Pathophysiology And Clinical Features Of Peripheral Nervous System .pptx

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Pathophysiol
ogy And
Clinical
Features Of
Peripheral
Nervous
System
PRESENTING BY : Dr. Nagaraj S Maka
(PT)
Mpt Neurological science

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Objectives
• To provide an overview of the anatomical structure and functional role of the peripheral
nervous system.
• To explore the pathophysiological processes underlying various peripheral neuropathies.
• To recognize the characteristic clinical manifestations, including signs and symptoms, of
peripheral nervous system disorders.
• To categorize peripheral neuropathies based on established classifications and correlate them
with fundamental clinical findings.
• To highlight the clinical implications of peripheral nervous system dysfunctions in
physiotherapy evaluation and intervention.

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CONTENTS
• Introduction
• Peripheral nervous system
• Pathophysiology of peripheral neuropathies
• Clinical features of PNS
• Signs and symptoms
• Basic clinical findings in polyneuropathies
• Classifiation of peripheral neuropathies
• Clinical translation of PNS in physiotherapy.

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INTRODUCTION
• The Peripheral Nervous System (PNS) is responsible for connecting the Central Nervous
System (CNS) to the rest of the body, enabling motor control, sensory input, and autonomic
functions.
• It consists of cranial nerves, spinal nerves, peripheral nerves, and the neuromuscular
junctions.
• Disorders affecting the PNS are known as peripheral neuropathies and can arise from various
causes, including diabetes, infections, autoimmune diseases, toxins, trauma, and genetic
mutations.
• These neuropathies may affect sensory, motor, or autonomic fibers, often leading to mixed
symptoms.
• The two main types of pathophysiological changes in PNS disorders are axonopathy, which is
damage to the nerve fiber, and demyelination, which is damage to the myelin sheath.
• Both conditions interfere with normal nerve signal transmission and can lead to significant
functional impairment.

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Peripheral nervous system
Contents
• Organization of PNS
• Spinal nerves
• Cranial nerves
• Structure and composition of a peripheral nerve
• Axonal transport
Fredericks CM. Pathophysiology of motor systems: Principles and clinical presentations. 2nd ed. Philadelphia: F.A. Davis Company; 2001.

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Organization of PNS

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Spinal
Nerves

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Cranial
nerves

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Structure and
composition
of a
peripheral
nerve

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Axonal transport
• Nerve fibers are unique because the cell body maintains an axon of enormous length
and volume, containing hundreds of times more cytoplasm than the cell body.
• Since axons lack ribosomes for protein synthesis, essential materials must be
produced in the cell body and transported to axonal sites.
• Structural components, organelles, and nutrients are transported from cell body to
nerve terminal (anterograde transport) and also in reverse direction (retrograde
transport).
• Used neurotransmitter vesicles return to the cell body for recycling, while foreign
substances from nerve terminals can also be transported back.
• Transport defects significantly disturb neuronal function and likely cause many
peripheral nervous system disorders.
• Axonal injury causes rapid degeneration beyond the injury site, and blocked
retrograde transport of trophic factors harms neuronal activity.

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Pathophysiology of Peripheral
Neuropathies
• Disease and injury can disturb peripheral nerve function in a number of ways
,and the particular signs and symptoms that characterize a specific disorder
will reflect the nature of these underlying disturbances ,as well as the
particular fibers disrupted.
• The pathological process afflicting peripheral nerve are few and can be
divided into those that primarily affect the axon and those that primarily
affect its ensheathments ,the surrounding myelin or syhwann cells .

