RE: Autoimmune encephalopathies

[Guest guest]

,

Thanks for this. I've always understood from Dr. G that my son has

encephalopathy. He had a MRI when he was 3, but it did not show anything. Do

you think that's common?

Kristy Nardini

TazziniTM Stainless Steel Bottles

<http://www.tazzini.com/> http://www.tazzini.com

kristy@...

Phone: 858.243.1929

Fax: 858.724.1418

P Please consider the environment before printing this email.

From: [mailto: ] On Behalf Of

Sent: Thursday, May 06, 2010 11:38 AM

nids

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi.nlm.nih.gov/pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt-Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid-responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalography, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

This is very interesting! My son has low male hormone levels and extreme

hyperactivity and impulsivity. It says in the information below that

corticosteroid-responsive encephalopathy may improve with corticosteroids.

Are these meds that Dr. G prescribes? How do you get diagnosed?

From: [mailto: ] On Behalf Of

Sent: May-06-10 3:38 PM

nids

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi.nlm.nih.gov/pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt-Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid-responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalography, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

Hi Kristy,

My son also had an MRI done when he was 2 years old and it came back normal as

well.

Dr. Golberg also talks about non-inflammatory inflammation. Kind of hard to

understand what it means, but a real condition. In this condition the

inflammation is there, but it displays different, more subtle patterns. I don't

think doctors are actually looking for this kind of inflammation when an MRI is

performed. I don't even know if an MRI can detect this kind of inflammation. A

brain SPECT scan can detect the problem by looking a cerebral perfusion.

Please read the article below.

Take care,

's Story - Stop Calling It Autism!

http://www.stopcallingitautism.net

Neuronal damage in brain inflammation.

http://www.ncbi.nlm.nih.gov/pubmed/17296833

Abstract

In contrast to traditional textbook paradigms, recent studies indicate neuronal

damage in classic neuroinflammatory diseases of the brain, such as multiple

sclerosis or meningitis. In these cases, immune cells invade the central nervous

system compartments, accompanied by a massive breakdown of the blood-brain

barrier and typical changes of the cerebrospinal fluid. On the other hand,

inflammation within the central nervous system is a common phenomenon even in

classic noninflammatory brain diseases that are characterized by degeneration or

trauma of neuronal structures, such as Alzheimer disease, Parkinson disease, or

stroke. In these cases, inflammation is a frequent occurrence but displays

different, more subtle, patterns compared with, for example, multiple sclerosis.

Concepts for directly protecting neurons and axons in neuroinflammatory diseases

may improve the outcome of the patients. In parallel, epidemiological and animal

experimental evidences, as well as first clinical trials indicate the benefit of

immunomodulatory therapies for classic noninflammatory brain diseases. We review

the evidence for inflammatory neuronal damage and its clinical impact in the

context of these diseases.

From: knardini@...

Date: Thu, 6 May 2010 11:48:24 -0700

Subject: RE: Autoimmune encephalopathies

,

Thanks for this. I've always understood from Dr. G that my son has

encephalopathy. He had a MRI when he was 3, but it did not show anything. Do

you think that's common?

Kristy Nardini

TazziniTM Stainless Steel Bottles

<http://www.tazzini.com/> http://www.tazzini.com

kristy@...

Phone: 858.243.1929

Fax: 858.724.1418

P Please consider the environment before printing this email.

From: [mailto: ] On Behalf Of

Sent: Thursday, May 06, 2010 11:38 AM

nids

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi.nlm.nih.gov/pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt-Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid-responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalography, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

I don't think Dr. Goldberg prescribes corticosteroids.

Do you mean how you diagnose a child with encephalopathy?

Regards,

's Story - Stop Calling It Autism!

http://www.stopcallingitautism.net

From: freemanbk@...

