POLYNEUROPATHY

LONG ESSAY
1. Define Gulian barre syndrome pathophysiology, etiogensis,
clinical features and management of same-17,21
ANSWER: Guillain-Barré syndrome (GBS) is a heterogeneous group of immune-
mediated conditions.
GBS is the most common acute, severe fulminant
polyradiculopathy/polyneuropathy.
 Usually demyelinating or rarely axonal.
 Often postinfectious, post vaccinal basis
 Monophasic does not recur.

Guillain-Barré Syndrome (GBS) is characterized by rapid-onset muscle

weakness and areflexia, often preceded by an infection. It is
considered the most common cause of acute flaccid paralysis
worldwide

ETIOLOGY

GBS is an autoimmune disorder triggered by infections, vaccines, or other

immune stimuli. The immune system mistakenly attacks
peripheral nerves, leading to demyelination and/or axonal
degeneration.

Common Triggers:

 Infections:
o Campylobacter jejuni (most common)
o Cytomegalovirus (CMV)
o Epstein-Barr Virus (EBV)
o Mycoplasma pneumoniae
o Zika virus
 Frequently develop in patients with lymphoma, HIV seropositive,
and
SLE
 Vaccinations: Rarely post-influenza or other vaccines
 Surgery or trauma
 Other immune responses

PATHOGENESIS

• Exact pathogenesis not known.

• GB syndrome is a monophasic immunologically mediated inflammatory

disorder of peripheral nerves.

Multifocal demyelination with inflammation results in conduction block. Severe

forms show secondary axonal degeneration.

• GB syndrome commonly follows an infection. Antiganglioside antibodies are

seen in at least one-third of GBS patients. These antibodies appear to
cross-react with antigens in the lipopolysaccharides of some
antecedent infective agents.

These antibodies act against gangliosides, such as GM 1, distributed throughout

the myelin in the peripheral nervous system.

• Both cellular and humoral immune mechanisms probably play a role in its
development.

• Since inflammation is important in its pathogenesis, GB syndrome is also

known as acute inflammatory demyelinating polyneuropathy
(AIDP).

Key mechanisms:

 Molecular mimicry: Immune system forms antibodies against

pathogens (e.g., Campylobacter jejuni), which also react with
gangliosides on peripheral nerves (e.g., GM1, GD1a).
 Inflammation and demyelination:
o In AIDP (Acute Inflammatory Demyelinating
Polyradiculoneuropathy), macrophages and T-cells strip myelin
from nerves.
o In AMAN/AMSAN (Acute Motor/Sensory Axonal Neuropathy),
the attack is on axons themselves.
 Conduction block: Leads to weakness and paralysis.

1) Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

 Most common.
 Auto immune response against schwann cell.

2) Miller Fisher Syndrome (MFS)

 Rare variant
 Manifest as a descending paralysis.
 Usually affects the eve muscles first and presents with the triad
ophthalmoplegia, ataxia, and areflexia.

3) Acute Motor Axonal Neuropathy (AMAN)

 Also known as Chinese paralytic syndrome.
 Attacks motor nodes of Ranvier and is prevalent in China and
Mexico.

4) Acute Motor Sensory Axonal Neuropathy (AMSAN)

 Similar to AMAN
 Affect the sensory with several axonal damage.

5) Acute Panautonomic Neuropathy

 Is the most rare variant of GBS, sometimes accompanied by
encephalopathy.
 Frequently occurring symptoms include impaired sweating, lack of
tear formation, photophobia, dryness of nasal and oral mucosa,
itching and peeling of skin, nausea, dysphagia, and constipation
unrelieved by laxatives or alternating with diarrhea.

• Initial nonspecific symptoms of lethargy, fatigue, headache, and decreased

initiative are followed by autonomic symptoms including orthostatic
light-headedness, blurring of vision, abdominal pain, diarrhoea,
dryness of eyes, and disturbed micturition.

Bickerstaff's brainstem encephalitis (BBE)

 It is characterized by acute onset of ophthalmoplegia, ataxia,
disturbance of consciousness, hyperreflexia.
 Large, irregular hyper intense lesions located mainly in the
brainstem, especially in the pons, midbrain and medulla, are
described in the literature.

Clinical Features:

Onset and Progression:

 Symptoms usually begin 1 to 3 weeks after a triggering infection.

 Ascending paralysis: Starts in the legs and progresses upwards.

Motor Symptoms:

 Symmetrical weakness, starting in lower limbs

 Loss of deep tendon reflexes (areflexia)
 Facial weakness (bilateral facial palsy)
 Bulbar palsy: difficulty swallowing, speaking
 Respiratory muscle weakness → may need ventilation

Sensory Symptoms:

 Tingling or numbness (paresthesia)

 Mild sensory loss

Autonomic Dysfunction (in 70% of cases):

 Fluctuating blood pressure

 Cardiac arrhythmias
 Urinary retention
 Sweating abnormalities

Variants of GBS:

 AIDP: Most common variant in Western countries

 AMAN/AMSAN: Common in Asia and Latin America
 Miller Fisher Syndrome: Triad of ophthalmoplegia, ataxia,
areflexia
Investigations/Diagnosis

CSF findings: Develop after 1 week of illness:

– Raised protein (100–1000 mg/dL), normal sugar

– CSF pleocytosis (up to 50 cells) is common in patients who have GBS and
concurrent HIV infection.

