Peripheral Nerve
• Peripheralnerve is a term used to describe
the peripheral nervous system.
• The peripheral nervous system connect the
brain and spinal cord to the entire human
body.
3.
Classification of nervefibers
1. Depending upon structure :
– Myelinated
– Non myelinated
2. Depending upon distribution :
– Somatic
– Autonomic
4.
3. Depending uponorigin :
– Cranial nerves (12 pair)
– Spinal nerves (31 pair)
4. Depending upon function :
– Motor
– sensory
5.
5. ERLANGER GASSERCLASSIFICATION :
Depending upon length of fibers and rate of
conduction of impulses
Type Diameter Velocity (m/s)
A alpha 12 to 24 70 to 120
A beta 6 to 12 30 to 70
A gamma 5 to 6 15 to 30
A delta 2 to 5 12 to 15
B 1 to 2 3 to 10
C <1.5 0.5 to 2
Peripheral neuropathy
• Peripheralneuropathy refers to the conditions
that result when nerves that carry messages
to and from the brain and spinal cord from
and to the rest of the body are damaged or
diseased.
• Damage to these nerves can impair muscle
movement, prevent normal sensation in the
arms and legs, and cause pain.
8.
• Peripheral neuropathymay be classified
according to :
– The number and distribution of nerves affected
(mononeuropathy, mononeuritis multiplex, or
polyneuropathy)
– Type of nerve fiber predominantly affected
(motor, sensory, autonomic)
– Based on duration chronic or acute
9.
• Neuropathy affectingjust one nerve is called
"mononeuropathy"
• Neuropathy involving multiple nerves in roughly the same
areas on both sides of the body (symmetrical) is called
"symmetrical polyneuropathy" or simply
"polyneuropathy".
• When two or more (typically just a few, but sometimes
many) separate nerves in disparate areas (asymmetrical)
are affected it is called "mononeuritis multiplex",
"multifocal mononeuropathy", or "multiple
mononeuropathy"
10.
Classification of peripheralnerve injuries
(anatomical classification)
Based on the extent of damage to nerve
1. Seddon’s Classification
2. Sunderland’s classification
Neuropraxia
• Mildest type
•Occurs due to temporary compression or
stretch of nerve
• Temporary interruption of conduction without
loss of axonal continuity (conduction block)
• Endoneurium, perineurium and epineurium
and are intact.
13.
• Oedema ofaxons and displacement of myelin
occures. But no wallerian degeneration
occures.
• Sensory and motor problems distal to the site
of injury
• Stimulaion distal to injury - Response present
• Prognosis – Good
• Recovery – week or month
14.
Axonotmesis
• More severestage
• Loss of continuity of axon and its covering myelin.
• Rupture of axon or nerve fibers and its covering of
myelin, but preservation of the connective tissue
framework of the nerve
• Epineurium and perinurium are intact.
• Wallerian degeneration occurs below the site of injury.
• It begins at 2nd
week and complete at 3rd
week after onset
of injury.
• Retrograde degeneration occurs up to proximal node of
ranvier.
15.
• Sensory, motorand sometimes autonomic deficits distal
to the site of injury.
• Stimulation proximal or distal to the site of nerve
injuries will produce no response.
• Recovery depends on rate and extent of regeneration.
• If lesion is proximal – 3 mm per day
• If lesion is distal – 1 to 1.5mm per day
• Prognosis – Better than neurotmesis (upto months)
16.
Neurotmesis
• Most severe
•Complete Transaction
• Total disruption of nerve fiber
• Epineurium and perineurium are also affected
• Wallerian degeneration occurs distal to the site of injury
• Prognosis : Poor compared to axonotmesis and
neuropraxia
• Surgery needed.
17.
2. Sunderland classification
•Builds upon seddons classification
• Divides seddon’s last stage into 3 sub
categories
• Total 5 grades
18.
• First degree: Neuropraxia.
– Recovery within few hours to weeks without surgical
intervention
• Second degree : Axonotmesis.
– Recovery within 18 months
• Third degree : Neurotmesis with preservation of
perineurium and epineurium
– Recovery is poor and incomplete
19.
• Forth degree: Neurotmesis with preservation of
epineurium
– Recovery is poor and incomplete.
– Nerve Grafting is required
• Fifth degree : Neurotmesis with complete
transection.
– Recovery is not possible without surgery
– Bypass / jump Grafting is required
20.
Degeneration and regenerationof nerve
fibers
• Pathological changes after peripheral nerve
injury includes :
1. Segmental demyelination
2. Degenerative changes
1. Wallerian degeneration
2. Retrograde degeneration
3. Regeneration
21.
1. Segmental demyelination:
• Focal degeneration of the myelin sheath with
sparing of axon
• Occurs when axon is intact after nerve injury
• It is the act of demyelinating or loss of myelin
sheath
23.
