Peripheral Nerve Disorders Flashcards

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1
Q

Peripheral Nerve Disorders

Subtypes

A

Peripheral nerve ⇒ neuropathy

Nerve root ⇒ radiculopathy

Lumbar or brachial plexus ⇒ plexopathy

Anterior horn ⇒ motor neuron disease

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2
Q

Peripheral Nervous System

Basic Anatomy

A
  • Consists of nerves and ganglia outside of the brain and spinal cord
  • Peripheral nerves connected to spinal cord by two roots:
    • Ventral root ⇒ motor
    • Dorsal root ⇒ sensory
  • Interconnects all other tissues with the CNS
  • Innervates all voluntary muscles
  • Transmits the sensory impulses to the whole body
  • Individual nerve fibers ⇒ vary widely in diameter and may be heavily myelinated, lightly myelinated or unmyelinated
    • Amount of myelin ∝ conduction speed
  • Largely under conscious (cerebral) control
  • Injury results in both sensory and motor loss
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3
Q

Sensory Innervation

A
  • A sensory nerve (afferent nerve) carries sensory information toward the CNS
  • It is a bundle of nerve fibers coming from sensory receptors in the PNS
  • Afferent nerve fibers leave the sensory neuron from the dorsal root ganglia of the spinal cord
  • Large myelinated sensory fibers ⇒ vibration and proprioception
  • Small myelinated and unmyelinated sensory fibers ⇒ pain and temperature
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4
Q

Motor Innervation

A
  • Upper Motor Neuron
    • Neuron in the motor cortex
    • Travels down and decussates at the level of the medulla
    • Travels down the spinal cord
  • Lower Motor Neuron
    • Neuron in the spinal cord or cranial nerve of brainstem
    • Travel to the skeletal muscle
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5
Q

Motor Unit

A

A motor neuron and all the skeletal fibers it innervates.

  • Groups of motor units work together to coordinate contraction of a single muscle
  • It is a functional unit made up of:
    • Lower motor neuron
    • Motor axon
    • NMJs
    • Muscle fibers innervated by the motor neuron
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6
Q

Upper Motor Neuron

Signs

A
  • Weakness
  • Hyperreflexia
  • Spasticity
  • Stiffness
  • Babinski sign
  • Brisk jaw jerk
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7
Q

Lower Motor Neuron

Signs

A
  • Fasciculations
  • Atrophy/muscle wasting
  • Weakness
  • Muscle cramps
  • Loss of reflexes
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8
Q

Disease Localization

A

Differentiating PNS from CNS disease

  • Weakness or sensory loss confined to one limbperipheral nerve problem
    • Associated pain in the extremity ⇒ ↑ likelihood of a peripheral process
  • Localization less obvious when weakness/sensory loss involves > 1 extremity or when there is no associated pain or discomfort
  • The patient approach will include taking a detailed hx including family hx of similar sx, time course of sx, and comorbidities (ex. DM)
  • Complete neurologic exam will be extremely helpful
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9
Q

Peripheral Nerve

Composition

A

Peripheral nerve is composed of:

  • Motor axon/neuron
  • Sensory axon/neuron
  • Autonomic fibers
  • Myelin
  • Other supporting structures
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10
Q

Peripheral Nerve

Characteristics

A
  • Individual nerve fibers ⇒ vary widely in diameter and may be heavily myelinated, lightly myelinated or unmyelinated
    • Amount of myelin ∝ conduction speed
    • Myelin made by Schwann cells
    • Distance b/t nodes of Ranvier determines conduction rate
  • Largely under conscious (cerebral) control
  • Injury results in both sensory and motor loss
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11
Q

Peripheral Nerve Damage

A
  • Segmental demyelination
    • Diseases primarily affect Schwann cells ⇒ loss of myelin
  • Nerve injury/transection
    • Primary destruction of the axon ⇒ secondary disintegration of its myelin sheath
    • Results in axonal degeneration
      • Distal portion ⇒ Wallerian degeneration
      • Proximal portion ⇒ retrograde degeneration
      • Begins in the periphery and proceeds back toward the cell body ⇒ “dying back“
    • Cell body may become chromatolytic
    • If process reversed early phases, some regeneration may be possible
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12
Q