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Axonopathies
• Axonopathies involve primary axonal damage that typically begins at the
distal terminals and progresses proximally, often referred to as "dying-back"
neuropathy.
• The pathophysiology includes impaired energy metabolism, disruption of
cytoskeletal proteins, accumulation of toxic metabolites, and failure of
axonal transport systems.
• These mechanisms collectively result in axonal degeneration and the clinical
features of neuropathy.
Pathophysiology of
Peripheral Neuropathies

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Wallerian degeneration
• Wallerian degeneration is the process that occurs when an axon is acutely
injured, such as by transection, crush, or ischemia, resulting in disruption of
the axonal continuity.
• Following injury, the distal segment of the axon deteriorates rapidly due to
loss of essential materials transported from the cell body.
• Synaptic transmission fails within hours of injury, even before visible
degeneration begins.
• By around two weeks post-injury, the entire distal axon undergoes
degeneration—the axon breaks down and myelin is phagocytosed.
• In myelinated fibers, Schwann cells help clean up debris and later assist in
regeneration; in unmyelinated fibers, Schwann cell proliferation is less
marked.
Pathophysiology of

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• Chromatolysis occurs in the cell body, involving swelling and reorganization of the rough
endoplasmic reticulum for axonal repair.
• Wallerian degeneration progresses faster in the peripheral nervous system (PNS) than in the
central nervous system (CNS).
• Regeneration is possible in the PNS if the cell body remains intact, but does not occur in the
CNS, leading to permanent loss.
• Regeneration begins with sprouting from the proximal stump, with Schwann cells and
connective tissue guiding axons toward their targets.
• Crush injuries show better recovery than transections, as the guiding structures remain
more intact and promote accurate reinnervation.
Pathophysiology of

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Pathophysiology of

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Axonal
Degeneration
(Distal
Axonopathy)
• Axonal degeneration, also known as distal
axonopathy, occurs gradually due to chronic diseases,
metabolic disorders, or toxic insults to the nervous
system.
• It is the most common pathological response of
peripheral nerves to chronic injury.
• The degeneration typically begins at the distal end of
the axon and progresses back toward the cell body—
this process is called “dying back.”
• It is often seen in conditions like diabetic neuropathy,
alcoholism, chemotherapy toxicity, and certain
hereditary neuropathies.
• Initially, the axon sheaths and Schwann cells may
remain intact, but prolonged degeneration can lead to
secondary demyelination.
Pathophysiology of

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Effects of axonopathy on skeletal
muscle
• Denervation due to axonopathy leads to predictable
changes in skeletal muscle, with the most noticeable
effect being rapid muscle atrophy.
• Muscle atrophy develops quickly within weeks, then
slows but continues progressively—permanent
muscle fiber loss begins after 6–9 months and is
extensive by 3 years.
• Atrophied muscle fibers become angulated or
elongated in cross-section, a classic sign of
neurogenic atrophy.
• Type II (fast-twitch) fibers typically atrophy earlier
and more severely than type I (slow-twitch) fibers.
• In partially denervated muscles, remaining healthy
fibers undergo compensatory hypertrophy due to
increased workload.
• Denervation also leads to capillary loss and
connective tissue proliferation around muscle fibers,
Pathophysiology of

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Myelinopathies
• Myelinopathies are disorders where the myelin
sheath or Schwann cells are primarily damaged,
while the axon remains relatively intact.
• This leads to segmental demyelination, where
entire internodal segments of myelin are lost.
• Primary demyelination often occurs in immune-
mediated inflammatory conditions like Guillain-
Barré syndrome or diphtheritic neuropathy.
• Secondary demyelination can occur as a result of
underlying axon damage, such as in axonopathies.
• Loss of myelin results in slowed or blocked nerve
conduction, which can impair nerve function.
• Even when conduction is maintained, it may be
intermittent and unreliable, especially during
prolonged stimulation.
Pathophysiology of

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Neuronopathies
• Neuronopathies are disorders where the primary pathological change occurs in the nerve cell
body, also called perikaryal disorders.
• These conditions may affect either motor neurons or primary sensory neurons.
• Neuronopathies can arise due to infectious, hereditary, or toxic factors.
• A hallmark feature is the selective vulnerability of certain neuronal populations—e.g.,
poliovirus selectively affects anterior horn cells.
• The clinical presentation of neuronopathies can resemble axonopathies, even though the
primary site of damage is the cell body.
• For sensory and autonomic fibers, the cell bodies lie outside the CNS, so neuronopathies
affecting these are considered peripheral nervous system disorders.
Pathophysiology of

