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CLINICAL APPROACH
UMN
•Weakness entire limb/side
•Hypertonia /Spasticity
•Brisk reflex
•Barbinski +ve
Spinal cord
•No/slight muscle atrophy
contain both UMN
•Clonus
and LMN, if
damage :
•UMN /
•LMN /
•combination
LMN
•Paralysis muscle in discrete
area
•Hypotonia / Flacidity
•Reflex absent /normal
•Muscle wasting (atrophy)
•fasciculation
Anterior horn cell Peripheral nerve NMJ Muscle
1. Demyelination
2. Axonal degeneration
3. Wallerian degeneration
4. Compression
5. Infarction
6. Infiltration
Motor.
Weakness
(usually Sensory
start Positive phenomena
distally)
Paresthesia, Dysesthesia,
Cramps Hyperalgesia, Causalgia-
Fasciculatio spontaneous burning pain,
n Lightning pain
Tremor Negative phenomena
Hyposthesisa,
Anesthesia
Ataxia
Peripheral
neuropathy
Autonomic
symptoms
Motor.
Wasting
Fasciculation
Peripheral Hypotonia
neuropathy Weakness
sign Absent DTR
P.N. Sensory.
Thickening Impaired in
Tendernes cutaneous Nerve
s distribution
Trophic Distal symmetric
Tinnel’s
sign
changes- “Glove and
ulcer/joints/ hair Stocking”
loss/brittle distribution
nail/cold blue Dermatomal
extremities distribution
Preferential loss of
History
• Onset
o Acute / Sub acute / Chronic
• Course
o Relapsing or not
• Function disturbance
o Sensory / Motor / Sensory motor / Autonomic
• Systemic illness
o Endocrine / Metabolic
• Drug history
• Exposure to toxins
• Family history
Diagnostic assessment
Mimickers
High
High cervical
cervical lesion
lesion
•• IfIf Gracilis
Gracilis column
column first,
first, then
then the
the
Cuneate
Cuneate column,
column, symptoms
symptoms develop
develop in
in
L.L
L.L followed
followed by by U.L
U.L
•• Preservation
Preservation of of Ankle
Ankle Jerk.
Jerk. Clue
Clue against
against
neuropathy
neuropathy
Psychogenic
Psychogenic
Myasthenia
Myasthenia
Investigations
Step wise approach
Diagnosis
Step-I
• FBC, ESR
• Urine-Glucose, Proteins
• FBS, RFT, LFT, TFT
• X-ray Chest
• Electro diagnostic Study Step –III
-Urine Bence Jones protein
-GTT
-CSF
-Immunology- HIV,antineural
antibody,antiganglioside antibody
Step-II -Search for ca
• Serum protein -Nerve biopsy
Electrophoresis
• Immunological -Molecular genetic study
Investigations
•No such thing as routine study- tailor made for each patient
•Even after a thorough work up, no cause identified in 15-20%
Nerve conduction study
• Confirm the presence of Neuropathy
• Differentiate from NMJ / Muscle
• Localize the pathology
– Neurons/Root/ Plexus/ Nerves.
– Mononeuritis/ Multiplex/
Polyneuropathy
– Sensory/ Motor.
• Characterize the pathology
– Axonal/ Demyelinating
• Severity and Chronicity
• Prognosis
• Sub clinical involvement
Nerve Biopsy
• Not required for most of routine cases
• Might show the pathological changes-
but may not clinch an etiology.
• May miss
– Patchy lesions
– Predominantly proximal conditions
– Selective motor involvement
• Indicated in cases of unknown
etiology.
• Expertise must be available
• Routine H&E, Axon/Myelin staining,
Immune studies, Teased fiber, EM
Treatment
Ganeral
• Protection from trauma
• Relief of pain
• Withdraw toxin/drugs
• Physiotheraphy
• Rehabilitation
Specific Surgery
• Treat etiology • Entrapment
neuropathy
• Treat systemic disease
• Correction of
• Immunosuppression deformities
• Immunomodulation
Rehabilitation