimental data in patients with
gluten sensitivity suggest that there is a range
of mucosal abnormalities affecting the small
bowel ranging from preinfiltrative
(histologically normal) to infiltrative, to
hyperplastic to flat destructive (seen in CD),
and finally to the irreversible hypoplastic
atrophic lesions.

Now that I have your attention, let’s dig into the details:

Increasing the gluten load may result in progression
of the severity of the lesion.
In those patients where
the histology is normal, staining of the T cell subpopulations
of the intraepithelium of the small bowel biopsies
shows alteration of T cell subpopulations of the
intraepithelial lymphocytes (increase of the / T
cells). This finding is said to be a marker of
potential CD. This procedure is only available
in a very few pathology laboratories, rendering
its use limited.

Finally, CD has a very strong association with
the human lymphocyte antigen (HLA) of the major
histocompatibility complex
. Ninety per cent of
patients with CD have the HLA DQ2; the rest have
DQ8.

These advances suggest that gastrointestinal
symptoms are absent in most patients with CD,
that the definition of gluten sensitivity can no
longer be solely based on the presence of an
enteropathy and that genetic susceptibility may
be an important additional marker for gluten
sensitivity
. Given the knowledge of these
advances and approaching gluten sensitivity from
a neurological perspective we set up to address
the following question: Does cryptic gluten
sensitivity play a part in neurological illness?

THE NEUROLOGY OF GLUTEN SENSITIVITY
Over the past 8 years we have used antigliadin
antibodies to screen patients with neurological
dysfunction of unknown aetiology. Our original
study concluded that gluten sensitivity played an
important part in neurological illness
.

The evidence was statistical: Patients with
neurological disease of unknown aetiology were
found to have a much higher prevalence of
circulating antigliadin antibodies (57%) in their
blood than either healthy control subjects (12%)
or those with neurological disorders of known
aetiology (5%).

Since then, we have identified 131 patients with
gluten sensitivity and neurological disorders of
unknown aetiology. [Table 2 in the full article shows the neurological
diagnoses we have encountered.] Perhaps not
surprisingly the commonest manifestations are
ataxia (also known as gluten ataxia) and
peripheral neuropathy.

CONTENTIOUS ISSUES
:
“But antigliadin antibodies lack specificity.”

IgG anti-gliadin antibodies have been the
best diagnostic marker in the neurological
population we have studied. IgG anti-gliadin
antibodies have a very high sensitivity for CD
but they are said to lack specificity. In the
context of a range of mucosal abnormalities and
the concept of potential CD, they may be the only
available immunological marker for the whole
range of gluten sensitivity of which CD is only a
part. Further support for our contention comes
from our HLA studies:

Within the group of patients with neurological
disease and gluten sensitivity (defined by the
presence of anti-gliadin antibodies) we have
found a similar HLA association to that seen in
patients with CD: 70% of patients have the HLA
DQ2 (30% in the general population), 9% have the
HLA DQ8, and the remainder have HLA DQ1. The
finding of an additional HLA marker (DQ1) seen in
the remaining 20% of our patients may represent
an important difference between the genetic
susceptibility of patients with neurological
presentation to those with gastrointestinal
presentation within the range of gluten
sensitivity.

REFERENCES FOR THE ENTIRE ARTICLE
-Aretaeus. Liber IV In: Corpus Medicorum
Graecorum
. Berlin: Akademie-Verlag GmbH 1956:74.
-Gee S. On the coeliac affection. St
Bartholomew’s Hospital reports 1888;24:17–20.
-Brown C W. Sprue and its treatment. London: J
Bale, sons, and Danielson, 1908.
-Elders C. Tropical sprue and pernicious anaemia,
aetiology and treatment
. Lancet 1925;i:75–7.
-Dicke W K, Weijers HA, Van De Kamer JH. Coeliac
disease II; the presence in wheat of a factor
having a deleterious effect in cases of coeliac
disease.
Acta Paediatrica 1953;42:34–42.[Medline]
-Taylor KB, Truelove SC, Thomson DL, et al. An
immunological study of coeliac disease and
idiopathic steatorrhoea
. BMJ 1961;2:1727–31.
-Marks J, Shuster S, Watson AJ. Small bowel
changes in dermatitis herpetiformis
.
Lancet
1966;ii:1280–2.
-Cooke WT, Thomas-Smith W. Neurological disorders
associated with adult coeliac disease
.
Brain
1966;89:683–722.[Free Full Text]
-Holmes GKT. Neurological and psychiatric
implications of celiac disease
In:Gobbi G,
Anderman F, Naccarato S, et al, eds. Epilepsy and
other neurological disorders in coeliac disease
.

