Monthly Archives: January 2017

ICD-1 (Well….near enough)

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I’ve taken a slight diversion while looking at Health Information Exchanges (HIE). HIE’s allow clinical information to follow a patient around the healthcare system. What is clear is that the task is made a lot easier if health data is stored in a standardised way. That is a function of the SNOMED/SNOP terminologies. However it is also a feature of the International Classification of Diseases which allows for the communication of diseases using codings.

In previous posts, we looked at the origins of the International Classification of Diseases in the 1893 congress of the International Statistical Institute. The original classification wasn’t a classification of disease but causes of death. The distinction is subtle. Not all diseases necessarily lead to death. Not all causes of death are diseases. In any case, at that point in time the classification scheme reflected the knowledge of the time which has been greatly expanded over the past 120 years.

We are now on ICD-10 and moving towards ICD-11. In previous posts, we looked at the original classification of causes of deaths. So the first revision, we might think of as ICD-1. The only problem there is that ICD now stands for the International Classification of Diseases. Strictly speaking therefore the first revision of the International Causes of Death is not ICD-1 but a revision of Bertillon’s Classification of Causes of Death. For the sake of convenience it seems nevertheless to be considered as ICD-1.

So what did ICD-1 look like? Well the World Health Organisation have an archived copy of ‘ICD-1’ found at their historical collections webpage. The classification is written in French. The revision was again headed by Dr Jacques Bertillon. There are 179 causes of death listed. The causes are classified in several ways – according to the system in the body, the stage in life as well as miscellaneous causes.

On a slightly separate note, there is a reference to the collection of population data by statistical bodies in many countries. The total population included is estimated at 121 million people.

On reflection there is some similarity between the compilation of statistical health data and the storage of health information in databases. There is utility in quantifying this information so as to more easily analyse or store it. There are however additional ways of managing the information which capture more qualitative (intuitive) aspects. The quantification and taxonomising of health information has led to a very stable information infrastructure.

Appendix A – Other Posts in the Series on Health Information Exchanges

A Literature Review of 40 years of SNOMED

Arizona Statewide Health Information Exchange

A History of The Health Information Exchange in Pennsylvania

The Arkansas Health Information Exchange – SHARE

The California Health Information Exchange – Cal Index

Creating a Health Information Exchange in Arizona

Health Information Exchanges

Health Information Exchanges and Chronic Conditions

HIPPA and Health Information Exchanges

ICD-11 and SNOMED CT®

ICD-SNOMED-CT® Harmonisation

Körner Data and SNOMED: A Snapshot from 1988

Mapping ICD 9 (or 10) to SNOMED CT®

Over 1 Million Relationships: SNOMED CT ®

Standardisation of Health Information Technology in New Zealand

Statisticians were Responsible for the Development of an International Classification of Diseases

Why Do We Need Electronic Record Systems to Talk to Each Other

Appendix B – Definition of Health Information Exchange

This is the definition of the Health Information Exchange that I use (Hersh et al, 2015)

Health information exchange (HIE), the electronic sharing of clinical information across the boundaries of health care organizations

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section.

 

 

 

 

 

 

 

 

Small and Duff’s Dual Pathway Hypothesis

Stylised Diagram of the Hippocampus - Frank Gaillard
Diagram showing Hippocampus, an area affected by Alzheimer’s Disease (credits Appendix A)

Small and Duff’s Dual Pathway hypothesis is widely cited (e.g see here). The interested reader is referred to the paper above. However I have outlined the salient features below as I have found them

(1) The Amyloid Cascade Hypothesis does not appear to explain all cases of Alzheimer’s Disease particularly when this is late in onset.

(2) Tau  gene mutations are described as leading to Frontotemporal Dementia rather than Alzheimer’s Type Dementia

(3) A dual pathway is hypothesised which describes processes upstream to the Amyloid deposition and tau phosphorylation and which influence both

(4) Small and Duff identify APOE4, GSK and the Retromer sorting pathway as three examples of upstream drivers

(5) When Amyloid deposition is absent or minimal but the other elements are present this has implications for Amyloid reducing strategies

Appendix A – Credits

Picture by FG Designs. Creative Commons License.

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section.