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Clinical features of PNS
• Neuropathies are classified broadly into mononeuropathies, multiple mononeuropathies
(mononeuropathies multiplex), and polyneuropathies based on the pattern of nerve
involvement.
• Mononeuropathy involves damage to a single nerve trunk, often due to localized factors like
entrapment, compression, or trauma.
• Multiple mononeuropathies involve several individual nerves affected by focal lesions, either
simultaneously or sequentially.
• Common causes of mononeuropathies include nerve trauma, vascular lesions,
granulomatous or neoplastic processes, and preexisting conditions like diabetes mellitus.
• In both mononeuropathies and multiple mononeuropathies, motor and sensory symptoms
are localized to the affected nerves, and tendon reflexes are usually preserved unless the
specific reflex arc is disrupted.
• Polyneuropathy is characterized by diffuse damage to many peripheral nerves, most often in
a bilateral, symmetric, and distal pattern, affecting large nerve fibers first.

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• The clinical features of polyneuropathy depend on the location,
severity, and nature of the underlying pathology.
• Demyelinating neuropathies and axonal neuropathies have
different clinical presentations, though many cases involve both
axons and myelin.
• Most polyneuropathies include a combination of motor, sensory,
and autonomic dysfunctions, though some may be purely one type.
• Polyneuropathies are usually associated with systemic causes like
toxins, nutritional deficiencies, metabolic disorders, or immune
responses, and may sometimes overlap with features of multiple
mononeuropathies as they progress.
Clinical features of

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Signs and symptoms
Category Signs and Symptoms
Motor
- Muscle weakness (often distal) - Muscle atrophy -
Fasciculations or cramps
Sensory
- Numbness, tingling, paresthesia - Burning or stabbing pain -
Loss of vibration and position sense
Reflex Changes
- Decreased or absent tendon reflexes - Reflex loss follows
nerve/root involvement
Autonomic
- Orthostatic hypotension - Abnormal sweating or dry skin - GI
symptoms (e.g., constipation) - Bladder dysfunction
Symptom Distribution
- Focal (mononeuropathy) - Multifocal (mononeuropathies
multiplex) - Symmetric distal (polyneuropathy - “stocking-glove”
pattern)
Progression Pattern
- Gradual in metabolic/hereditary causes - Rapid/subacute in
toxic, immune, or inflammatory causes

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Category Signs and Symptoms
Sensory Ataxia
- Unsteady gait - Difficulty walking in the dark or with eyes
closed
Pain
- Neuropathic pain - Often chronic and severe, especially in
small fiber neuropathy
Severity Factors
- Depends on fiber type (motor/sensory/autonomic) - Depends
on extent and site of damage
Associated Conditions
- Symptoms influenced by systemic diseases (e.g., diabetes,
autoimmune conditions)
Sensory Ataxia
- Unsteady gait - Difficulty walking in the dark or with eyes
closed
Pain
- Neuropathic pain - Often chronic and severe, especially in
small fiber neuropathy
Signs and symptoms

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Loss of Motor and Sensory Function
(Negative Signs and Symptoms)
• Persistent muscle weakness is the most common motor symptom in peripheral neuropathy.
• Motor weakness may be localized (in mononeuropathy) or widespread (in polyneuropathy or
multiple mononeuropathies).
• In polyneuropathy, weakness typically begins symmetrically and distally, affecting the feet and
legs first, followed by hands and forearms—known as a “glove-and-stocking” distribution.
• In milder polyneuropathies, only the lower limbs may be involved.
• Nutritional, metabolic, and toxic neuropathies often follow this distal symmetric pattern.
• In severe cases, such as Guillain-Barré Syndrome, patients may develop quadriplegia and
require respiratory support.
Signs and symptoms

