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Welcome to the diagnosis page of
CIDPUSA
Diagnosis of autoimmune diseases is simple. These diseases
present with complaints of fatigue, tiredness, weakness,
pain, stress, anger which often comes in cycles (remits and relapses) or (waxes and
wanes). If your disease comes in cycles which are
days, weeks, months apart then you have a autoimmune disease
process. The
autoimmune diseases are associated with a elevated SED
rate or ESR. (Sed Rate is a simple blood test which measures
inflammation). C-reactive protein (CRP) is a more sophisticated
blood test which also is used to measure inflammation, CRP will also
be elevated in autoimmune diseases. However in my personnel
experience sedimentation rate is a cost effective test as compared to CRP for mass
screening and disease follow up.
Some Fibromyalgia patients will present with pain only on the left
side of the body and in a similar way early Parkinson will only
affect the left side of the body. All the diseases are immune
mediated and if you follow the disease pattern you can diagnose and
treat the disease on the first visit without any tests or
procedures.
The human body is the most sensitive machine and I can just see and
diagnose most diseases. To me it looks like the diagnosis is written
on the face of the patient. I sense the disease, you can too if you
try. Don't depend on diagnostic tests. Most diseases will not show
up on the tests. Lets take the case of Fibromyalgia, the only test I
have seen come back positive in this diseases is IgG sub class
deficiency. But in reality the diagnosis can be seen as a anxious
look on the patients face who is begging for a diagnosis. Feel with
your fingers and feel the pain, if the patient has a headache then
feel the scalp and if the scalp is tender then two things should
come to mind either it is a vasculitis like Temporal arteritis or it
is a case of Myofacial pain/ Fibromyalgia.
I see patients from USA and UK who have seen a orthopedic surgeons
for their weak knees and have had several endoscopies, MRI, CT scans,
yet their disease remains a mystery. I frequently ask them did
the doctor examine the knee with is hands, you can feel the
swelling, the warmth and the speed bumps of myofacial pain.
The most common cause of knee pain is Statins.
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In CIDP, patients usually present with a history of weakness,
numbness, pain and difficulty in walking. Some patients may have a
sudden onset of back pain or neck pain radiating down the
extremities. This pain is usually diagnosed as radicular pain
(radiating pain or going down). The symptoms of CIDP are usually
progressive and may come and go. The patients have difficulty
climbing stairs and use their hands to pull themselves upstairs.
On examination the patients may have weakness in hips and
shoulders, loss of deep tendon reflexes (rarely increased or
normal).
There may be atrophy (shrinkage) of muscles, fasciculation's
(twitching) and loss of sensation in the feet and hands.
Some patients present with ALS (Lou Gehrig's Disease ) like
clinical picture. Who have MMF (Multi-Focal Motor neuropathy. As
these patients have no sensory loss, but just weakness. These
conditions are fully reversible.
The patients may present with a single cranial nerve or
peripheral nerve dysfunction. For example, double vision, loss of
hearing, ringing in the ear, face dropping on one side, hoarseness,
facial pain. They can have weak hand grip, numbness in the hands or
feet. Pain in the neck or back .
They may present with abdominal pains, fainting spells while
standing up. Burning pain in extremities.
Laboratory findings for CIDP
or Polyneuropathy
The major laboratory tests for CIDP are electrophysiologic studies,
CSF examination, and nerve biopsy.
Electrophysiological Tests consist of two parts.
- EMG or Electro-Myo-Graphy is a test where a
electrical needle is placed in a muscle to record its electrical
activity. It is used to differentiate other causes of muscle
weakness, such as myopathy (inflammation of muscle), axonal
neuropathies (Dysfunction in the center of the nerve) and
disorders of neuromuscular transmission (dysfunction at the
place where a nerve connects to a muscle) seen in Myasthenia.
NCV is a Nerve-conduction-Velocity is the second
part of the Electrophysiological Test. In NCV a nerve is shocked
by a electrical current and the time this current takes to
reach a second point is measured. If the speed of this measured
electrical conduction is slow, then the nerve conduction studies
show demyelination or CIDP. If the speed is slightly slow then a
axonal neuropathy is considered which may be due to vitamin
deficiency.
Some of the NCV findings include:
(see this link for EMG findings in CIDP)
(a) a slowing in the nerve conduction velocities ;
(meaning that the Myelin around a nerve is damaged or rarely the
axon is affected)
(b) the presence of conduction block or abnormal
temporal dispersion in at least one motor nerve (meaning no or
little electrical current is transmitted in the nerve). Is seen
in Mutli Focal Motor Neuropathy.
