DIFFERENTIAL DIAGNOSIS OF NEUROGENIC DISORDERS & …
[Pages:46]DIFFERENTIAL DIAGNOSIS OF NEUROGENIC DISORDERS & MYOPATHIES
NEUROPATHY
Weakness
distal
Sensory loss
+
Loss of reflexes
early
CSF protein
elevated
Electromyography neurogenic
Serum enzymes
+/-
MYOPATHY proximal 0 late normal myopathic ++++
CLASSIFICATION OF PERIPHERAL NERVE DISEASES
Myelinopathy Acute inflammatory polyneuropathy (AIP) Chronic inflammatory demyelinating polyneuropathy (CIDP) Charcot-Marie-Tooth, type 1 (CMT-1)
Axonopathy Vasculitis, amyloidosis Metabolic neuropathies (diabetic neuropathy) Toxic neuropathy (acrylamide neuropathy)
Neuronopathy Amyotrophic lateral sclerosis (ALS)
1
TEASED MYELINATED FIBER: NORMAL
2
3
TEASED MYELINATED FIBER: SEGMENTAL REMYELINATION
SAME TEASED FIBER AT HIGHER MAGNIFICATION
4
TEASED MYELINATED FIBER: AXONAL DEGENERATION
5
CLASSIFICATION OF PERIPHERAL NERVE DISEASES
Myelinopathy Acute inflammatory polyneuropathy (AIP) Chronic inflammatory demyelinating polyneuropathy (CIDP) Charcot-Marie-Tooth, type 1 (CMT-1)
Axonopathy Vasculitis, amyloidosis Metabolic neuropathies (diabetic neuropathy) Toxic neuropathy (acrylamide neuropathy)
Neuronopathy Amyotrophic lateral sclerosis (ALS)
ACUTE INFLAMMATORY POLYNEUROPATHY (GUILLAIN-BARRE SYNDROME [GBS])
? Rapidly progressive neuropathy, chiefly motor, reaching maximum weakness usually within 1 to 2 weeks.
? An acute infectious illness precedes weakness in two thirds. ? Electrophysiology: slow conduction velocity & conduction block
but also show axonal degeneration, usually of mild degree. ? Recovery takes weeks or months. Permanent handicap in 5%. ? Plasmapheresis or intravenous gamma globulin speeds recovery.
6
PATHOLOGY OF ACUTE INFLAMMATORY POLYNEUROPATHY (GBS)
? Immune complexes (C3, IgG, IgM) are detectable on the surface of myelin sheaths in the early stage.
? T cells, chiefly CD4 subset, infiltrate endoneurium. ? Monocytes and macrophages appear to attack myelin sheaths. ? Myelinated fibers show segmental demyelination during the
first few days. Segmental remyelination occurs subsequently. ? The lesions have a perivenular distribution.
GBS, DORSAL ROOT GANGLION, H&E
7
GBS, MOTOR NERVE, H&E GBS, MOTOR NERVE, SEMITHIN SECTION
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