Electrodiagnostic study: Nerve conduction studies:

– In mild/early stage: Normal

– In demyelination: Prolonged distal latencies, slow conduction, velocity,

conduction block,

– In primary axonal: Reduced amplitude of compound action potential without

slow conduction.

Antibodies:

a ganglioside component of nerve are found in about 25%, usually the motor
axonal form.

– Miller–Fisher syndrome: Antibodies against GQ1b (ganglioside) have 90%

sensitivity.

MANAGEMENT

Medical emergency

ICU management

Assessment of respiratory function- respiratory therapy and mechanical

ventilation

Prevention of complications of immobility- anticoagulant agents and thigh high

elastic compression stockings

Plasmapheresis and IVIG are used to directly affect the peripheral nerve myelin
antibody level.
Both therapies decrease circulating antibody levels and reduce the amount of
time the patient is immobilized and dependent on mechanical
ventilation.

Studies indicate that IVIG and plasmapheresis are equally effective in treating
GBS

Intravenous immunoglobin therapy: prevents immune system from further

attacking Schwann cells and myelin by blocking receptors on
microphages

Plasmapheresis: filters blood plasma to remove antibodies and aids in replacing

lost fluids

Corticosteroids: inhibit inflammation associated w/ symptoms

1. Supportive Care:

 Hospitalization and close monitoring

 Ventilatory support if respiratory failure (30% may need it)
 Monitoring autonomic function
 Prevention of complications (pressure sores, DVT)

2. Specific Treatments:

 Intravenous Immunoglobulin (IVIG):

o Dose: 0.4 g/kg/day for 5 days
o Preferred for ease of use and fewer complications
 Plasmapheresis (Plasma exchange):
o Removes circulating autoantibodies
o 4-6 sessions over 10–14 days
 Note: Steroids are not effective in GBS

3. Rehabilitation:

 Physiotherapy to improve muscle strength and prevent contractures

 Occupational therapy
 Psychological support
Prognosis:

 Most patients recover fully or with minimal deficits in 6–12

months.
 20% may have residual weakness
 3–5% mortality, mostly due to respiratory or autonomic
complications
 Poor prognostic indicators:
o Need for mechanical ventilation

Complications:
DVT
Cardiac arrhythmia
Pressure sores
Persistent pain
Contractures and deformity
Psychological imbalance

3.define chronic inflammatory demyelinating neuropathy. Explain

pathophysiology and management – 18
ANSWER:

🌟 Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

Definition:

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is a rare, acquired,

immune-mediated neuropathy characterized by chronic progressive
or relapsing sensorimotor neuropathy due to demyelination of
the peripheral nerves and nerve roots. It is considered the chronic
counterpart of Guillain-Barré Syndrome (GBS), with symptoms
progressing over at least 8 weeks.
Etiopathogenesis:

CIDP is thought to be an autoimmune disease in which the body's immune

system mistakenly attacks the myelin sheath (the protective
covering) of peripheral nerves.

 Immune mechanisms involved:

o Cell-mediated immunity: T-cells activate macrophages that attack
myelin.
o Humoral immunity: Autoantibodies against Schwann cell surface
proteins (e.g., neurofascin, contactin) may be involved.
 Segmental demyelination and remyelination leads to onion bulb
formation (concentric layers of Schwann cells).
 Inflammatory infiltrates (T-cells, macrophages) found in nerve
biopsies.

Predisposing Factors/Associations:

 Idiopathic (most common)

 Post-infectious or post-vaccination
 Diabetes mellitus
 Systemic autoimmune diseases (e.g., lupus, sarcoidosis)
 Monoclonal gammopathy
 HIV/AIDS and other chronic infections

🧠 Pathophysiology of CIDP:

CIDP is a chronic autoimmune disorder that affects the peripheral nervous

system, specifically causing inflammation and demyelination of
peripheral nerves and nerve roots.

🔬 Step-by-Step Mechanism:

1. Immune Dysregulation:

a. The exact trigger is unknown in most cases, but CIDP is thought to

result from abnormal immune responses.
b. T-lymphocytes and macrophages cross the blood-nerve barrier and
mistakenly recognize peripheral nerve myelin as foreign.

2. Cell-Mediated Immune Response:

a. Activated T-helper cells release inflammatory cytokines (e.g., IL-2,

IFN-γ).
b. These cytokines recruit macrophages to the site of the peripheral
nerve.