London: John Libbey, 1997.
-Henriksson K G, Hallert C, Norrby K, et al.
Polymyositis and adult coeliac disease. Acta
Neurol Scand 1982;65:301–19.[Medline]
-Lu C S, Thompson PD, Quin NP, et al. Ramsay Hunt
syndrome and coeliac disease: a new association.

Mov Disord 1986;1:209–19.[Medline]
-Gobbi G, Bouquet F, Greco L, et al. Coeliac
disease, epilepsy, and cerebral calcifications.

Lancet 1992;340:439–43.[Medline]
-Grodzinsky E, Franzen L, Hed J, et al. High
prevalence of celiac disease in healthy adults
revealed by antigliadin antibodies
.
Annals of
Allergy 1992;69:66–9.[Medline]
-Catassi C, Ratsch IM, Fabiani E, et al. Coeliac
disease in the year 2000: exploring the iceberg.

Lancet 1994;343:200–3.[Medline]
-Marsh MN. The natural history of gluten
sensitivity: defining, refining, and re-defining.

Q J Med 1995;85:9–13.
-Maki M, Holm K, Collin P, et al. Increase in
gamma/delta T-cell receptor bearing lymphocytes
in normal small bowel mucosa in latent coeliac
disease.
Gut 1991;32:1412–14.[Medline]
-Hadjivassiliou M, Gibson A, Davies-Jones G A B,
et al. Is cryptic gluten sensitivity an important
cause of neurological illness?
Lancet
1996;347:369–71.[Medline]
-Hadjivassiliou M, Grünewald RA, Chattopadhyay
AK, et al. Clinical, radiological,
neurophysiological and neuropathological
characteristics of gluten ataxia
. Lancet
1998;352:1582–5.[Medline]
-Hadjivassiliou M, Chattopadhyay AK, Davies-Jones
GAB, et al. Neuromuscular disorder as a
presenting feature of coeliac disease
.
J Neurol
Neurosurg Psychiatry 1997;63:770–5.[Abstract/Free
Full Text]
-Hadjivassiliou M, Grünewald RA, Davies-Jones
GAB. Causes of cerebellar degeneration: gluten
ataxia in perspective.
J Neurol Sci
2001;187(suppl 1):S520.
-Hahn JS, Sum JM, Crowley RS, et al. Coeliac
disease presenting as gait disturbance and ataxia
in infancy.
J Child Neurol
1998;13:351–3.[Medline]
-Hadjivassiliou M, Grünewald RAG, Lawden M, et
al. Headache and CNS white matter abnormalities
associated with gluten sensitivity
. Neurology
2001;56:385–8.[Abstract/Free Full Text]
-Ventura A. Coeliac disease and autoimmunity. In:
Lohiniemi S, Collin P, Maki M, eds. Changing
features of Coeliac disease.
Tampere: The Finnish
Coeliac Society 1998:67–72.
-Hadjivassiliou M, Grünewald RA, Davies Jones A,
et al. Gluten ataxia – insights into the
pathophysiology
. J Neurol Neurosurg Psychiatry
1999;67:262.
-Jensen K, Sollid LM, Scott H, et al.
Gliadin-specific T cell responses in peripheral
blood of healthy individuals involve T cell
clones restricted by the coeliac disease
associated DQ heterodimer
. Scand J Immunol
1995;42:166–70.[Medline]
-Chinnery PF, Reading PJ, Milne D, et al. CSF
antigliadin antibodies and the -Ramsay Hunt
syndrome
.
Neurology 1997;49:1131–3.[Abstract/Free
Full Text]
-Hadjivassiliou M, Grünewald RA, Davies-Jones
GAB, et al. The humoral response in the
pathogenesis of gluten ataxia
. Ann Neurol
2001;50(suppl 1):S37.
-Hadjivassiliou M. On the neurological
manifestations of gluten sensitivity
[MD thesis].
Sheffield: Department of Health Sciences,
University of Sheffield, 1999.
-Hadjivassiliou M, Grünewald RA, Davies-Jones
GAB. Gluten sensitivity: a many-headed hydra
[editorial]. BMJ 1999;318:1710–11.[Free Full
Text]

Just take a moment to look at the reference topics, and you will start to think more about the psych/neurologic implications of this overlooked problem.

Next post on Vitamin B12 deficiency those symptoms with the downstream findings from gluten sensitivity… and we’re only scratching the surface of the bowel thing.

Not to be discussed at dinner!

Make sure you take a look at these pages!
ADHD Medication Rules Purchase
“Rules” Affiliate Link
Neuroscience Details

If you found this article interesting please SHARE it:
Bookmark and Share

{ 3 comments }