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Peripheral Neuropathies - Coggle Diagram
Peripheral Neuropathies
PNS
Organization
Bundles of axons running to and from the CNS
Motor Axons; Single axons stretch from anterior horn to NMJ
Sensory Axons: Single axons stretch from receptors to central sensory pathways via pseudo-unipolar dorsal root ganglion
Anatomy
Individual nerve trunks made up of many nerve fasicles which in turn are composed of axons
Myelination
Speed up conduction in order to conduct faster than unmyelinated fibers due to saltatory conduction
CNS and PNS
Oligodendrocytes: Myelinating glial cells, direction of myelination centripetal, and Several per cell
Schwann cells: Centrifugal and one per cell
Physiology of Function
nerve fiber and diameter correlate with function (Large myelin - Spindle, Golgi, Sensory, Motor, Small/Inter - Touch, hair, pain, motor, Unmyelin - Temp, pain (slow sympathetic)
Symptoms of Neuromuscular Disease
Motor Symptoms (weakness)
Sensory symptoms (Numbness, tingling, burning)
Neurogenic Process: Atrophy, fasciculations, normal/hypotonic tone, diminished reflex, weakness pattern
Myopathic Process: Little/no atrophy, normal tone, normal reflexes
NMJ: No sensory symptoms, weakness variable
Sensory Exam
Pattern is anatomic based on nerve/root distribution
Amyotrophic Lateral Scleoriss
Description
Clinical Diagnossis based on UMN, and LMN Signs
Absence of significant sensory abnormalities
Bulbar Symptoms (Dysphagia, speech abnormalities)
Pseudobulbar affect (emotional incontinence)
Denervation on EMG
Degenerative Disc Disease
Commonest cause of isolated radiculopathy, cervical, thorcic, lumbar, sacral, radicular pain, numbness/paresthesia in dermatome of nerve root, loss of strength in myotome
Plexopathies
Brachial Plexopathies
Traumatic: Following shoulder disclocation
Malignant: With apical lung cancer, painful, lower trunk, associated with horner's syndrome
Inflammatory: Brachial Plexitis, neuralgic amyotrophy, parsonage-Turner Syndrome
Diabetic Lumbosacral Plexopathies
Abrubt onset of unilateral leg pain, weakness follows pain
Believed to be ischemic, often good recovery but residual weakness
Mono neuropathies
Median Nerve at Wrist: Carpal Tunnel
Ulnar at Elbow: Ulnar claw
Radial at Spiral Groove: Saturday night palsy -> Wrist drop
Lateral Femoral Cutaneous : Meralgia paresthetica
Peroneal at fibular head: Foot drop, steppage gait
Polyneuropathies
Classification Methods
Type of Nerve involved: Sensory, motor, sensorimotor, autonomic, generalized
Mechanism of Damage: Axonal, demyelinating, Mixed
Distribution: Length-dependent, mononeuritis multiplex
Time Course: Acute, subacute, chronic
Approach to Neuropathies
Typical
Chronic, sensorimotor, axonal, length dependent (diabetes)
Others: Toxic, Alcoholic, B12 deficiency, uremic, thyroid
Atypical
Mononeuritis multiplex: Vasculitis
Pure Motor: Lead
Pure sensory: Paraneoplastic, Platinum derived Chemo
Hereditary: Charcot marie tooth
Acquired demyelinating: GBS
Polyneuropathy
Motor symptoms: Weakness, loss of muscle bulk, cramps
Sensory symptoms: Numbness, loss of feeling, tingling, burning, pain, poor balance, autonomic symptoms
Nerve Conudction Study
Determine which nerve is involved
Determine sensory/motor, small vs large fiber, axonal vs demyelinating, acute vs chronic
Diabetic Neuropathy
Most diabetics will have some neuropathy after 10 years
Seneveral Clinnical Patters
Distal tingling/numbness
Small fibre predominant (burning dysesthetic pain)
Large fibre predominant (very little/no pain, prominent ataxia)
Autonomic Neuropathy
Resting Tachycarida, loss of sinus arrhythmia, postural hypotension, erectile dysfunction/impotence, bladder dysfunction, swearing/pupillary abnormaltiies
Diabetic 3rd nerve palsy
Ptosis, diplopia, Spares pupil
Guillain Barre Syndrom
Description
Acute inflammatory demyelinating polyradiculoneuropathy
Autoimmune attach on myelin sheaths
Clinical Features
Acute illness developing over few days-weeeks
Tingling paresthesia and pain are often the first symptoms
Dominant Feature is weakness (aschending paralysis is a bad term but legs before arms)
Symetric, faicla fweakness, and resp failure
Diagnosis
Primarily clinical diagnosis, nerve conduction study (often normal or minimally non sepcific), lumbar puncture (CSF protein elevated and albuminocytologic dissociation)
Pathophysiology
Loss of myelin sheath leading to slowed conduction velocity or conudctiion block
Treatment
Immunomodulatory, supportive therapy
IVIg Intravenous
Plasmapheresis
Initiate treatment quickly
General Management
Close monitorying of respiratory status (Bedisde spirometry) autonomic instability, DVT prophylaxis, Stress ulcer, Nosocomial infections, Bowel routine, urinary catheter, swallowing issues, pain control, SIADH