Further Details of the PART Hypothesis

Stylised Diagram of the Hippocampus - Frank Gaillard

Diagram showing Hippocampus, an area affected by Alzheimer’s Disease (credits Appendix A)

Crary and colleagues have written this 2014 paper on PART (Primary Age Related Tauopathy) (see also this paper by Crary). I’ve highlighted a few key points about the hypothesis from this paper

(1) The PART hypothesis is driven by pathological findings

(2) PART distinguishes between pathology and clinical manifestation

(3) Comorbid pathology presents a challenge when identifying ‘pure’ clinical correlates of PART

(4) Ambiguity in the hypothesis. PART has been described as:

(a) Distinct from Alzheimer’s Disease

(b) A subset of Alzheimer’s Disease cases

(c) An early stage of Alzheimer’s Disease (i.e. the Amyloid plaques may be expected to follow the appearance of the tangles)

(d) On a continuum with Alzheimer’s Disease

(5) PART also maps onto the pathology associated with several previous descriptors

(a) ‘Tangle Predominant Senile Dementia’

(b) ‘Tangle only Dementia’

(c) ‘Preferential Development of NFT without senile plaques’

(d) ‘Senile Dementia of the Neurofibrillary Tangle Type’

(6) TPSD (5a above) has previously been classed as a Frontotemporal Lobar Degeneration

The reader can see from the above that there are many possible variations of the hypothesis.

Appendix A – Credits

Picture by FG Designs. Creative Commons License.

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section.

Statisticians were Responsible for the Development of an International Classification of Diseases

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I wrote about the origins of the International Classification of Disease (ICD) in a previous post. The original classification described causes of deaths and was first presented and approved at the congress of the International Statistical Institute (ISI).

I checked out the schedule for the last conference of the ISI in Brazil in 2015 and was impressed by the breadth of topics (and intrigued by one topic – neurostatistics). It is particularly interesting to note that ICD which has led to the creation of diagnoses and influenced the lives of clinicians and patients alike was born in a statistical congress in 1893.

The mission statement of the International Statistical Institute is stated thus:

Founded in 1885, the International Statistical Institute (ISI) is among the oldest scientific societies. Its mission is to promote the understanding, development and good practice of statistics worldwide‘.

The society for advancing the study of a branch of mathematics has generated one of the most significant changes to clinical practice in the last few hundred years. I still don’t properly understand the details of how this was actualised but the longevity of ICD is testimony to the utility of a statistical (as well as clinical) underpinning.

I found it interesting that the statistical underpinnings are also referenced in the discussion of SNOMED-CT® by Schulz and colleagues

Health statistics over time should be affected as minimally as possible by changes in the underlying coding vocabulary. ICD has evolved for more than 120 years, which explains most of its structure, especially the single-hierarchy principle

Appendix A – Other Posts in the Series on Health Information Exchanges

A Literature Review of 40 years of SNOMED

Arizona Statewide Health Information Exchange

A History of The Health Information Exchange in Pennsylvania

The Arkansas Health Information Exchange – SHARE

The California Health Information Exchange – Cal Index

Creating a Health Information Exchange in Arizona

Health Information Exchanges

Health Information Exchanges and Chronic Conditions

HIPPA and Health Information Exchanges

ICD-11 and SNOMED CT®

ICD-SNOMED-CT® Harmonisation

Körner Data and SNOMED: A Snapshot from 1988

Mapping ICD 9 (or 10) to SNOMED CT®

Over 1 Million Relationships: SNOMED CT ®

Standardisation of Health Information Technology in New Zealand

Why Do We Need Electronic Record Systems to Talk to Each Other

Appendix B – Definition of Health Information Exchange

This is the definition of the Health Information Exchange that I use (Hersh et al, 2015)

Health information exchange (HIE), the electronic sharing of clinical information across the boundaries of health care organizations

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section.

 

 

 

PART and the Amyloid Cascade Hypothesis

Stylised Diagram of the Hippocampus - Frank Gaillard

Diagram showing Hippocampus, an area affected by Alzheimer’s Disease (credits Appendix A)

Pathologist and Associate Professor John Crary has written an interesting piece on PART and the relationship to the Amyloid Cascade Hypothesis. PART is an acronym for Primary Age Related Tauopathy. Whilst the Amyloid Cascade Hypothesis has a great deal of supporting evidence there is data which contradicts the hypothesis.

Professor Crary references pathological findings where people with clinically diagnosed Alzheimer’s Type Dementia are found to lack evidence of Amyloid toxicity but there is the presence of tangles. He hypothesises that PART, if it is a valid construct reflects an aging mechanism in the brain independent of Amyloid plaque. He also cites evidence that the pathology is found in areas including the medial temporal lobe structures that are likely to be exposed to mechanical injury during the lifespan.

Appendix A – Credits

Picture by FG Designs. Creative Commons License.