3. Macrophage-Mediated Demyelination:

a. Macrophages infiltrate the peripheral nerve and strip away the

myelin sheath that surrounds axons.
b. This causes segmental demyelination, resulting in conduction
slowing or block.

4. Antibody-Mediated Damage (in some cases):

a. In some CIDP variants, autoantibodies target specific proteins on

Schwann cells or nodes of Ranvier (e.g., contactin-1, neurofascin-
155).
b. This may lead to nodopathy or paranodopathy (disruption at the
node of Ranvier).

5. Remyelination Attempts:

a. Schwann cells attempt to repair damage, leading to onion bulb

formation (concentric layers of Schwann cell processes).
b. However, continuous immune attacks disrupt this process, resulting
in chronic nerve dysfunction.

6. Resulting Deficits:

a. Demyelination and inflammation impair the conduction of nerve

signals, resulting in motor weakness, sensory loss, and aref
Clinical Features:

CIDP presents gradually over weeks to months and includes motor and
sensory deficits in a symmetric, proximal and distal distribution.

1. Motor Symptoms:

 Progressive muscle weakness (both proximal and distal)

 Weakness of legs more than arms initially
 Difficulty walking, climbing stairs, lifting objects
 May progress to inability to walk or stand

2. Sensory Symptoms:

 Tingling, numbness
 Sensory ataxia (uncoordinated movement due to impaired
proprioception)
 Paresthesias in hands and feet

3. Reflexes:

 Reduced or absent deep tendon reflexes

4. Other Features:

 Fatigue
 Mild facial weakness (rare)
 Cranial nerve and respiratory muscle involvement (uncommon but
possible)

Diagnostic Criteria:

According to EFNS/PNS (European Federation of Neurological

Societies/Peripheral Nerve Society):

1. Clinical criteria:
a. Chronic progression >8 weeks
b. Symmetrical weakness and sensory involvement in limbs
2. Electrophysiological studies (NCS/EMG):
a. Slowed conduction velocity
b. Prolonged distal latencies
c. Conduction blocks
d. Absent F-waves
3. Cerebrospinal Fluid (CSF):
a. Elevated protein (>45 mg/dL)
b. Normal or mildly elevated cell count (albuminocytologic
dissociation)
4. MRI of spinal roots or nerves:
a. May show nerve root hypertrophy or contrast enhancement
5. Nerve biopsy (if needed):
a. Segmental demyelination
b. Onion bulb formation

Differential Diagnosis:

 Guillain-Barré Syndrome (GBS)

 Multifocal motor neuropathy
 Hereditary neuropathies (e.g., Charcot-Marie-Tooth)
 Vasculitic neuropathies
 Diabetic neuropathy

Management:

A. Medical Management:

1. First-line therapies:
a. Corticosteroids (e.g., Prednisolone)
b. Intravenous Immunoglobulin (IVIG) – preferred in elderly or
diabetics
c. Plasma Exchange (Plasmapheresis) – useful in severe cases
2. Second-line / Immunosuppressive agents (if refractory):
a. Azathioprine
b. Mycophenolate mofetil
c. Methotrexate
d. Cyclosporine
e. Rituximab (in antibody-positive CIDP)
3. Monitoring:
a. Repeated neurological examinations
b. Periodic NCS/EMG
c. Assess treatment response and side effects

B. Physiotherapy Management:

Physiotherapy plays a key role in rehabilitation and improving function in CIDP

patients.

Goals:

 Prevent muscle atrophy and joint contractures

 Improve muscle strength and endurance
 Enhance balance and coordination
 Promote mobility and independence
 Reduce fatigue and prevent complications

Phases of Physiotherapy:

1. Acute Phase (in hospital):

 Positioning to prevent pressure sores and contractures

 Gentle passive range of motion (PROM) exercises
 Breathing exercises and chest physiotherapy if needed
 Splinting for limb support

2. Subacute Phase:

 Gradual introduction of active-assisted and active ROM

 Low-resistance strengthening exercises
 Bed mobility and transfer training
 Gentle balance training in sitting and standing
 Walking with support (parallel bars, walkers)
3. Recovery Phase:

 Progressive resistive exercises

 Proprioceptive training
 Endurance training (low-impact aerobic exercises: cycling,
walking)
 Gait training with or without orthotics
 ADL (Activity of Daily Living) retraining

4. Maintenance Phase (Home program):

 Continue exercise routine

 Use of assistive devices if needed
 Energy conservation techniques
 Education on fatigue management and fall prevention

SHORT ESSAY
1. mononeuritis multiplex-cause and nerve involved – 22

ANSWER:

🧠 Mononeuritis Multiplex

✅ Definition:

Mononeuritis multiplex is a neurological condition characterized by

asymmetric involvement of two or more non-contiguous
peripheral nerves. It presents as painful, patchy, multifocal
neuropathy, often with acute or subacute onset.