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• Muscle paralysis results from the failure of motor nerve impulse conduction from the CNS to
the periphery.
• The severity of weakness correlates with the number of motor neurons affected.
• Motor deficits can be worsened by concurrent sensory loss, especially proprioceptive input.
• All sensory modalities may be reduced in polyneuropathy, but some disorders show selective
sensory loss.
• Vibratory and positional senses may be diminished in some neuropathies, with vibration
sense more often affected.
• Pain and temperature sensation may be reduced in other types, especially those involving
small sensory fibers.
Signs and symptoms

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Distorted or Exaggerated Motor and Sensory
Activity (Positive Signs and Symptoms)
• Positive signs occur due to abnormal generation of action potentials in damaged motor or
sensory neurons.
• These symptoms may coexist with or follow negative signs like weakness and sensory loss.
• Involuntary muscle activation can occur even in the presence of weakness.
• Fasciculations (muscle twitching) and cramps may be seen, especially in motor fiber involvement.
• Fasciculations and cramps are more prominent in anterior horn cell disorders, but may also be
present in neuropathies.
• Neuro myotonia, myokymia, or continuous motor unit activity syndrome involve repetitive,
asynchronous motor unit firing.
• This abnormal motor activity can cause generalized muscle stiffness.

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• Such motor hyperactivity is reported in both demyelinating and axonal neuropathies.
• The activity often originates from damaged peripheral nerve regions and persists during sleep
or spinal anesthesia.
• It typically decreases with distal nerve blocks or neuromuscular junction blockade, confirming a
peripheral origin.
• Paresthesias (abnormal sensations) like numbness, tingling, prickling, or pins-and-needles are
common in sensory or mixed neuropathies.
• If paresthesias are unpleasant, they are termed dysesthesias.
• These sensations are most evident in the hands and feet, following the “stocking-glove”
distribution.

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Basic Clinical Findings in
Polyneuropathies
Feature Axonopathy Myelinopathy
Onset
Gradual and insidious; often
preceded by subclinical disease
Rapid onset, especially
following trauma
Initial Clinical Manifestations
Symmetric, diffuse weakness
and mild sensory loss in lower
limbs; may involve bulbar
muscles
Earliest signs are usually
sensory; symmetric distal limb
involvement (“glove-and-
stocking”)
Sensory Loss
May be limited to distal
extremities
Common in distal limbs
Tendon Reflexes
Loss of ankle jerks; proximal
reflexes preserved
Abnormalities and loss of ankle
jerks; proximal reflexes
preserved
Motor Nerve Conduction
Velocity
Normal or slightly slowed
Markedly slowed or completely
blocked conduction

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Feature Axonopathy Myelinopathy
Muscle Atrophy
Denervation atrophy (if axonal
loss present)
Disuse atrophy; denervation
atrophy if axonal damage
occurs
CNS Involvement Some involvement Rarely involved
Common Causes
Exogenous toxins, metabolic
and hereditary factors
Immune-mediated
inflammation (most common);
rarely toxic, infectious, or
hereditary
Clinical findings

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• Tendon Hyporeflexia and Areflexia :It refers to reduced or absent reflexes, commonly seen in
peripheral nerve disorders.
It often results from early damage to muscle spindle afferent fibers due to axon
degeneration or impaired nerve conduction from demyelination.
• Ataxia and Tremor: In sensory neuropathies, loss of proprioception despite preserved muscle
strength can cause uncoordinated movements, known as sensory ataxia.
Tremors during movement may also occur due to distorted proprioceptive feedback.
• Autonomic Dysfunction: In polyneuropathy commonly causes anhidrosis, genitourinary
issues, and orthostatic hypotension, often due to damage to small nerve fibers.
It usually coexists with motor or sensory symptoms and is most often seen in diabetic,
amyloid, or hereditary neuropathies, with sympathetic involvement being more common.
• Deformity and Trophic Changes: Long-standing polyneuropathies can lead to deformities like
high-arched feet (pes cavus), claw toes, hand clawing, and spinal curvatures, mainly due to
muscle imbalance.
Trophic changes such as muscle wasting, skin and nail changes, joint damage, and ulcers occur
with denervation, disuse, sensory loss, and poor blood flow—commonly seen in diabetic
neuropathy.