Appendix B – Summary of the Amyloid Cascade Hypothesis

For further details see here

(1) Amyloid is central to all pathophysiological processes that lead to Alzheimer’s Disease
(2) Amyloid (including the ABeta components) is toxic
(3) An increase in Amyloid through increased production, reduced removal or both leads to increased toxicity
(4) Amyloid/ABeta leads to tangle pathophysiology
(5) Tangle pathophysiology leads to neuronal cell death
(6) Reducing Amyloid/A Beta would improve symptoms resulting from the Alzheimer’s Disease process

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

The Origins of the International Classification of Diseases

023715-black-inlay-steel-square-icon-culture-books3-stacked

In this series, we have been looking at health information exchanges, interfaces that allow medical information to follow a person between organisations and different clinical informatics systems. Along the way we have seen that the exchange of information is facilitated by using standardised frameworks for recording clinical information. This bifurcates into the classification of diseases on one hand (e.g the International Classification of Diseases) and a database driven clinical ontology on the other hand (e.g SNOMED-CT ®). We have seen that SNOMED began as SNOP in 1965 and then developed into SNOMED-RT before merging with the UK Read codes to form SNOMED-CT ®.

The development of SNOMED is a little complex but what about the World Health Organisation’s International Classification of Diseases (ICD)? Where did that begin? Well a brief and very helpful overview of the development of ICD can be found on the WHO website. Although there had been a number of classification systems developed in the 19th and 18th centuries, ICD began as a classification of deaths.

The International Statistical Institute established a committee to draw up a classification of the causes of death. Jacques Bertillon was the central figure in these efforts and was the chair of the committee drawing up the classification. Interestingly enough Bertillon’s brother Alphonse Bertillon worked in law enforcement in Paris and established the use of biometrics and the mugshot. Bertillon’s grandfather Achille Guillard was a statistician who had coined the term demographics and requested a resolution for a ‘uniform classification’ in the first Statistical Congress in 1853.

The Bertillon Classification of Causes of Death was in essence the first version of the International Classification of Disease but of course had a different meaning. ICD editions are referred to as revisions – they are revisions of this original classification of causes of deaths. Bertillon’s classification was presented and adopted at the meeting of the International Statistical Institute in 1893.

Appendix A – Other Posts in the Series on Health Information Exchanges

A Literature Review of 40 years of SNOMED

Arizona Statewide Health Information Exchange

A History of The Health Information Exchange in Pennsylvania

The Arkansas Health Information Exchange – SHARE

The California Health Information Exchange – Cal Index

Creating a Health Information Exchange in Arizona

Health Information Exchanges

Health Information Exchanges and Chronic Conditions

HIPPA and Health Information Exchanges

ICD-11 and SNOMED CT®

ICD-SNOMED-CT® Harmonisation

Körner Data and SNOMED: A Snapshot from 1988

Mapping ICD 9 (or 10) to SNOMED CT®

Over 1 Million Relationships: SNOMED CT ®

Standardisation of Health Information Technology in New Zealand

Why Do We Need Electronic Record Systems to Talk to Each Other

Appendix B – Definition of Health Information Exchange

This is the definition of the Health Information Exchange that I use (Hersh et al, 2015)

Health information exchange (HIE), the electronic sharing of clinical information across the boundaries of health care organizations

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section.

Alternatives to the Amyloid Cascade Hypothesis

Stylised Diagram of the Hippocampus - Frank Gaillard

Diagram showing Hippocampus, an area affected by Alzheimer’s Disease (credits Appendix A)

In his paper on the Amyloid Cascade Hypothesis, Professor Hardy references two alternative hypotheses which are worth bearing in mind

(a) The Presenilin inhibition hypothesis. The Presenilins genes have been clearly linked to Alzheimer’s Disease and so understanding of the function of their phenotypes (the translation of the gene into molecule product) is important.  The Presenilin inhibition hypothesis states that the Presenilins, as subunits of an enzyme are inhibited in their actions. Professor Hardy identifies some critiques of this model.

(b) The Double Hit hypothesis states that as well as changes in the Amyloid Precursor Protein there is a second independent step which leads to changes in the tau protein in late-onset disease. Again Professor Hardy identifies difficulties with this hypothesis.

Appendix A – Credits

Picture by FG Designs. Creative Commons License.

Index: There are indices for the TAWOP site here and here

Twitter: You can follow ‘The Amazing World of Psychiatry’ Twitter by clicking on this link.

TAWOP Channel: You can follow the TAWOP Channel on YouTube by clicking on this link.

Responses: If you have any comments, you can leave them below or alternatively e-mail justinmarley17@yahoo.co.uk.

Disclaimer: The comments made here represent the opinions of the author and do not represent the profession or any body/organisation. The comments made here are not meant as a source of medical advice and those seeking medical advice are advised to consult with their own doctor. The author is not responsible for the contents of any external sites that are linked to in this blog.

Conflicts of Interest: *For potential conflicts of interest please see the About section.