It differs from polyneuropathy (which is typically symmetric and distal) by its

asymmetry, focal deficits, and often painful presentation.
🔍 Etiology / Causes:

Mononeuritis multiplex is commonly caused by underlying systemic diseases,

particularly vasculitic, metabolic, infectious, or infiltrative
conditions.

Category Common Causes

- Polyarteritis nodosa (PAN) - Microscopic

polyangiitis (MPA) -
Vasculitis Granulomatosis with polyangiitis
(Wegener’s) - Churg-Strauss
syndrome (EGPA)

Ischemic nerve damage due to microvascular

Diabetes mellitus
disease
- Hepatitis B/C - HIV/AIDS - Leprosy - Lyme
Infections
disease

- Rheumatoid arthritis - Systemic lupus

Autoimmune diseases
erythematosus (SLE)

Amyloidosis Deposition of abnormal proteins in nerves

Sarcoidosis Granulomatous nerve inflammation

Paraneoplastic syndromes, lymphoma

Neoplastic
infiltration

Drugs/Toxins Chemotherapy agents, isoniazid

🧠 Pathophysiology:

 The primary mechanism is vasculitis of the vasa nervorum (blood

supply to nerves), leading to:
 o Ischemic infarction of individual nerves
o Patchy and asymmetric nerve damage
 Other mechanisms:
o Direct infiltration (e.g., in lymphoma, amyloidosis)
o Immune complex deposition (e.g., in SLE)

✅ Common Nerves Involved in Mononeuritis Multiplex

🔹 Upper Limb Nerves:

Nerve Clinical Features

Wrist drop, finger extension weakness, sensory loss on

Radial nerve
dorsum of hand and forearm

Claw hand, weakness of hand grip, sensory loss on

Ulnar nerve
medial 1½ fingers

Thenar atrophy, weak thumb opposition, sensory loss in

Median nerve
lateral 3½ fingers (carpal tunnel symptoms)

Musculocutaneo
Weak elbow flexion, sensory loss on lateral forearm
us
(less common)
nerve

Shoulder abduction weakness, sensory loss over deltoid

Axillary nerve
area (less common)

🔹 Lower Limb Nerves:

Nerve Clinical Features

Common peroneal Foot drop, steppage gait, sensory loss on lateral leg
nerve and dorsum of foot
Tibial nerve Weak plantar flexion, sensory loss on sole of foot

Weak hip flexion and knee extension, sensory loss

Femoral nerve
over anterior thigh and medial leg

Obturator nerve Weak thigh adduction, sensory loss over medial thigh

Lateral femoral
Numbness or burning over lateral thigh (meralgia
cutaneous
paresthetica)
nerve

🔹 Cranial Nerves (occasionally):

Nerve Clinical Features

Facial nerve (CN VII) Facial weakness (Bell’s palsy-like), asymmetrical

Trigeminal nerve (CN

Facial numbness, pain
V)
Oculomotor nerve (CN Ptosis, diplopia, pupillary involvement (rare, but can
III) occur in vasculitis or diabetes)

⚠️Clinical Features:

 Acute/subacute onset
 Asymmetric, patchy motor and sensory loss
 Painful neuropathy (burning, stabbing)
 Weakness in distribution of affected nerve(s)
 Mixed upper and lower limb involvement
 May progress to generalized polyneuropathy if untreated
🔬 Investigations:

Test Findings
Nerve Conduction
Reduced amplitude, conduction block in multiple
Studies /
non-contiguous nerves
EMG
CBC, ESR, CRP (inflammation), ANA, RF, ANCA
Blood tests (vasculitis), HbA1c (diabetes), Hep
B/C, HIV

May show vasculitic changes, axonal

Nerve biopsy
degeneration, inflammation

May show elevated protein (in inflammatory

CSF analysis
causes)
Imaging
(MRI/Ult To assess nerve thickening or mass lesions
rasound)

💊 Management:

1. Treat underlying cause:

 Diabetes: Good glycemic control

 Infections: Antiviral, antileprosy, or antibiotics depending on the
cause
 Autoimmune/Vasculitis:
o Corticosteroids (e.g., Prednisolone)
o Immunosuppressants: Azathioprine, Cyclophosphamide,
Methotrexate
o IVIG or Plasmapheresis (in severe immune-mediated cases)

2. Symptomatic treatment:

 Neuropathic pain: Gabapentin, Pregabalin, Amitriptyline

 Physical therapy: Maintain strength, prevent contractures
 Orthotic devices: AFO for foot drop, wrist splints
 Occupational therapy: Support with ADLs (activities of daily
living)

FOCAL PERIPHERAL NEUROPATHY

LONG ESSAY
1.classify peripheral nerve injury. Add a note on different surgical
procedures for the same –19

ANSWER: 📘 II. Definition:

Peripheral Nerve Injury refers to any damage to the structure or function of a

peripheral nerve due to trauma, compression, ischemia, or disease,
leading to motor, sensory, or autonomic dysfunction in the
distribution of the affected nerve.
⚙️III. Mechanism of Injury:

