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Peripheral neuropathy
1. Dr. Sabir Kumar Khadka
Dept of Orthopedics
PERIPHERAL NEUROPATHY
2. Refers to nervesoutside
the brainand spinal
cord.
Broken downinto
Sensory
Motor
Autonomic
▪ Parasympathetic
▪ Sympathetic
3. May affect one nerve (mononeuropathy),
Several nerves together (polyneuropathy)
Several nerves not contiguous
(Mononeuropathy multiplex)
Further classified into those that primarily affect the
cell body (e.g., neuronopathy or ganglionopathy),
myelin (myelinopathy), and the axon (axonopathy)
4. Pathology
Acute axonal interruption
Loss of motor and sensory function is immediate and complete
Detectable at early stage by nerve conduction and EMG.
Chronic axonal degeneration
Symptoms tend to appear in feet and legs before arms and
hands(stocking and glove distribution)
NCV:reduction in size of CMAP and SNAP responses
Demyelinating neuropathies
Focal entrapment most common in nerve entrapment syndrome
and blunt soft tissue trauma.
Slowing of conduction and complete nerve block
Eg: GBS and HMSN
5. Possible mechanisms of peripheral nervedegeneration
Demyelination –e.g. Guillain-BarreSyndrome
Axonal degeneration - e.g. toxic neuropathies
Compression –e.g. carpal tunnelsyndrome
Infarction –e.g.diabetes
Infiltration –e.g. leprosy and granulomas
6. Causes of polyneuropathy
Hereditary
Hereditary motor and sensory neuropathy
Friedreich ataxia
Hereditary sensory neuropathy
Infections
Viral infections
Herpes zoster
Neuralgic amyotrophy
Leprosy
8. Disease
Diabetes
Paraproteinaemia
Alcohol misuse
Renal failure
Vitamin B-12 deficiency
HIV infection
Chronic idiopathic
axonal neuropathy
Prevalence
11-41% (depending on
duration, type,and
control)
9-10%
7%
4%
3.6%
16% (depending on the
population studied,
usually much lower)
10-40% of different
hospital series
BMJ 2010:341:c6100
9. Loss of function
“- symptoms”
Disordered function
“+ symptoms”
Sensory
“Large Fiber”
↓ Vibration
↓ Proprioception
Hyporeflexia
Sensory ataxia
Paresthesias
Sensory
“Small Fiber”
↓ Pain
↓ Temperature
Dysesthesias
Allodynia
The clinical response to sensory nerve injury
10. Loss of function
“- symptoms”
Disturbed function
“+ symptoms”
Motor nerves Wasting Fasciculation
Large fibre Hypotonia Cramps
Weakness
Hyporeflexia
Orthopedic deformity
The clinical response to motor nerve injury
11. Loss of function
“- symptoms”
Disturbed function
“+ symptoms”
Autonomic nerves ↓ Sweating
Hypotension
↑ Sweating
Hypertension
Urinary retention
Impotence
Vascular color changes
The clinical response to autonomic nerve injury
12.
13. Peripheral nerve compressionand
entrapment
Carpaltunnel syndromeisacommon
mononeuropathy –Median nerve
entrapement
Clinicalpresentation
Pain, tinglingand paraesthesia on
palmaraspectof handandfingers
Weaknessof thenar muscles and
wasting of abductor pollicis brevis
Painmay extend to arm andshoulder
Tinel’sand Phalen’stests arepositive.
16. Clinical presentation:
Progressive weakness orclumsiness
Difficulty walking (falling or stumbling)
Respiratory difficulties (falling vital capacity)
Wasting
Foot or wrist drop might be seen
Reflexes absent orreduced
17. MONONEUROPATHY
Focal involvement
of a single nerve
Weakness &
sensory loss in the
territory of a single
peripheral nerve
Pain along the
pathway of the
nerve
Direct
trauma
compression
entrapment Vascular
lesions
neoplasms
18. Random pattern of nerve involvement
In distribution of separate
nerves,asymmetric
May/may not be painful
Not length dependent
Isolated reflex loss
Mononeuropathy Multiplex
22. POLYRADICULOPATHY
Disease of multiple peripheral nerve roots
Asymmetric with erratic distribution-proximal in
one,distal in another
Pain is a common feature
MONORADICULOPATHY
Root disease by disease of spinal column
Changes in distribution of spinal nerve root
23. SENSORYNEURONOPATHY
Ganglion cells predominantly affected
Both proximal & distal involvement
Sensory ataxia is common
No weakness
But awkward movement d/t sensory disturbances
MOTOR NEURONOPATHY
Disorder of ant horn cells
Weakness,fasciculation,atrophy
24. PLEXOPATHY
Asymmetric
Painful onset
Multiple nerves in a single limb
Rapid onset of weakness,atrophy
Isolated reflex loss
Brachial plexus traction injury
Lumbosacral plexopathy in
pelvic trauma
Compression by local
tumor(pancoast’s tumor)
25. Directly related to the duration and degree of
abnormal metabolic control –occurring relatively
early indisease
Due to metabolic disturbance and accumulation of
fructose and sorbitol in Scwanncells
Types of Diabeticneuropathy
Symmetrical mainly sensoryneuropathy
Acute painfulneuropathy
Mononeuropathy and mononeuritismultiplex
Diabetic amyotrophy
Autonomic Neuropathy
26. Chronic alcohol abuseleads
to polyneuropathy
Calf pain iscommon
Deficiency in thiamine dueto
alcoholism also causes
neuropathy
Canlead to Wernicke-Korsakoff
syndrome
Commonpresentation
▪ Eyesigns
▪ Ataxia
▪ Cognitive change
▪ Deliriumtremens
▪ Hypothermia andhypotension
27. Acute polyneuropathy –acute inflammatory or postinfective
neuropathy
Usually demyelinating but canbe axonal
Following Campylobacter jejuni and CMV infections
Infection inducesantibody responses against peripheral nerves
Paralysis 1-3weeks followinginfection
Weaknessof distal limb musclesand/or distal numbness
Symptoms progressproximally
Lossof tendonreflexes
Facial muscleweakness
Autonomic features -uncommon
Might need ventilatorysupport
SCheparin is required to reduce risk of thrombosis
Spontaneousrecovery beginsafter several weeks
28.