Axonal Injury

A

Traumatic transection of a nerve

  • Distal portion of the nerve fiber degenerates ⇒ Wallerian degeneration
    • Axons begin to break down
    • Schwann cells begin to catabolize myelin and later engulf axon fragments, forming myelin ovoids
    • MΦ recruited and phagocytose axonal and myelin-derived debris
  • Proximal portion of severed nerve degenerates ⇒ retrograde degeneration
    • Degenerative changes involving only the most distal two or three internodes
    • Proximal stump then undergoes regenerative activity
    • Regenerated fiber has shorter internodes
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13
Q

Segmental Demyelination

A
  • Selective loss of individual myelin internodes with preservation of the axon
  • Process affects some Schwann cells and their corresponding internodes while sparing others
  • Disintegrating myelin is engulfed initially by Schwann cells and later by MΦ
  • After segmental demyelination, Schwann cells can proliferate and remyelinate
  • Example: Guillain-Barré Syndrome
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14
Q

Regenerative Processes

A
  • Axonal Sprouting
    • After axonal damage, the axon may sprout from the distal end
    • Regenerating axons re-grow at ~ 1 mm/day
  • Remyelination stimulated by denuded axon
    • Segmentally demyelinated axons may remyelinate ⇒ shorter internodes = slower conduction
    • Axonal sprouts will be re-myelinated by surviving Schwann cells
    • Remyelination may restore some function
    • Repeated episodes of demyelination and remyelination → accumulation of layers of Schwann cell processes
      • Onion Bulb: a single thinly myelinated axon surrounded by concentrically arranged Schwann Cells and redundant BM
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15
Q

Neurodiagnostic Testing

A

Electromyography (EMG) and Nerve conduction studies (NCS)

  • Most common diagnostic tests for dx of nerve and muscle disease after hx and exam
  • Both are complementary and are always performed together during the same setting
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16
Q

Nerve Conduction Studies (NCS)

A

Measure the ability of sensory and motor fibers to conduct an action potential

Used mainly for eval of paresthesias and/or weakness of arms and legs

  • Axonal injury/neuropathy
    • ↓ amplitude of AP
    • Mild slowing
    • Can see mix of both
  • Demyelination neuropathy
    • Conduction block (failure of AP to propogate)
    • Slow conduction
    • Amplitude of AP may be normal or reduced
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17
Q

Electromyography (EMG)

A

Measures muscle response or electrical activity in response to nerve stimulation of the muscle

Used to determine NMJ abnormalities, myopathy, and denervation

  • Increased insertion activity
    • Denervation ⇒ will fire spontaneously as a “Fibrillation potential”
    • Polymyositis
  • Decreased insertional activity
    • Myopathy ⇒ loss of response of motor units
      • Small motor units
      • Early recruitment of other motor units
      • Muscle is replaced by fat
  • Muscle fibers s/p denervation and reinnervated ⇒ very large due to reorganization and formation of large motor units
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18
Q

Peripheral Nerve Biopsy

A
  • Used when the pathology is in question and when therapy is contemplated
  • Superficial sensory branches of the sural or radial nerves are often sampled and examined pathologically
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19
Q

Peripheral Neuropathy Patterns

A

Patterns of peripheral neuropathy aids in clinical dx and finding underlying pathologic processes:

  • Mononeuropathy
  • Mononeuropathy Multiplex
  • Polyneuropathy
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20
Q

Focal Neuropathies

(Mononeuropathies)

A
  • Typically have damage to a single nerve
  • Etiologic agents are focal ⇒ process tends to be asymmetric
  • Classic cause is vasculitis ⇒ produces discrete infarctions in nerve trunks
  • NO distal-proximal gradient b/c an individual nerve trunk is affected
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21
Q

Median Nerve

A

Responsible for:

  • Flexion of the thumb, index, and middle fingers
  • Wrist flexion
  • Thumb opposition
  • Forearm protonation
  • Hand abduction
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22
Q

Median Nerve Entrapment

(Carpal Tunnel Syndrome)

A

Secondary to compression of the median nerve as it passes through the carpal tunnel

Most common nerve entrapment

  • Due to any condition that causes decreased space within the carpal tunnel
    • Tissue edema, pregnancy, inflammatory arthritis, hypothyroidism, amyloidosis acromegaly, DM, and excessive repetitive motions of the wrist
  • Pain primarily at the wrist, may radiate to forearm, arm, or shoulder
  • Sensory findings: paresthesia and sensory loss in the thumb, index and lateral half of ring fingers of affected hand
    • Often noted more at night
  • Motor findings: Weakness of thumb abduction and atrophy of the thenar eminence
  • Diagnostic signs:
    • Phalen’s Sign: elicited when wrist flexion produces paresthesias in the median nerve distribution
    • Tinel’s Sign: present when tapping over the median nerve at the wrist elicits paresthesias in the median nerve distribution
  • NCS: focal slowing or conduction block of median nerve fibers
  • Treatment: wrist splints in mild cases and surgical decompression in severe cases
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23
Q