1. Trauma:
a. Lacerations (knife, glass), blunt force, crush injuries
b. Bone fractures causing nerve damage (e.g., humeral shaft → radial
nerve)
c. Traction injuries (e.g., brachial plexus from shoulder dislocation)
2. Compression:
a. Chronic pressure (e.g., carpal tunnel syndrome)
b. Tumors or cysts compressing nerves
3. Ischemia:
a. Vascular occlusion or vasculitis reduces blood flow to nerves
4. Injection Injury:
a. Injections given near nerves (e.g., sciatic nerve injury from gluteal
injection)
5. Entrapment Neuropathies:
a. Nerves trapped in anatomical tunnels (e.g., ulnar nerve in cubital
tunnel)

Classification of Nerve injury: - by Seddon's classificiation

1. Transient ischaemia.
2. Neurapraxia
3. Axonotmesis
4. neurotmesis

Type Description Recovery Pathology

Myelin sheath
Temporary
Complete affect
conduc
recov ed, no
tion
Neuropraxi ery in Walle
block
a days rian
without
to degen
axonal
weeks eratio
damage
n
Axonotmesi Axon damaged, but Recovery possible Wallerian
 but
connect slow
ive (axon degen
tissue regen eratio
s
(endon erates n
eurium ~1 occurs
) intact mm/d
ay)
Complete
No recovery
disrupti Wallerian
witho
on of degen
ut
axon eratio
Neurotmesis surgic
and n,
al
connect fibrosi
interv
ive s
ention
tissue

Transient ischemia:-

 Due to transient endoneurial anoxia (due to acute nerve

compression)
 Reversible condition
 Within 15 min: numbness and tingling
 After 30 min: loss of pain sensibility
 After 45 min: muscle weakness
 Relief of compression is followed by intense paresthesia upto 5 min.
 Feeling restored within 30 seconds and full muscle power after 10
minutes.

Neurapraxia:-

 Physiological interruption, anatomically normal.

 No proximal or distal degenration and neuroma formation.
 Seen in crutch palsy, Saturday night palsy, tourniquet palsy.
 Recovery is Complete and Excellent.

Axonotmesis
  Due to axonal interruption but the nerve is in continuity and the
neural tubes are intact.
 Wallerian degeneration distal to the lesion and few millimeters
retrograde.
 Neuroma in continuity will formed.
 Axonal regeneration occurs within hours of nerve damage (1-2
mm/day), and recover in few weeks.
 Seen in Tardy Ulnar nerve palsy.
 Recovery is usually Good.

Neurotmesis:-

 Division of nerve trunk (Axons as well as nerve).

 Rapid wallerian degeneration.
 End or side neuroma will formed.
 Destruction of endoneurial tubes over a variable segment and
scarring prevents regeneration of axons.
 Surgical repair required
 Recovery/Function may be adequate but is never normal (poor).

2. Sunderland’s Classification (1951):

Grade Description Structures Involved Recovery

Grade Conduction block Myelin only Full recovery

I
Axon only;
Grade endoneur
Axonal injury Good recovery
ium
intact
Axon and
Grade
Axon + endoneurium injury endoneur Incomplete recovery
ium
Grade Axon + endoneurium + Only epineurium
Poor recovery
perineurium injury intact
Grade No recovery without
Complete transection of nerve All layers disrupted
surgery

Examination

• Following observation should be made:

1. Attitude and deformity: Some peripheral nerve injuries present with classic
attitude and deformity of limb.

 Wrist drop
 Foot drop
 Winging of scapula
 Claw hand
 Ape-hand deformity
 Pointing index

* Policeman-tip deformity

Scoliosis and Cobb angle

2. Wasting of muscles:

 Will become obvious some time after paralysis.

 Compare opposite sound side. Slight wasting may go missed.

3.Skin changes:

 Dry(No sweating), glossy and smooth.

 Pallor or cyanosis
 Trophic changes such as ridged and brittle nails, shiny atrophic skin,
trophic ulcersetc
1. Temperature: Paralysed part is usually colder and drier due to loss of
sweating. Always compare with normal side.
2. Sensory examination: Different forms of sensation to be tested in
suspected case of nerve palsy.
3. Sweat test: To detect sympathetic function in the skin supplied by a
nerve.
 Presence of sweating within an autonomous zone of an injured
peripheral nerve reassures that complete inteurrption of the nerve has
not occurred.
 Starch test or Ninhydrin print test.

