NPTE - PNS Disorders

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35 Terms

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PNS Anatomy

CNs 3-12, spinal nerves, and the peripheral nerves

Motor (efferent) and sensory (afferent) fibers

Lesions cause LMN signs

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LMN signs

Flaccid paralysis

Mm atrophy

Fasciculations

Hyporeflexia

Hypotonia

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Neurapraxia

Mild injury, myelin damage only

full recovery within weeks

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Axonotmesis

axonal damage, intact endoneurium

recovery via axonal regrowth

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Neurotmesis

Complete nerve severance

Requires surgery, poor prognosis

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Boards Tip Pt 1

Neurapraxia = temporary block (Saturday Night Palsy)

Neurotmesis = worst

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Common PNS Disorders

GBS

Charcot-Marie-Tooth Disease

MG

Post-Polio Syndrome

Bell’s Palsy

Trigeminal Neuralgia (CN V)

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GBS Pathophys

Autoimmune, demyelinating polyneuropathy

Rapid ascending weakness (LE —> UE), areflexia

Often follows infection/vaccination

No cognitive involvement

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PT Role in GBS

Avoid overfatiguing!

Focus on respiratory care, PROM —> AAROM —> strengthening

Progress slowly with functional tasks

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GBS Outcome Measures

FIM

MMT

Vital Capacity

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Charcot-Marie-Tooth Disease

Genetic, progressive polyneuropathy

Weakness in distal LE > UE, foot drop, pes cavus

Sensory loss may occur

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PT Role in Charcot-Marie-Tooth

Orthotic management (AFO)

Balance and gait training

Avoid overwork weakness

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MG

Autoimmune, affects the NM junction (ACh receptors)

Fluctuating weakness, worse with activity, better with rest

Affects face, eyes, speech, and swallowing (ptosis, dysphagia)

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PT Role in treating MG

Energy conservation, pacing

Respiratory monitoring

Avoid heat, overexertion

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What test is used to confirm MG dx?

Tensilon Test

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Post-Polio Syndrome

Occurs years after the initial polio infection

Progressive new weakness, fatigue, joint pain

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PT Role in Post-polio syndrome

Avoid overuse

Submaximal exercise, orthoses, pacing

Energy conservation and adaptive strategies

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Bell’s Palsy

LMN lesion of the Facial Nerve (CN VII)

Sudden, UL facial paralysis

Often idiopathic/post-viral

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PT Role in Bell’s Palsy

Facial exercises, massage, and eye protection

E-stim is controversial

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Differentiate Bell’s Palsy from a stroke

Bell’s palsy = entire face

Stroke = lower face only

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Trigeminal Neuralgia (CN V)

Sudden, severe facial p! (jaw, cheek)

Often triggered by light touch, chewing

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PT Role in Trigeminal Neuralgia

Ed on triggers, desensitization strategies

Modalities for p! control

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Median Nerve Entrapment

Entrapment at Carpal tunnel

S&S: numbness in thumb-3rd digit, atrophy

Tx: splinting, ergonomic training

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Ulnar Nerve Entrapment

Entrapment at Cubital Tunnel, Guyon’s Canal

S&S: claw hand, sensory loss

Tx: activity mod, ulnar glides

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Radial Nerve Entrapment

Entrapped at the spiral groove (humerus)

S&S: Wrist drop

Tx: dynamic splint, strengthening

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Peroneal Nerve Entrapment

Entrapped at the fibular head

S&S: foot drop

Tx: AFO, gait training

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Tarsal Tunnel Entrapment

Entrapped post to med mall

S&S: foot p!, tingling

Tx: orthotics, activity modification

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Diagnostic Tests

EMG - evals motor unit ftn

Nerve Conduction Study - assesses speed and amplitude of signals

Tensilon test - dx MG

Lumbar puncture - high protein in GBS

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PT Interventions for PNS disorders

ROM and contracture prevention (esp in flaccid limbs)

Orthotics for foot drop/hand ftn

Task-specific gait training

Fatigue management: GBS, post-polio, MG

Sensory re-ed for sensory loss

NM re-ed for motor control

Avoid overwork weakness in chronic NM disorders!

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Red flags for PNS disorders

Rapidly ascending weakness —> GBS —> hospital referral

Respiratory weakness/fatigue —> emergency (MG, GBS)

Unexplained new weakness years after polio —> post-polio

B facial weakness/eye involvement —> refer for neuro eval

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Boards Tips Pt 2

PNS = LMN signs (hypotonia, decreased reflexes, atrophy, fasciculations)

Know the difference btw myopathy and neuropathy

MG = fatigue worsens with activity

GBS = careful not to over-fatigue during rehab

Foot drop = peroneal nerve injury/CPN entrapment

Stroke spares the upper face; Bell’s Palsy affects the whole face

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Myopathy

Disease/dysfunction of mm fibers

Mm itself is weak

Proximal > distal (shoulders, hips)

Typically normal/slightly decreased reflexes

Sensation intact

Mild mm atrophy (late stage)

Typically normal tone

No fasciculations

Short-duration, low-amplitude APs on EMG

Ex: MD, polymyositis, statin-induced myopathy

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Neuropathy

Disease/famage of the peripheral nerves

The nerve signal to the mm is disrupted

Distal > proximal (hands, feet)

Decreased/absent reflexes

Sensation often impaired (N&T)

Mm atrophy is more pronounced, often early

Often hypotonia with LMN lesions

Fasciculations present (esp in LMN neuropathies)

Fibrillations, sharp waves, abnormal MUs on EMG

Ex: GBS, diabetic neuropathy, CTS

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If a pt has distal weakness, numbness, absent reflexes, and fasciculations

they probably have neuropathy

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If a pt has proximal weakness, normal sensation, and intact reflexes

they probably have myopathy