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• Deformity (clawing) and scarring
of the fingers is due longstanding
weakness and wasting of small
hand muscles and distal
anesthesia in the polyneuropathic
patient
Claw Hand in Parsonage Turner syndrome | Published in Journal of Brown Hospital Medicine.

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• Ulcerated Feet in Sensory
Neuropathy. In this patient
with a sensory neuropathy
distal sensory impairment
led to the development of
painless perforating ulcers
on the soles of both feet.
Full article: Cutaneous manifestations of diabetic peripheral neuropathy.

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Classification of Peripheral
Neuropathies
Type Subtypes
Pathologic
- Axonal dysfunction - Wallerian degeneration (after acute injury) -
Distal axonopathy - Myelinopathy
Etiologic Acquired Forms
- Mononeuropathy: • Entrapment or compression • Traumatic •
Infectious/inflammatory • Neoplastic
- Multiple Mononeuropathy: • Vascular/ischemic • Entrapment or
compression • Metabolic • Infiltration or neoplasm
- Polyneuropathy: • Metabolic • Toxic • Deficiency •
Infectious/inflammatory • Malignancy-associated • Idiopathic
Hereditary Forms
- Mixed sensorimotor neuropathy (Metabolic, Idiopathic) -
Sensory/autonomic neuropathy
Syndromic
- Acute sensorimotor polyneuropathy - Subacute sensorimotor
polyneuropathy - Chronic sensorimotor polyneuropathy - Recurrent or
relapsing polyneuropathy - Mononeuropathy or multiple
mononeuropathy - Acquired and genetically determined forms

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feature Inherited Neuropathies Acquired Neuropathies
Onset
Often begins in childhood; slow and
insidious
Can be acute, subacute, or chronic
Progression Slow, over years or decades Variable—can be rapid or gradual
Distribution Symmetric, distal > proximal
Often distal; may be symmetric or
asymmetric
Motor/Sensory Involvement
Mixed motor and sensory; often both
affected
Variable; may involve sensory, motor,
or both
Deformities
Common (e.g., pes cavus, claw toes,
kyphoscoliosis)
Rare unless long-standing or severe
Common Types
HMSN (Hereditary Motor and Sensory
Neuropathies), HSAN (Hereditary Sensory
and Autonomic Neuropathies)
Guillain-Barré Syndrome, diabetic
neuropathy, toxic/nutritional
neuropathies
Etiology
Genetic mutations; hereditary
transmission (dominant, recessive, X-
linked)
External/systemic causes (trauma,
toxins, infections, metabolic,
autoimmune)
Recovery Progressive and often irreversible
Recovery possible, especially in
demyelinating forms
Biochemical Basis
May be idiopathic or linked to
Pathology-dependent (e.g.,
demyelination or axonal

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Diabetic Polyneuropathy
• Diabetic polyneuropathy is the most common complication of diabetes and the most frequent
cause of peripheral neuropathy.
• The most common type is distal, symmetric polyneuropathy, affecting about 75% of diabetic
neuropathy cases.
• It typically develops in long-term diabetes patients, especially those with poor blood sugar
control.
• Large-fiber involvement causes painless paresthesias in the feet and legs, loss of vibration and
joint position sense, and reduced reflexes like ankle jerks.
• A less common small-fiber form presents with burning sensations, deep aching pain, and
impaired temperature and pain sensations.
• Some rare forms involve primarily motor or autonomic symptoms.