7. Motor examination

Treatment of nerve injury

• Conservative management

*Splintage of the paralysed limb

Preserve mobility of the joint

*Care of skin and nails

•Physiotherapy

*Relief of pain: analgesics

• Operative management

1. Neurolysis
2. Nerve repair
3. Nerve grafting
4. Nerve transfer

Neurolysis

 Application of physical or chemical agents to a nerve in order to

cause a temporary degeneration of targeted nerve fibres
 Operation where nerve is freed from enveloping scar (perineural
fibrosis) ; called external neurolysis
 The nerve sheath may be dissected longitudinally to relieve the
pressure from the fibrous tissue within the nerve(intraneural fibrosis;
internal neurolysis

Nerve repair

 May be performed within a few days of injury or

later.
Types:

 Primary repair: Indicated in clean sharp nerve injuries;

 done in the first 6 to 8 hours of injury
 Delayed primary repair: Done in the first 7 to 18 days of injury when
the wound is clean and there are no other major complicating
injuries
 Secondary repair: Done in crushed, avulsed injuries; done at a delay
of 3-6 weeks

Techniques of nerve repair

1. Nerve suture

 Indicated when the nerve ends can be brought close to each other
 Techniques：
 Epineural suture
 Epi-perineural suture
 Perineural suture
 Group fascicular repair

✅ 2. Nerve Grafting:

Indications:

 When nerve ends cannot be approximated without tension

 Gaps >1–2 cm
Procedure:

 Interpose an autograft (usually sural nerve, less commonly

medial/lateral antebrachial cutaneous nerve)

Types:

 Cable grafts: Multiple small-caliber grafts for large nerves

 Vascularized nerve grafts: Used in scarred beds or previous failed
repairs

✅ 3. Nerve Transfer (Neurotization):

Indications:

 Root avulsion injuries (e.g., brachial plexus)

 When proximal nerve not available or recovery is not feasible

Procedure:

 Transfer of a functional nearby motor nerve (or branch) to

reinnervate the denervated muscle
 Example: Spinal accessory nerve → musculocutaneous nerve

Advantages:

 Shorter reinnervation time

 Useful in late presentations

✅ 4. Tendon Transfers (Supportive):

Indications:

 Chronic cases where nerve recovery is not expected

 When muscles are permanently denervated
Procedure:

 Redirect a functional tendon/muscle to replace lost function (e.g.,

palmaris longus to extensor tendon in radial nerve palsy)

✅ 5. Nerve Decompression:

Indications:

 Chronic nerve entrapments

 Example: Carpal tunnel release (median nerve), cubital tunnel
release (ulnar nerve)

Procedure:

 Relieve pressure by cutting surrounding ligaments or fibrous tissue

SHORT ESSAY

1.radial nerve palsy –22,19

ANSWER: Radial Nerve Palsy – In Detail

(For physiotherapy/BPT-level understanding – textbook style)

Anatomy of Radial Nerve

The radial nerve arises from the posterior cord of the brachial plexus, with
nerve roots from C5 to T1. It is the major motor and sensory
nerve of the posterior arm and forearm.

 Course:
o Originates from posterior cord.
o Travels posteriorly through the triangular interval.
o Passes through the spiral groove of the humerus.
o Pierces the lateral intermuscular septum to enter the anterior
compartment.
o At the level of the lateral epicondyle, it divides into:
 Superficial branch: Sensory to dorsum of the hand.
 Deep branch (posterior interosseous nerve): Motor to extensor
muscles of the forearm.

Definition

Radial nerve palsy refers to a condition where the function of the radial nerve is
impaired due to injury or compression. It leads to motor and
sensory deficits, particularly affecting the extension of the wrist,
fingers, and thumb, and causes wrist drop.

Etiology / Causes

1. Trauma:
a. Mid-shaft humeral fractures (most common).
b. Shoulder dislocation.
c. Penetrating injuries (e.g., stab wounds).
2. Compression neuropathy:
a. “Saturday night palsy”: Prolonged compression of the nerve in the
spiral groove due to falling asleep with the arm over a chair.
b. Improper use of crutches (crutch palsy).
c. Tourniquet use or tight plaster casts.
3. Iatrogenic:
a. Surgical injuries during humeral fixation.
4. Systemic/neurological conditions:
a. Diabetes mellitus (neuropathy).
b. Vasculitis (leading to mononeuritis multiplex).
 Pathophysiology

When the radial nerve is compressed, stretched, or severed, there is disruption in

the transmission of motor and sensory impulses:

 Axonotmesis or neuropraxia is common in compressive cases.

 Neurotmesis occurs in severe trauma.
 Muscles supplied by the nerve lose their innervation, resulting in
paralysis and eventual atrophy if not recovered.

Clinical Features

Motor Deficits:

 Wrist drop: Inability to extend the wrist.

 Finger drop: Inability to extend fingers and thumb at the
metacarpophalangeal joints.
 Weak elbow extension (if lesion is proximal to triceps innervation).
 Difficulty in grip due to poor wrist stabilization.

Sensory Loss:

 Posterior arm (variable).

 Posterior forearm.
 Dorsal aspect of the lateral hand, thumb, and proximal dorsal 2½
fingers (excluding finger tips).