Date: Thu, 6 May 2010 16:09:21 -0300

Subject: RE: Autoimmune encephalopathies

This is very interesting! My son has low male hormone levels and extreme

hyperactivity and impulsivity. It says in the information below that

corticosteroid-responsive encephalopathy may improve with corticosteroids.

Are these meds that Dr. G prescribes? How do you get diagnosed?

From: [mailto: ] On Behalf Of

Sent: May-06-10 3:38 PM

nids

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi.nlm.nih.gov/pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt-Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid-responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalography, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

Yes, how do you get diagnosed and it did say that this

corticosteroid-responsive encephalopathies are treated with corticosteroids.

Could this help our child?

Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi.nlm.nih.gov/pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt-Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid-responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalography, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

Hey Kristi,

 

It is very common to not find inflammation on an MRI. I remember when my son had

an MRI done and I asked the neurologist for the results and she said that ASD

children have the most beautiful brains. I thought I need a new neurologist

because something was not right. Anyway, it was not until 2005 that it was

discovered that ASD brains do have inflammation. Vargas et al from s Hopkins

did a post-mortem study on ASD brains and found inflammation. Of course, Dr. G

and perhaps a few others knew well before this but even now, the basic medical

community is not taking this seriously because they are unobservant, ambivalent

and slow. I am thinking other choice words but I will refrain. Here is the link

to the Hopkins 2005 paper.

 

http://www.ncbi.nlm.nih.gov/pubmed/15546155

 

Cheers,

 

Jill

From: Kristy Nardini <knardini@...>

Subject: RE: Autoimmune encephalopathies

Date: Thursday, May 6, 2010, 2:48 PM

 

,

Thanks for this. I've always understood from Dr. G that my son has

encephalopathy. He had a MRI when he was 3, but it did not show anything. Do

you think that's common?

Kristy Nardini

TazziniTM Stainless Steel Bottles

<http://www.tazzini. com/> http://www.tazzini. com

kristytazzini (DOT) com

Phone: 858.243.1929

Fax: 858.724.1418

P Please consider the environment before printing this email.

From: groups (DOT) com [mailto:groups (DOT) com] On Behalf Of

Sent: Thursday, May 06, 2010 11:38 AM

nidsgroups (DOT) com

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi. nlm.nih.gov/ pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt- Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid- responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalogra phy, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

Thanks to everyone who responded and for the information!

Kristy Nardini

TazziniTM Stainless Steel Bottles

<http://www.tazzini.com/> http://www.tazzini.com

kristy@...

Phone: 858.243.1929

Fax: 858.724.1418

P Please consider the environment before printing this email.

From: [mailto: ] On Behalf Of Jill Boyer

Sent: Thursday, May 06, 2010 4:50 PM

Subject: RE: Autoimmune encephalopathies

Hey Kristi,

It is very common to not find inflammation on an MRI. I remember when my son had

an MRI done and I asked the neurologist for the results and she said that ASD

children have the most beautiful brains. I thought I need a new neurologist

because something was not right. Anyway, it was not until 2005 that it was

discovered that ASD brains do have inflammation. Vargas et al from s Hopkins

did a post-mortem study on ASD brains and found inflammation. Of course, Dr. G

and perhaps a few others knew well before this but even now, the basic medical

community is not taking this seriously because they are unobservant, ambivalent

and slow. I am thinking other choice words but I will refrain. Here is the link

to the Hopkins 2005 paper.

http://www.ncbi.nlm.nih.gov/pubmed/15546155

Cheers,

Jill

From: Kristy Nardini <knardini@... <mailto:knardini%40roadrunner.com>

>

Subject: RE: Autoimmune encephalopathies

<mailto:%40>

Date: Thursday, May 6, 2010, 2:48 PM

,

Thanks for this. I've always understood from Dr. G that my son has

encephalopathy. He had a MRI when he was 3, but it did not show anything. Do

you think that's common?

Kristy Nardini

TazziniTM Stainless Steel Bottles

<http://www.tazzini. com/> http://www.tazzini. com

kristytazzini (DOT) com

Phone: 858.243.1929

Fax: 858.724.1418

P Please consider the environment before printing this email.