(c) prolonged distal latencies in at least two nerves; (means
that it takes a long time for the current to get past the ends
of the shocked nerve) This portion is a good way to measure for
carpal tunnel syndrome. At CIDPUSA we believe CTS is due to the
inflammation of a nerve and does not need surgery.
(d) This F wave is a stimulation of the nerve in the opposite
direction, towards the spin and the distance from the spine back
to the nerve is measured. F wave will be absent in Diabetic
Amyotrophy or swelling of the spinal discs causing inflammation
on the nerve. Absent F waves or prolonged minimum F wave
latencies in at least two motor nerves is a rule in CIDP
diagnosis. Or that a F wave is not seen in these patients.
(In some case EMG/NCV can be normal). EMG does not tell what
is the cause of your disease, it can only locate the site of the
damage.
- CSF Examination: Cerebro Spinal Fuid is the fluid
that bathes your brain and spinal cord. Cytoalbuminologic
dissociation (means elevated CSF protein >45 in the absence of a
high cell count <10) is characteristic of CIDP & GBS. CSF
pleocytosis (excess of white cells) is rare except in
HIV-associated CIDP. An elevated IgG index and IgG synthesis
rate is consistent with the immune-related nature of CIDP.
Dr. Imran Khan Nanotech Neurology Lahore
Not all the patients will have lab abnormalities. In many the
EMG/NCV findings will not show that they have CIDP yet they will
still have the disease.
Is EMG/NCV Insensitive in the Diagnosis of CIDP?
The clinical profile of chronic inflammatory demyelinating
polyneuropathy (CIDP) is variable. Nerve conduction
studies are essential for the diagnosis of CIDP; however,
current electrophysiologic criteria for CIDP may not be
sensitive. These authors analyzed results of nerve
conduction studies and nerve biopsies in 8 patients with
CIDP who did not fulfill standard electrophysiologic criteria
(of 44 patients with CIDP confirmed by nerve histology). Two
standard electrophysiologic criteria were used: one proposed
by an ad hoc committee of the AAN (Neurology 1991;
41:617) and another by the Inflammatory Neuropathy Cause
and Treatment Group (Ann Neurol 2001; 50:195).
The main electrophysiologic abnormalities were those of simple
axonopathy in 7 patients; the other patient had almost normal
electrophysiologic results. In contrast, examination of
nerve
biopsies in all 8 patients revealed substantial loss of
myelinated fibers; in addition, frequent histologic
findings were naked axons, thinly myelinated fibers, and
various degrees of onion bulbs. These histology findings
were identical to those of the 36 other CIDP patients.
The authors conclude that many patients with
unrecognized CIDP are erroneously classified by electrodiagnosis
as having chronic axonal neuropathy and that nerve biopsy should
be considered to further investigate a chronic idiopathic
neuropathy.
Click to view different size nerve fibers.
| : Neurology. 2002 Dec 24;59(12 Suppl 6):S2-6. |
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Diagnosis of CIDP.
Latov N.
Peripheral Neuropathy Center, Weill Medical College of Cornell
University, New York, NY 10022, USA.
Chronic inflammatory demyelinating polyneuropathy (CIDP) is an
autoimmune disease that targets the myelin sheaths of peripheral
nerves. In clinical practice the diagnosis is often difficult to
make because of the clinical heterogeneity of the disease, its
multifocality and predilection for proximal nerve segments, and the
limitations of our electrophysiologic and pathologic techniques.
Although there are rather stringent research criteria for selecting
patients to clinical trials, there are no generally agreed-on
clinical diagnostic criteria for CIDP, and application of the
research criteria to routine clinical practice would miss the
diagnosis in a majority of patients. Because of this uncertainty,
the prevalence of CIDP is greatly underestimated, and patients are
often left untreated despite progression of their disease. However,
given what is known about the clinical presentation and
pathophysiology of CIDP, patients with neuropathy of otherwise
unknown etiology are more likely to have CIDP than idiopathic axonal
neuropathy, and warrant a trial of therapy if they have nerve
conduction velocities below the lower limits of normal, prolongation
of F-waves beyond the normal range, or presence of conduction block
or temporal dispersion. A favorable response to therapy,
consisting of stabilization or improvement of the neuropathy, would
confirm the diagnosis
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