Classification Based on Level of Injury

Level Type of Deficit

Loss of elbow, wrist, and finger extension. Sensory
Axilla (e.g., crutch palsy)
loss on posterior arm.
Spiral groove (e.g., humeral
Loss of wrist and finger extension, triceps spared.
fracture)
Elbow (posterior Motor loss to finger and wrist extensors, no sensory
 interosseous
loss.
nerve)
Superficial branch (sensory
Sensory loss only, no motor involvement.
only)

Investigations

1. Clinical Examination – Tinel’s sign, muscle power testing.

2. Electromyography (EMG) – To assess nerve and muscle
involvement.
3. Nerve Conduction Studies (NCS) – Measures conduction velocity
and block.
4. MRI/Ultrasound – In traumatic or compressive lesions.
5. X-ray – If fracture suspected.

Management

Conservative:

 For neuropraxia or mild compression:

o Rest and activity modification.
o Splinting: Cock-up splint to prevent contractures and wrist drop.
o NSAIDs for inflammation.
o Physiotherapy:
 Electrical stimulation for muscle re-education.
 Passive and active ROM exercises.
 Strengthening exercises as recovery begins.
 Sensory re-education.

Medical:

 Treatment of underlying conditions (e.g., diabetes).

 Corticosteroids (in inflammatory neuropathies).
Surgical:

 Indicated if:
o No improvement in 3–6 months.
o Evidence of neurotmesis or entrapment.
 Options:
o Neurolysis: Decompression of the nerve.
o Nerve grafting: In case of severed nerve.
o Tendon transfer surgery: For irreversible palsy (e.g., pronator teres
to extensor carpi radialis).

Prognosis

 Depends on the type of nerve injury:

o Neuropraxia – Complete recovery in weeks to months.
o Axonotmesis – Recovery takes months; may need surgical aid.
o Neurotmesis – Poor prognosis without surgical repair.

Complications

 Muscle wasting and contractures.

 Loss of fine motor skills.
 Chronic neuropathic pain.
 Psychological impact due to disability.

2.erbs palsy-cause and c/f -23,18

Answer: Definition

 Erb's palsy is a paralysis of the arm caused by injury to the upper

group of the arm's main nerves, specifically the CS-C6 nerves roots.
 Erb's palsy is a form of obstetric brachial plexus palsy.
 The injury can either stretch, rupture or avulse the roots of the plexus
from the spinal cord
 Depending on the nature of the damage, the paralysis can either
resolve on its own over a period of months, require rehabilitative
therapy, or surgery.

Mechanism of injury
Bending or stretching of the neck in a direction away from the side of injury

Causes
 The nerves of the brachial plexus can be injured during a difficult
delivery from:
 The infant's head and neck pulling toward the side as the shoulders
pass through the birth canal
 Pulling on the infant's shoulders during a head-first delivery
 Pressure on the baby's raised arms during a breech (feet-first)
delivery

Other situations where the brachial plexus can be damaged are:

 A trauma to the side of the neck, for instance a motor vehicle

accident, fall or heavy blow
 A stretch injury sustained while participating in a sport
 An attempt to reduce a dislocated shoulder
Pathophysiology:

 Sudden stretching or tearing of the upper brachial plexus (C5-C6).

 Results in neuropraxia, axonotmesis, or neurotmesis depending on
severity.
 Muscles innervated by affected nerves become weak or paralyzed,
while others are spared, leading to characteristic posturing and
functional loss.

Clinical Features:

Posture of the Limb (Classical Appearance):

 Known as “Waiter’s Tip” position:

o Arm adducted (held close to body)
o Arm internally rotated
o Elbow extended
o Forearm pronated
o Wrist flexed
Motor Loss:

 Inability to abduct the shoulder.

 Loss of elbow flexion.
 Weak supination of forearm.
 Reduced or absent biceps reflex.

Sensory Loss:

 Over the lateral aspect of the arm and forearm, corresponding to

the C5–C6 dermatomes.

Other Signs (in infants):

 Asymmetric Moro reflex.

 Decreased spontaneous movement of the affected limb.

Muscles Affected & Resulting Motor Deficits:

Muscle Innervation Function Lost

Deltoid Axillary (C5, C6) Shoulder abduction

Supraspinatus Suprascapular (C5, C6) Shoulder abduction

External rotation of
Infraspinatus Suprascapular (C5, C6)
shoulder

Musculocutaneous (C5, Elbow flexion &

Biceps brachii
C6) supination

Musculocutaneous (C5,
Brachialis Elbow flexion
C6)
Brachioradialis Radial (C5, C6) Elbow flexion
Diagnosis:

Clinical Examination:

 Observation of posture and spontaneous movement.

 Reflex testing (especially biceps reflex).
 Sensory testing (in older children and adults).

Imaging:

 MRI / CT Myelogram: To assess nerve root avulsion.

 X-rays: To rule out associated fractures.
 Ultrasound: To detect muscle atrophy in infants.

Electrophysiology:

 Nerve Conduction Studies (NCS)

 Electromyography (EMG) – to assess denervation and
reinnervation.

