‫مرحبا بالحضور الكرام‬
‫بسم هللا الرحمن الرحيم‬
‫وما أوتيتم من ألعلم إال ق ليال•‬
‫صدق اهلل العظيم •‬
Peripheral Neuropathy In
Dyslipidemia with special
Emphasis on diabetes
mellitus
(Biochemical & Electrophysiological study)
Peripheral neuropathy
• Def: PNP is a generic term for peripheral
nerve disorders of any cause.
• Mononeuropathy refers to involvement of
a single nerve whereas polyneuropathy
refers to involvement of multiple nerves.
PNP in Dyslipidemia
1. dyslipidemia could be associated with subclinical peripheral
neuropathy, which may occur more frequently in patients
with very high mean serum level of T.G, T.C and LDL.
2. The type of peripheral neuropathy that occurs in
Dyslipidemia is mainly a sensory type, although motor
neuropathy can not be excluded.
3. The underlying mechanism is mixed axonal degeneration
and segmental demyelination; however, the
demyelination is thought to be secondary to the axonal
degeneration. The peripheral neuropathy associated
with dyslipidemia is symmetrical type.
Pathogenesis of Peripheral Neuropathy in
Dyslipidemia
I.
II.
Involvement of structural lipids
The action of lipoproteins as enzyme
co-factor and as a bound intermediate
in the biosynthesis of polysaccharides
and proteins.
III. Nerve infarction which is mediated via
fat embolism or lipid induced platelet
aggregation.
Types of peripheral neuropathy in
DM
• PNP affect 30% of diabetic patients.
• Diabetic neuropathy divided into:
A. somatic: include:
1. polyneuropathy
symmetrical
(mainly sensory and distal)
Asymmetrical (mainly
motor and proximal)
2. Mononeuropathy (including mononeuritis
multiplex)
B. Visceral (autonomic)
Pathogenesis of peripheral
neuropathy in DM
The pathogenesis of sensorimotor
neuropathy in D.M is multifactorial and
related metabolic disturbances, such as
hyperglycemia, dyslipidemia, oxidative
stress and growth factor deficiency all
contribute to the development of this
complication.
Several metabolic products, such as:
1. Advanced glycated end products.
2. Activation of protein kinase C enzyme.
3. Sorbitol aldose reductase (polyol)
pathway flux, are claimed to have a role
in pathogenesis of neuropathy
Dyslipidemia as a contributory factor in
etiopathogenesis of diabetic neuropathy
Dyslipidemia leads to high levels of oxLDLs
that may injure DRG neurons via LOX-1
receptor and contribute to the development
of diabetic neuropathy.
 Also these oxLDLs that carry lipids to the
periphery could be one factor that acts in
concert with glucose to increase sensory
nerve injury.
These same mechanisms also occur in the
blood microvessels, leading to multiple
neurovascular targets for oxidative stress
mediated injury.
Role of Electrophysiology in Dyslipidemia
Neurological complications of dyslipidemia were
firstly noticed in hereditary lipid disorders like
Tangier disease, abetalipoprotienemia, later on
many studies was carried out to disclose the
relation between peripheral neuropathy and
dyslipidemia, but in spite of all these studies the
proportion of dyslipidemic patients with peripheral
neuropathy is still unknown and based on
literature review.
ELECTROPHYSIOLOGICAL ASSESSMENT OF
THE PERIPHERAL NERVOUS SYSTEM:Electrophysiological methods have made an
important contribution in elucidating the
pathophysiology of peripheral nerve disorders by
ELECTRONEUROGRAPHY which include:A. SENSORY NERVE CONDUCTION.
B. MOTOR NERVE CONDUCTION.
C. F -WAVE CONDUCTION STUDY.
PARAMETER
DSL
(msec)
Subject
N
O.
Rt. Median
N.
Mean ±S.D
Rt. Ulnar
N.
Mean ± S.D
Rt.Com.Per.
N.
Mean ± S.D
Rt. Post.Tib.
N.
Mean ± S.D
Patients
68
2.65 ± 0.58
2.44 ± 0.50
3.52± 0.88
3.60± 0.96
Control
42
2.44 ± 0.17
2.29 ± 0.16
3.05 ± 0.22
3.12 ± 0.27
P.value
Amplitude
(µv)
(S)
(H.S)
(H.S)
Patients
68
22.63 ±5.56
20.75±3.69
9.65± 2.97
9.92± 3.75
Control
42
25.25 ±2.24
22.04 ±1.71
11.07 ±1.37
11.66 ±1.81
P.value
C.V
(m/sec)
(N.S)
(H.S)
(S)
(H.S)
(H.S)
Patients
68
57.34 ±7.12
57.55 ±6.77
47.70±8.19
47.88±8.01
Control
42
59.67 ±3.07
59.41 ±3.44
51.48 ±4.55
51.61 ±3.97
(H.S)
(H.S)
P.value
(S)
(N.S)
Patients with Abnormal
Electrophysiologic Results
PARAM
ETER
DSL
(msec)
SUBJECT N
O.
Rt.Median
Rt.Ulnar
Rt.Com.
N.
N.
Per. N
Mean ± S.D Mean ± S.D Mean ±S.D
Rt.Post.
Tib. N.
Mean ± S.D
Control
42
2.44 ± 0.17
2.29 ± 0.16
3.05± 0.22
3.12 ± 0.27
Affected
21
3.11 ± 0.84
2.79 ± 0.75
4.39 ± 1.06
4.73 ± 0.96
P.value
AMPLIT Control
UDE
Affected
(µv)
P.value
C.V
(m/sec)
(H.S)
(H.S)
(H.S)
(H.S)
42
25.25 ±2.24
22.04±1.71
11.07 ±1.37
11.66 ±1.81
21
18.25 ±5.87
17.76±4.92
6.62 ± 3.23
5.96 ± 3.46
(H.S)
(H.S)
(H.S)
(H.S)
Control
42
59.67 ±3.07
59.4 ±3.44
51.48 ±4.55
51.61 ±3.97
Affected
21
51.45 ±9.58
54.0 ±8.56
39.19 ±7.25
38.85 ±6.91
P.value
(H.S)
(H.S)
(H.S)
(H.S)
Recommendations

Dyslipidemia is a causative factor for peripheral
neuropathy, which stresses the importance of screening
patients with peripheral neuropathy of unknown origin for
dyslipidemia, as it is a potentially treatable condition.

Electrophysiologically, we recommend to examine the
patients, at first, for nerves of lower limbs, as they are
usually the first to be affected. Starting with sensory fibers
assessment and further tests are done according to these
findings.

Unilateral sensory nerve conduction study will
be reasonably informative since the disease
process found to affect both sides of the body
equally. Examination of upper limbs mainly
median nerve sensory conduction study will be
supportive and helpful to see the degree of
extension of the disease process.
 Motor nerve conduction study could
be helpful and informative if the
patients have abnormal sensory nerve
conduction study.
 So further evaluation of patients by
MNCS and F-wave conduction study
is recommended.
Thank you