Ulnar Nerve

A

Responsible for:

  • Wrist flexion
  • Flexion of 4th and 5th digits
  • Thumb adduction
  • Finger abduction and adduction
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24
Q

Ulnar Neuropathy

(Cubital Tunnel Syndrome)

A

Nerve entrapment due to compression of the ulnar nerve in the cubital tunnel at the elbow.

  • Sensory signs: numbness of the little finger and half of the ring finger
  • Motor signs: decreased grip and problems with finger dexterity
  • NCS: Slow conduction velocity at the elbow, or conduction block
  • Treatment: avoidance of behaviors involving leaning on elbows, elbow pads or surgical decompression in severe cases
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25
Q

Radial Nerve

A

Responsible for:

  • Supination of forearm
  • Brachioradialis reflex
  • Extension of fingers, thumb, wrist, and elbow
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26
Q

Radial neuropathy

“Saturday Night Palsy”

A

Results from compression of the radial nerve at the radial/spiral groove.

  • Classic case seen with sleeping with arm draped over a chair
  • Can also be seen with humerus fracture or other insult
  • Sensory sx: sensory loss over lateral dorsal hand
  • Motor sx: wrist drop, finger drop, weakness of supination, mild elbow flexion weakness
  • Treatment is supportive with generally spontaneous recovery
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27
Q

Peroneal (Fibular) Nerve

A
  • Deep peroneal nerve
    • Ankle and toe dorsiflexion
    • Foot eversion
  • Superficial peroneal nerve
    • Sensory over anterior and lateral lower leg
28
Q

Peroneal Neuropathy

A

Results from compression of the peroneal nerve as it wraps around the fibular head.

  • Often results from leg crossing, prolonged bedrest, knees casts, fibular fractures
  • Motor sx: weakness of toe and foot dorsiflexion and foot eversion
  • Sensory sx: sensory loss over the dorsum of the foot and lateral distal lower extremity
  • NCS: Slow conduction velocity at fibular head
  • Management is usually supportive with removing cause of compression
29
Q

Lateral Femoral Cutaneous Nerve

A

Provides sensation to the:

  • Anterior thigh
  • Knee
  • Upper part of lateral thigh
30
Q

Lateral Femoral Cutaneous Neuropathy

(Meralgia Paresthetica)

A

Results from entrapment of the lateral femoral cutaneous nerve as it passes under the inguinal ligament.

  • Causes include tight clothing, obesity, and pregnancy
  • Presents with paresthesias in the lateral thigh
  • NCS/EMG not helpful
  • Tx: supportive, meds
31
Q

Mononeuritis Multiplex

A
  • Less common focal neuropathy
  • Painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy
  • Involves isolated damage to at least two separate nerve areas
  • Multiple nerves can be affected
    • Can be confused with polyneuropathies
  • As condition worsens, becomes less multifocal and more symmetrical
  • Has variable etiologies including vasculitis, DM, HIV, CMV
32
Q

Polyneuropathy

Overview

A

Generalized process affecting many peripheral nerves.

  • Most common pattern of peripheral nerve disease
  • Usu. occurs as a side effect of medication or manifestation of systemic disease
  • Can be caused by both axonal degeneration and demyelinating disease
  • Affects longest nerves most severely
  • Presents first with distal signs in the arms and legs
    • Muscle weakness of the hands and feet
    • Loss of sensation in what is refer to as the “glove and stocking” distribution
  • Tends to be symmetric
33
Q

Polyneuropathy

Etiologies

A
  • Usu. occurs as a side effect of medication or manifestation of systemic disease
    • DM, ETOH, HIV, CMT
  • Peripheral nerves susceptible to various factors ⇒ ∆ health & function ⇒ polyneuropathy
    • Toxins (acrylamide and hexacarbons)
    • Chemotherapeutic agents such as Vincristine and Isoniazid
    • Inflammation (Amyloidosis)
    • Dietary
    • Metabolic (B12, hypothyroid)
    • Hereditary
    • Infection (VZV, Leprosy)
    • Parainfectious
34
Q