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Alcoholic Polyneuropathy
1. Alcoholic polyneuropathy is a common complication of chronic alcohol abuse, affecting the
peripheral nerves.
2. It usually presents as a slowly progressive, distal, symmetric polyneuropathy, but may
occasionally worsen acutely.
3. Sensory symptoms (pain, burning, paresthesias) typically appear before motor weakness.
4. Early symptoms may include aching in calves and discomfort in the soles, while severe cases
involve significant distal muscle weakness and wasting.
5. Reflexes (especially in the lower limbs) are often reduced or lost, and sensory loss in the feet
can lead to sensory ataxia.
6. Severe pain and hypersensitivity to touch on the plantar surface are common, sometimes
making shoes or socks intolerable.

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Guillain-Barré Syndrome
• Guillain-Barré Syndrome (GBS) is an acquired, acute polyneuropathy characterized primarily
by motor dysfunction.
• It is the most common acute paralytic disease in developed countries.
• The condition presents with rapidly progressive, symmetric muscle weakness, often starting
in the distal lower limbs and ascending upward.
• Patients may quickly progress to severe weakness, including complete flaccid quadriplegia,
and even respiratory failure.
• Facial weakness is common, though extraocular and lower cranial nerve involvement is less
frequent.
• Absent tendon reflexes are a consistent feature.
• Sensory symptoms like paresthesias (tingling, burning, numbness) are common, but objective
sensory loss is usually mild.

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• Pain and dysesthesias may significantly affect comfort and hinder rehabilitation.
• Autonomic disturbances—such as tachycardia, fluctuating blood pressure, facial flushing, and
abnormal sweating—are common and can be difficult to manage.
• The peak of neurological deficit is typically reached within a few days to two weeks.
• Recovery often starts within 2–4 weeks after progression stops, and 85% of patients are
ambulatory within 6 months.
• Despite good prognosis, 5% may die, and around 20% remain significantly impaired.
• Pathology shows inflammation and segmental demyelination, most prominent in ventral
roots, plexuses, and proximal nerves.
• It is believed to be an autoimmune condition, often preceded by a respiratory or
gastrointestinal infection in ~60% of cases.
• Management includes respiratory support, prevention of complications, and early physical
and occupational therapy to prevent contractures and maintain mobility.

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Hereditary Motor and Sensory
Neuropathy (HMSN) Type I:
• HMSN Type I, also known as Charcot-Marie-Tooth disease, is a genetically inherited
neuropathy, and one of the most common hereditary neuropathies.
• It usually begins in late childhood or adolescence, with initial symptoms including pes cavus
(high-arched foot) and difficulty walking or running.
• Symmetrical weakness and wasting first affect the intrinsic foot, peroneal, and anterior tibial
muscles, progressing slowly over years.
• Later, hand and forearm muscles may also be involved, sometimes causing clawhand
deformity, though weakness rarely extends beyond the midthigh or above the elbow.
• Tendon reflexes are typically absent in affected limbs, and paresthesias (tingling or
numbness) are common.
• Sensory loss is usually distal and mild, involving diminished vibration and light touch,
especially in the feet and hands, and is rarely bothersome to patients.

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• The condition progresses very slowly, with long periods of stability and minimal functional
impairment in many cases.
• Walking difficulty arises due to footdrop, ankle instability, weakness, and sensory ataxia
(impaired coordination from sensory loss).
• Pathologically, the disorder involves axonal degeneration with secondary segmental
demyelination, particularly affecting large myelinated fibers.
• No specific treatment exists, but braces, orthotic devices, and corrective surgery can improve
mobility and reduce deformity, helping maintain ambulation.