From: groups (DOT) com [mailto:groups (DOT) com] On Behalf Of

Sent: Thursday, May 06, 2010 11:38 AM

nidsgroups (DOT) com

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi. nlm.nih.gov/ pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt- Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid- responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalogra phy, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.

[Guest guest]

Dr G avoids steroids in our kids at all costs.  The only time he would use them

is in a serious illness that demands them.

Steroids will work, BUT our kids have serious immune issues, and steroids will

'set free' the viruses that are the *cause* of the inflammation.  Much better to

treat the viruses, limit all the triggers of inflammation (diet, antibiotics

when required, antifungals) by suppressing the immune system from the other end.

There are serious side effects to the steroids, and desperate parents using them

often see several other serious problems aside from worsening the body's already

diminished ability to fight infection - actually blasting it.  And the steroids

have to be stopped at some time, and then you have a rebound and often lose all

those gains.

So yes, steroids do work, but the nids protocol works better and without the

consequences.

HTH

________________________________

From: <jrodrig6605@...>

nids

Sent: Thu, May 6, 2010 4:08:59 PM

Subject: RE: Autoimmune encephalopathies

I don't think Dr. Goldberg prescribes corticosteroids.

Do you mean how you diagnose a child with encephalopathy?

Regards,

's Story - Stop Calling It Autism!

http://www.stopcallingitautism.net

From: freemanbk@...

Date: Thu, 6 May 2010 16:09:21 -0300

Subject: RE: Autoimmune encephalopathies

 

This is very interesting! My son has low male hormone levels and extreme

hyperactivity and impulsivity. It says in the information below that

corticosteroid-responsive encephalopathy may improve with corticosteroids.

Are these meds that Dr. G prescribes? How do you get diagnosed?

From: [mailto: ] On Behalf Of

Sent: May-06-10 3:38 PM

nids

Subject: Autoimmune encephalopathies

Autoimmune encephalopathies

http://www.ncbi.nlm.nih.gov/pubmed/17495758

Abstract

BACKGROUND: Evaluation of patients with recent onset of progressive

cognitive and behavioral problems can be challenging. Psychiatric disorders,

metabolic derangements, toxins and infections are generally considered in

the differential diagnosis along with prion disorders (Creutzfeldt-Jakob

disease) and rapidly progressive degenerative dementias. Some subacute

encephalopathies are caused by autoimmune or inflammatory mechanisms,

recognized by the association with autoantibody markers and/or clear

response to immunomodulatory treatment. This review describes the clinical

features of these potentially reversible autoimmune encephalopathies. REVIEW

SUMMARY: Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and

nonparaneoplastic autoimmune limbic encephalitis have characteristic

clinical and serological features. Limbic encephalitis is characterized by

short-term memory impairment, complex partial temporal lobe seizures and

psychiatric symptoms. Signal abnormalities in the mesial temporal lobes

without contrast enhancement are the typical MRI findings. Morvan syndrome

presents with behavioral changes, hallucinations, severe insomnia, autonomic

hyperactivity and neuromyotonia (spontaneous muscle activity).

Corticosteroid-responsive encephalopathy associated with evidence of thyroid

autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range

of clinical presentation. Cognitive impairment with tremor, seizures,

stroke-like events (including transient aphasia) and normal thyroid hormone

levels is a common scenario. In the absence of diagnostic serological

findings, clinical improvement with corticosteroids may be the only evidence

of autoimmune encephalopathy. CONCLUSIONS: Autoimmune encephalopathies are

an important cause of rapidly progressive cognitive and behavioral decline

that probably remain under recognized. Electroencephalography, brain MRI,

cerebrospinal fluid examination and serological tests are useful diagnostic

tools. With increased clinical suspicion, these diseases may be diagnosed

and treated successfully.