Management:

Conservative Management (Initial):

 For infants with neuropraxia (mild cases), observation for

spontaneous recovery in 3–6 months.
 Physiotherapy is the mainstay during this period.

Physiotherapy Management:

1. Positioning and Splinting:

a. Prevent contractures.
b. Maintain functional positioning.
2. Passive Range of Motion (PROM):
a. To prevent joint stiffness and muscle contracture.
b. Gentle exercises for shoulder, elbow, wrist, and fingers.
3. Stimulation Techniques:
a. Tactile and proprioceptive stimulation.
b. Electrical muscle stimulation to prevent disuse atrophy.
4. Motor Re-education and Strengthening:
a. Encouraging active movements as the nerve recovers.
b. Functional tasks and play-based therapy in infants.
5. Parental Education:
a. Home exercise programs.
b. Handling and positioning advice.

Surgical Management:

 Considered if no functional improvement by 3–6 months.

 Types of surgery:
o Nerve grafting.
o Nerve transfers.
o Muscle/tendon transfers in older children for functional
improvement.

3.nerve repair-its indication and surgeries –22

ANSWER: Definition:

Nerve repair refers to surgical procedures aimed at restoring the continuity

and function of a damaged peripheral nerve. It is performed when a
nerve has been severed, ruptured, or severely damaged, and
spontaneous recovery is unlikely or inadequate.

✅ Indications for Nerve Repair Surgery

Nerve repair is considered when a peripheral nerve has been severely injured or
transected, and spontaneous recovery is unlikely. Surgical
intervention aims to restore the continuity and function of the nerve.

1. Complete Nerve Transection

 Sharp trauma (e.g., knife or glass injury)

 Accidental surgical damage (iatrogenic)

2. Open Nerve Injury

 Open wounds with visible nerve damage.

 Risk of infection mandates early exploration and repair.

3. Nerve Gaps >5 mm

 Gaps between nerve ends due to retraction or tissue loss.

 Cannot be approximated without tension.

4. No Improvement After Conservative Management

 If there's no functional recovery in 3–6 months, especially in

axonotmesis.

5. Neuroma Formation

 Painful or non-functional neuroma formation after nerve trauma.

6. Brachial Plexus Injury

 Avulsion or severe upper limb paralysis.

 Early intervention improves outcome.

7. Birth-related Brachial Plexus Palsy (e.g., Erb’s Palsy)

 Surgery if no functional improvement by 3–6 months.

8. Nerve Compression with Structural Damage

 Severe chronic compression (e.g., in carpal tunnel syndrome) with

axonal loss.

🔧 Types of Nerve Repair Surgeries

The choice of surgery depends on the type, site, and severity of injury, and the
time elapsed since the injury.
1. Direct (End-to-End) Neurorrhaphy

 Indication: Clean, sharp injuries with no or minimal gap.

 Procedure: The two ends of the severed nerve are directly sutured
together using microsurgical techniques, without tension.
 Note: Best results when done within 6–12 hours (primary repair).

2. Nerve Grafting

 Indication: When there is a nerve gap >5 mm that cannot be

approximated without tension.
 Procedure: A segment of donor nerve (usually sural nerve) is
harvested and used to bridge the gap.
 Types:
o Cable grafting: Multiple grafts placed side by side.
o Interfascicular grafting: Aligns matching fascicles.
 Timing: Usually done after 2–3 weeks (delayed primary/secondary
repair).

3. Nerve Transfer (Neurotization)

 Indication: Proximal nerve root avulsion or severe injury where the

original nerve cannot be used.
 Procedure: A functioning donor nerve or branch is redirected to
the distal part of the injured nerve.
 Examples:
o Spinal accessory nerve → musculocutaneous nerve
o Intercostal nerves → brachial plexus
o Ulnar nerve → radial nerve (partial transfers)
 Used extensively in: brachial plexus injuries, especially root
avulsions.
4. Nerve Conduits / Tubes

 Indication: Small nerve gaps (<3 cm) where grafts aren't ideal.
 Procedure: A synthetic or biological tube/conduit is placed
between nerve ends to guide axonal regrowth.
 Materials: Collagen, polyglycolic acid, or silicone.

5. Neuroma Excision with Repair

 Indication: Painful neuromas or ineffective regeneration.

 Procedure: Excision of the neuroma followed by direct repair or
grafting.

6. Tendon Transfers (in Late or Irreparable Injuries)

 Indication: When nerve repair is not possible or has failed, and

function must be restored.
 Procedure: Tendons from functioning muscles are transferred to
restore lost motion (e.g., wrist or finger extension).
 Common in radial nerve palsy.

Timing of Nerve Repair:

Type of
Timing Description

Immediately or
Done during the initial surgery if wound
Primary within
is clean and nerve ends are
6–12
healthy.
hours

Delayed 1–3 weeks after After infection risk subsides; allows

injury wound stabilization.
 >3 weeks to months
Secondary Often used when patient presents late or
after
wound was contaminated.
injury