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Syndromic Classification of Neuropathies based on
onset/time course, clinical features, and common causes:
Classification Clinical Features Common Causes
Acute Neuropathy
- Rapid onset (hours to days) -
Symmetric weakness starting
in feet - Sensory symptoms
(pain, paresthesia) - May
include autonomic dysfunction
- Guillain-Barré syndrome
(post-infectious) - Toxins (e.g.,
thallium) - Trauma (laceration,
compression, ischemia) -
Diphtheria (rare)
Subacute Neuropathy
- Develops over weeks to
months - Pain, numbness,
paresthesias (glove-stocking) -
Weakness and muscle wasting
- Nutritional deficiency (e.g.,
alcoholism) - Toxins (e.g.,
arsenic, solvents) - Drug
intoxication - Metabolic
disorders (e.g., diabetes) -
Inflammatory neuropathies
Chronic Neuropathy
- Evolves over months to
years - Similar
signs/symptoms as subacute -
- Diabetes mellitus - Chronic
alcoholism - Hereditary
neuropathies - Chronic

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Disorders of Cranial Nerves:
1. Cranial nerves can be affected by similar disorders and injuries as spinal nerves, such as
axonal degeneration and demyelination.
2. They are often involved in peripheral neuropathies like Guillain-Barré syndrome, Lyme
disease, and diabetic neuropathy.
3. In polyneuropathies, cranial nerve symptoms typically appear later in the disease course,
following symptoms in distal limbs.
4. Cranial nerve damage may result from vascular insults or central nervous system tumors,
particularly near the brainstem.
5. They are more vulnerable than spinal nerves to CNS-originating pathology, such as tumors
and strokes.
6. Unlike spinal nerves, cranial nerves are involved in unique sensory and motor functions,
including olfaction, vision, hearing, taste, and balance.

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• Dysfunction can lead to craniofacial pain, sensory loss, and impairments in facial expressions,
eye movement, and swallowing.
• Autonomic disturbances may also occur, similar to those from spinal nerve dysfunction.
• Damage to cranial nerves may result in significant discomfort and functional impairments,
affecting quality of life.
• Therefore, cranial nerve disorders are crucial to identify and manage in neurological and
rehabilitative care.

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Disorders of Spinal Roots
(Radiculopathies):
• Radiculopathies are disorders of spinal nerve roots and are among the most common
neurological problems.
• Spinal roots are anatomically delicate and exit through narrow foramina, making them
vulnerable to compression or injury.
• They lack the strong protective sheaths (epineurium and perineurium) and endoneurial
collagen present in peripheral nerves, reducing their tensile strength.
• Unlike peripheral nerves, spinal roots lack an effective blood-nerve barrier, making them more
susceptible to toxic, infectious, and inflammatory agents.
• The blood supply to spinal roots is relatively poor, increasing the risk of ischemic injury,
especially in conditions like diabetes or mechanical compression.
• Proximity to the leptomeninges (pia and arachnoid mater) makes spinal roots vulnerable to
meningeal infections, inflammatory diseases, and tumors.

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• Pathological changes in radiculopathies typically include segmental demyelination,
axonal degeneration, or both.
• Compressive radiculopathies mainly cause axonal degeneration, while inflammatory
radiculoneuropathies like Guillain-Barré syndrome typically show demyelination.
• Recovery is usually faster and more complete with demyelination (via remyelination),
but axonal damage leads to slower and often incomplete recovery.
• Damage to dorsal root ganglia may result in regenerating axons failing to reconnect
with the spinal cord due to glial scarring.
• A typical clinical presentation of radiculopathy includes radicular pain, sensory loss,
muscle weakness, and reduced reflexes.
• In most cases, both motor (ventral) and sensory (dorsal) roots are equally affected,
but some diseases may preferentially involve one (e.g., ventral root involvement in
inflammatory conditions).