Polyneuropathy

Clinical Manifestations

A
  • Length dependent sensory loss and weakness
  • Reflexes are decreased
  • Autonomic dysfunction can occur in severe cases
  • Sx may be variable
35
Q

Polyneuropathy

Neurodiagnostic Testing

A

Abnormal studies provide a higher level of specificity

Unclear etiology ⇒ NCS/EMG testing

  • EMG w/ axonal neuropathy
    • Systemic disorder, toxins, drugs
  • EMG w/ demyelinating neuropathy
    • Autoimmune or hereditary d/o
  • EMG w/ mixed neuropathy
    • Work-up same as demyelinating physiology
    • If not diagnostic, then evaluate for axonal causes
36
Q

Diabetic Polyneuropathy

A
  • Most common cause of neuropathy
  • Most common complication of DM
  • Involves peripheral and autonomic nervous system
  • Has a distal-proximal gradient
  • Duration and severity of hyperglycemia ⇒ crucial risk factor for development of diabetic neuropathy
  • Microvascular injury to blood vessels that supply the nerve
  • Prominent axonal degeneration w/ myelin debris, distal > proximal
  • Sx vary depending on areas affected:
    • Sensitive to touch
    • Pain
    • Anesthesia
    • Burning sensation
    • Muscle weakness or wasting
    • Ataxia
  • Treatment includes better glycemic control, gabapentin, pregabalin, SSNRI
37
Q

Vitamin B12 Deficiency Neuropathy

A
  • Vit B12 is an essential nutrient
  • Deficiency is common in the US
    • 10-25% of people > 80 y/o may have Vit B12 deficiency
  • Multiple etiologies:
    • Strict vegetarian diet
    • Inability of stomach acid to aid in absorption
    • Pernicious anemia
  • Ass. w/ impaired erythropoiesis and nervous system demyelination
  • Early dx is important
  • Treatment: ↑ Vit B12 in diet, oral or subcutaneous supplements if needed
38
Q

Alcoholic Neuropathy

A
  • ETOH abuse ⇒ high incidence of polyneuropathy
  • Primarily an axonal neuropathy
  • Complicated by demyelination when associated w/ nutritional deficiency
  • Predominant ↓in density of small myelinated and unmyelinated fibers
  • Gradually progressive
  • Clinically sx usually symmetric and predominantly distal
  • Sx include numbness, paresthesias, burning pain, weakness, cramps and ataxia
  • Specific treatment is not available
  • Pts should receive thiamine
  • Improved nutrition and cessation of drinking have been associated with sx improvement
39
Q

Guillain-Barre Syndrome (GBS)

(“Acute Inflammatory Demyelinating Polyneuropathy (AIDP)”

A

Severe ascending, symmetric weakness with areflexia.

  • Rapidly progressive acute segmental demyelination
  • ± Preceding illness
  • Distal to proximal gradient
    • Begins with distal paresthesias, pain in back/neck, and leg weakness
    • ± Cranial nerve involvement
    • ± Secondary respiratory failure
    • ± Autonomic instability ⇒ arrythmia and BP changes
  • Progresses for up to several weeks
  • ↑ CSF protein but normal WBC count (albumnio-cytological dissociation)
  • NCS/EMG: slow conduction velocities or conduction block
  • Management: Plasmapheresis or IVIG ⇒ slows progression
40
Q

Chronic Inflammatory Demyelinating Polyneuropathy

A
  • Immune mediated attack of peripheral myelin
  • Slowly progressive, usually symmetric weakness and sensory loss over months to years
  • Sensory loss to all modalities, usually worse in BLE
  • Generalized hyporeflexia
  • ± Nerves enlargement
  • ↑ CSF protein
  • NCS/EMG: prolonged distal latencies, significantly slowed conduction velocities, conduction block
  • Treatment includes steroids, plasmapheresis, IVIG, and immunosuppressants
41
Q

Demyelinating Neuropathies

Other Etiologies

A
  • Infectious mononucleosis (occasionally)
  • Toxic polyneuropathies
    • tri-(ortho) cresyl phosphate
    • [Ginger Jake (leg) Paralysis]
  • Reactions to immunization: Vaccination for the swine flu scare [1976]
42
Q