29. DM
hypothyroidism
chronic renal failure
liver disease
intestinal
malabsorption
malignancy
connective tissue
diseases
[HIV]
drug use
Vitamin B6 toxicity
alcohol and dietary
habits
• Weight loss, malaise, and anorexia.
30. Diabetes and Pre-Diabetes
Alcohol neuropathy
Chemotherapy
◦ Platinum-based
Paraproteinemia
Vasculitis and Connective Tissue Diseases
Heavy metals and other toxins
HIV
Amyloidosis
Porphyria
32. The temporal course of a neuropathy varies,
based on the etiology.
◦ With trauma or ischemic infarction, the onset will
be acute, with the most severe symptoms at
onset.
◦ Inflammatory neuropathies have a subacute
course extending over days to weeks.
◦ A chronic course over weeks to months is the
hallmark of most toxic and metabolic
neuropathies.
33. A chronic, slowly progressive neuropathy over
many years occurs with most hereditary
neuropathies or with chronic inflammatory
demyelinating polyradiculoneuropathy (CIDP).
Neuropathies with a relapsing and remitting
course include CIDP, acute porphyria,
Refsum's disease, hereditary neuropathy with
liability to pressure palsies (HNPP), familial
brachial plexus neuropathy, and repeated
episodes of toxin exposure.
34. Ischemic neuropathies often have pain as a
prominent feature.
Small-fiber neuropathies often present with
burning pain, lightning-like or lancinating
pain, aching, or uncomfortable paresthesias
(dysesthesias).
35. Peripheral neuropathy can present as restless
leg syndrome.
Proximal involvement may result in difficulty
climbing stairs, getting out of a chair, lifting
and bulbar involvement can also be seen
36. The clinical assessment should include:
◦ careful past medical history, looking for systemic
diseases that can be associated with neuropathy,
such as diabetes or hypothyroidism.
37. All patients should be questioned regarding
◦ HIV risk factors
◦ diet (nutrition)
◦ vitamin use (especially B6)
◦ possibility of a tick bite (Lyme disease)
◦ Constitutional symtoms (malignancy)
38. A cranial nerve examination can provide
evidence of mononeuropathies.
Funduscopic examination may show
abnormalities such as optic pallor, which can
be present in leukodystrophies and vitamin
B12 deficiency.
39. Tests with the highest yield of abnormality:
1. blood glucose (fasting)
2.serum B12 with metabolites
(methylmalonic acid, homocysteine)
3. SPEP(serum protein electrophoresis)
43. Antibodies against Gangliosides
GM1 :
GM1, GD1a :
GQ1b :
Multifocal motor neuropathy
Guillain-Barré syndrome
Miller Fisher variant
Antibodies against Glycoproteins
Myelin- associated glycoprotein
Antibodies against RNA-binding proteins
Anti-Hu, antineuronal nuclear antibody 1: Malignant
inflammatory polyganglionopathy
44. (1) Confirming the presence of neuropathy,
(2) Locating focal nerve lesions,
(3) Nature of the underlying nerve pathology
45. The limitations of EMG/NCS should be
taken into account when interpreting the
findings.
◦ There is no reliable means of studying proximal
sensory nerves.
◦ NCS results can be normal in patients with small-
fiber neuropathies
◦ Lower extremity sensory responses can be absent
in normal elderly patients.
EMG/NCS are not substitutes for a good
clinical examination.
47. In vasculitis, amyloid neuropathy, leprosy, CIDP,
Inherited disorders of myelin, and rare
axonopathies
The Sural nerve is selected most commonly
The superficial peroneal nerve – alternative;
:advantage of allowing simultaneous biopsy of
the peroneus brevis muscle through the same
incision.
This combined nerve and muscle biopsy
procedure increases the yield of identifying
suspected vasculitis
48. “For symptomatic patients with suspected
polyneuropathy, skin biopsy may be
considered to diagnose the presence of a
polyneuropathy, particularly SFSN.”
49. Slow progression
◦ Treat causative factors if possible
◦ If rapidly progressing
IVIG
Immunomodulating agents