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Clinical translation of PNS
1. Pain Management
Interventions:
Transcutaneous Electrical Nerve Stimulation (TENS): Utilizes electrical impulses to alleviate
pain by modulating nerve activity.
Manual Therapy: Includes massage and joint mobilizations to reduce muscle tension and
improve circulation.
Low-Level Laser Therapy (LLLT): Promotes tissue healing and reduces pain through
photobiomodulation.
Evidence:
A systematic review and meta-analysis indicated that TENS effectively reduces neuropathic pain
intensity in various conditions, including diabetic and chemotherapy-induced neuropathy.
Manual therapy techniques have been shown to decrease pain and stiffness, enhancing overall
mobility.
Kannan P, Bello UM, Winser SJ. Physiotherapy interventions for pain relief in individuals with peripheral neuropathic pain: A systematic review and meta-analyses of randomized
controlled trials. Contemp Clin Trials. 2023 Feb;125:107055. doi: 10.1016/j.cct.2022.107055. Epub 2022 Dec 16. PMID: 36535605.

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2. Strengthening and Muscle Function
Interventions : Resistance Training: Incorporates exercises using weights or resistance bands to build
muscle strength.
Functional Electrical Stimulation (FES): Applies electrical impulses to stimulate muscle contractions,
improving strength and function.
Evidence : Studies have demonstrated that resistance training enhances muscle strength and endurance
in individuals with peripheral neuropathy, leading to improved functional capacity.
FES has been found to improve motor performance and reduce symptoms in patients with diabetic
peripheral neuropathy.
3. Balance and Gait Training
Interventions: Balance Exercises: Activities like standing on one leg, heel-to-toe walking, and using
balance boards to improve stability.
Gait Training: Focused exercises to enhance walking patterns and reduce fall risk
Evidence:A systematic review highlighted that balance and gait training significantly reduce fall risk and
improve mobility in individuals with peripheral neuropathy.
Jahantigh Akbari N, Hosseinifar M, Naimi SS, Mikaili S, Rahbar S. The efficacy of physiotherapy interventions in mitigating the symptoms and complications of diabetic
peripheral neuropathy: A systematic review. J Diabetes Metab Disord. 2020 Oct 12;19(2):1995-2004. doi: 10.1007/s40200-020-00652-8. PMID: 33553048; PMCID: PMC7843894.

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4. Sensory Re-education
Interventions:
Sensory Stimulation: Techniques such as brushing, tapping, or using textured materials to
stimulate sensory receptors.
Proprioceptive Training: Exercises that enhance awareness of body position and movement.
Evidence:
Sensory re-education methods have been shown to improve sensory perception and reduce
discomfort in patients with neuropathy.
5. Foot Care and Education
Interventions:
Foot Inspections: Regular checks for injuries, ulcers, or deformities.
Footwear Advice: Recommendations for appropriate shoes to prevent pressure sores.
Education: Teaching patients about the importance of foot hygiene and self-care practices.
Evidence:
Proper foot care education has been associated with a reduction in foot complications and
improved quality of life in individuals with diabetic peripheral neuropathy.
Cervoni B. What Is Diabetic Peripheral Neuropathy? [Internet]. Verywell Health; 2023 Feb 8 [cited 2025 Jun 2]. Available from: https://www.verywellhealth.com/diabetic-
peripheral-neuropathy-5208619

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6. Aerobic Exercise
Interventions:
Activities: Brisk walking, cycling, or swimming to improve cardiovascular health.
Intensity: Moderate-intensity exercises performed regularly.
Evidence:
Regular aerobic exercise has been found to alleviate pain and improve overall function in individuals with
peripheral neuropathy.
7. Assistive Devices
Interventions:
Orthotics: Devices like foot orthoses to support foot structure and function.
Walking Aids: Canes or walkers to enhance stability and mobility.
Evidence:
The use of assistive devices has been shown to improve gait and reduce fall risk in patients with peripheral
neuropathy.
https://activeability.com.au/physiotherapy/peripheral-neuropathy-physiotherapy/?utm_source

Pathophysiology And Clinical Features Of Peripheral Nervous System .pptx

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