Varicella-Zoster Virus

A
  • Infectious Polyneuropathy
  • One of the most common viral infections of the PNS
  • Latent infection of neurons in the sensory ganglia of the spinal cord and brain stem follows chickenpox
  • Reactivation ⇒ painful, vesicular skin eruptions in the distribution of sensory dermatomes (shingles)
    • Most frequently thoracic or trigeminal
  • Virus may be transported along the sensory nerves to the skin ⇒ active infection of epidermal cells
  • Affected ganglianeuronal destruction, mononuclear infiltrates
  • Peripheral nerveaxonal degeneration after the death of the sensory neurons
43
Q

Leprosy

A
  • Infectious polyneuropathy caused by Mycobacterium leprae
  • Lepromatous leprosy:
    • Schwann cells invaded by M. leprae → proliferates and infects other cells
    • Segmental demyelination and remyelination
  • Tuberculoid leprosy:
    • CMI response to M. lepraegranulomatous inflammation in the dermis
    • Injures nearby cutaneous nerves → localized nerve involvement
44
Q

Hereditary Neuropathies

A

Heterogeneous, usu. progressive, and often disabling syndromes that affect peripheral nerves.

45
Q

Hereditary motor and sensory neuropathies

(HMSN)

A
  • Most common form of hereditary neuropathies
  • Charcot-Marie-Tooth disease and Dejerine-Sottas disease
  • Caused by mutations in genes involved in the formation and maintenance of myelin
46
Q

Charcot Marie Tooth (CMT)

A

Hereditary motor and sensory neuropathy

  • Clinical manifestations:
    • Foot drop
    • Claw toe / hammer toes
    • Pes cavus (high arch of foot)
    • Wasting of hands, feet, and distal leg muscles
    • Mild sensory loss
    • Enlarged nerves
  • Pathology: demyelination and onion bulbs
  • Multiple variants with different transmission patterns: autosomal dominant, autosomal recessive, or X-linked
47
Q

Hereditary Sensory and Autonomic Neuropathies

(HSAN)

A

Numbness, pain, and autonomic dysfunction → orthostatic hypotension

48
Q

Familial Amyloid Polyneuropathies

(FAP)

A
  • Deposition of amyloid within the PNS
  • Most types exhibit mutations of the transthyretin gene
  • Clinical presentation is similar to that of HSAN
  • Numbness, pain, and autonomic dysfunction
49
Q

Traumatic Neuropathies

A
  • Peripheral nerves commonly injured in the course of trauma
  • Lesions include lacerations and avulsions
  • Re-growth may be complicated by discontinuity b/t proximal and distal portions of the nerve sheath as well as by the misalignment of individual fascicles
  • Dysregulated/abnormal axonal growth ⇒ mass of tangled axonal processes called a traumatic neuronal (pseudoneuroma or amputation neuroma)
50
Q

Other Etiologies of Polyneuropathy

A
  • Long standing HIV
  • Critical Illness
  • Uremic polyneuropathy
  • Amyloidosis
  • Hypothyroidism
  • Vitamin Deficiencies
  • Lyme disease
  • Paraneoplastic
  • Heavy metal
  • Connective Tissue Disease (Sjogrens)
    *
51
Q

Pressure Palsy

A

Nerve dysfunction seen after pressure is applied to nerve

52
Q

Radiculopathy

Overview

A
  • Due to damage to a nerve root
  • Disc herniation is the most common cause
  • Characterized by sensory complaints in a dermatomal distribution and weakness in the muscles innervated by the root
  • If nerve root involved in a reflex, reflex may be decreased
  • Pain
  • NCS/EMG: sensory AP’s are normal, EMG w/ fibrillations in paraspinal muscles (acute)
  • Treatment:
    • Supportive - PT, pain management
    • Surgery
53
Q

Cervical Radiculopathy

A

Presents with neck pain, arm pain, or both

Sensory and/or motor deficits

54
Q

C6 Radiculopathy

A
  • C5-C6 disc herniation
  • Weakness of shoulder abduction, elbow flexion, wrist flexion/extension
  • Sensory loss of the lateral forearm, thumb, and index finger
  • Loss of bicep and brachioradialis reflex
55
Q

C7 Radiculopathy

A
  • C6-C7 disc herniation
  • Most common cervical radiculopathy
  • Weakness of elbow and wrist extension
  • Sensory disturbance of middle finger
  • Pain in neck and dorsum of forearm
  • Loss of triceps reflex
56
Q

Lumbosacral Radiculopathy

A
  • Pain syndrome caused by compression or irritation of nerve roots in the lower back
  • Caused by lumbar or sacral disc herniation, DDD, and narrowing of foramen where nerve exits
  • Results in low back pain with radiation to the leg
57
Q

L2,3,4 Radiculopathy

A
  • Marked overlap of L2, L3, L4 innervation
    • Radiculopathies considered as a group
  • Most commonly involved in older pts with sx of spinal stenosis
  • Acute back pain anterior thigh knee medial lower leg arch of the foot
  • Weakness: hip flexion, knee extension, hip adduction
  • ↓ Sensation: anterior thigh to medial lower leg
58
Q

L5 Radiculopathy

A
  • Most common radiculopathy affecting the lumbosacral spine
  • Back pain lateral aspect of the leg dorsum foot
  • ↓ Strength in foot dorsiflexion, toe extension, and foot eversion
  • ± Weakness of leg abduction in severe cases
  • Atrophy of the extensor digitorum brevis of muscle of the foot and tibialis anterior of the lower leg
  • Reflexes are normal
59
Q

S1 Radiculopathy

A
  • Pain posterior aspect of the leg foot from the back
  • Weakness of plantar flexion
  • ± Weakness of leg extension and knee flexion
  • Sensation is reduced on the posterior aspect of the leg and lateral edge of the foot
  • Loss of ankle reflex
60
Q

Plexopathy

A
  • Disorder affecting a network of nerves, blood vessels, or lymph vessels
  • Brachial or lumbosacral plexus
  • Sx include pain, loss of motor control, atrophy and sensory deficits
  • The entire plexus, or just portions may be involved
61
Q

Brachial Plexopathy

A
  • Can be d/t compression, transection, ischemia, inflammation, metabolic abnormalities, neoplasia, radiation therapy, trauma, burns, postoperatively, autoimmune or post-infectious, or direct infiltration
  • Muscle weakness, atrophy, sensory loss, and pain
  • Acute onset ⇒ pain in the shoulder and upper arm
  • Insidious onset ⇒ progressive pain, evolving numbness, weakness of selected muscle groups
62
Q

Lumbosacral Plexopathy

Clinical Manifestations

A

Pattern of weakness/numbness helps localize lesion:

  • Lumbar plexus:
    • Weakness of hip flexion and adduction and/or knee extension
    • Sensory disturbance in anterior thigh and medial leg
  • Lumbosacral trunk and upper sacral plexus:
    • Foot drop, flail foot, weakness of knee flexion or hip abduction
    • Sensory disturbance in leg, dorsum of foot, posterior thigh, perineum
63
Q

Lumbosacral Plexopathy

A
  • Secondary to various causes including: DM, neoplasms, ischemia, post-op, trauma, surgery (OB), infection, CT disorder
  • Often results from mass lesions
  • Compression from pelvic tumors
  • Psoas abscess
  • Retroperitoneal hemorrhage
  • Asymmetric, focal weakness, numbness, dysesthesia and/or paresthesia in multiple lumbosacral nerve root distributions
  • Pattern of weakness/numbness helps localize lesion
  • Lumbar plexus:
  • Weakness of hip flexion and adduction and/or knee extension
  • Sensory disturbance in anterior thigh and medial leg
  • Lumbosacral trunk and upper sacral plexus:
  • Foot drop, flail foot, weakness of knee flexion or hip abduction
  • Sensory disturbance in leg, dorsum of foot, posterior thigh, perineum
64
Q

Motor Neuron Disease

A

Neurodegenerative disorders that selectively affect motor neurons of the spinal cord

  • ALS is most common
  • Can have UMN + LMN signs or just LMN
  • Progressive
65
Q

Amyotrophic Lateral Sclerosis

(ALS)

A

Neurodegenerative disease of the upper and lower motor neurons.

  • Onset 55-75 years
  • UMN dysfunctionincreased tone, spasticity, hyperreflexia and positive Babinski
  • LMN dysfunctionatrophy, weakness, fasciculation and loss of reflexes
  • Extraocular muscles and sensation usually spared
  • Late in course, spasticity may occur
  • Bulbar weaknessdysarthria, dysphagia
  • Pts present with asymmetric distal weakness
    • Usually weakness starts in one region then spreads to adjacent regions then spreads to contralateral limb
  • Pts often die with respiratory insufficiency or aspiration pneumonia
  • Management: Supportive (multidisciplinary clinics), Riluzole (may prolong survival)