2. Degenerative changes
•Wallerian degeneration :
– Wallerian degeneration is the pathological change
that occurs in the distal cut end of nerve fiber
(axon) after axonal injury.
– It is also called orthograde degeneration.
– Wallerian degeneration starts within 24 hours of
injury.
24.
– After injuryaxonal skeleton disintegrates and axonal
membrane breaks apart.
– It is followed by degradation of myelin and infiltration of
miacrophages and schwann cells
– Neurilemmal sheath is unaffected, but the Schwann cells
multiply rapidly and clear the debris from the
degeneration
– So, the neurilemmal tube becomes empty.
– Later it is filled by the cytoplasm of Schwann cell. All these
changes take place for about 2 months from the day of
injury.
25.
• RETROGRADE DEGENERATION
–It is the pathological changes, which occur in the nerve cell body
and axon proximal to the cut end
• Changes in Nerve Cell Body
i. First, the Nissl granules disintegrate into fragments
ii. Golgi apparatus is disintegrated
iii. Nerve cell body swells due to accumulation of fluid and
becomes round
iv. Neurofibrils disappear followed by displacement of the nucleus
towards the periphery
• Changes in Axon Proximal to Cut End
In the axon, changes occur only up to first node of
Ranvier from the site of injury. Degenerative changes that
occur in proximal cut end of axon are similar to those
changes occurring in distal cut end of the nerve fiber.
26.
3. Regeneration ofnerve fiber :
1. It starts as early as 4th day after injury, but becomes more
effective only after 30 days and is completed in about 80
days.
2. Regenerative sprouts grow from the proximal cut end of
the nerve.
3. Fibrils move towards the distal cut end of the nerve Fiber
and Some enter the neurilemmal tube of distal end actually
guide the fibrils into the tube.
4. Schwann cells also synthesize nerve growth factors, which
attract the fibrils form proximal segment.
5. Axis cylinder is fully established inside the neurilemmal
tube (3 months)
27.
6. Myelin sheathis formed by Schwann cells slowly.
(1 year)
7. Diameter of the nerve fiber gradually increases.
8. In the nerve cell body, first the Nissi granules
appear followed by Golgi apparatus
9. Nucleus occupies the central portion
10. Though anatomical regeneration occurs in the
nerve, functional recovery occurs after a long
period.
28.
Causes
• Peripheral neuropathymay be either
inherited or acquired through disease
processes or trauma.
• Causes of Heriditory neuropathy :
- HMSN
- Friedrich’s ataxia
- Porphyria
29.
• Causes ofacquired peripheral neuropathy include:
– Physical injury (trauma) : Sudden injury, repeatitive stretch
– Metabolic and endocrine disease : Diabetic neuropathy,
Uremia, reduction in thyroid hormone
– Small vessel disease
– Autoimmune disease
– Infection/ Inflammation : Leprosy, AIDS, Vasculitis,
– Cancer
– Toxins : Heavy metals, pestisides
– Drugs
– Heavy alcohol consumption
• Causes :
–Tennis elbow (Inflammation of common extensor tendon)
– Fracture of upper end of radius and ulna
– Direct bolw to posterior interosseous nerve
– Fibrous arch covers the post interossei nerve as it passes
through supinator muscle and get compressed during
forcefull contraction (i.e. Arcade of frohse syndrome)
– Compression of the nerve between the two layers of
supinator (i.e Supinator syndrome)
– Compression due to ganglia, neoplasm, bursae, VIC and
fibrosis after trauma
43.
• Sensory :Sensations are spared (Pure Motor
syndrome)
• Motor : Weakness in distal extensors supplied
by radial nerve
» ED
» ECU
» EDM
» EI
» EPL
» EPB
» APL
• Symptoms
– Puresensory syndrome
– No muscle involvement
– Sensory abnormality (burning, numbness, tingling)
over dorsal radial aspect of the hand
– Discomfort may get worsen with palmar and ulnar
wrist flexion or forced pronation
47.
Deformity in radialnerve palsy
• Wrist drop
• Wrist - 45 of palmar flexion
• Thumb – Palmar abduction and slight flexion
• MP joints – 30 flexion
• IP joints – slight flexion
48.
Functional Disability
• Poorgrip due to weak wrist extensors as
fixators, can not put objects like cup or glass
flat on table
49.
Trick movements
• Reboundphenomena :
– Attempt to produce wrist extension wrist flexor
forcefully contracts and relaxes.
– Attempt to produce extension of DIP of thumb FPL
forcefully contracts and relaxes.
• Dorsal interossei produces MCP extension but
fingers will go into abduction as well
• While doing ulnar deviation wrist goes into flexion
• Paralysis of triceps – pt use gravitational force for
elbow extension
Causes
Traction injury/stretch injury
Brachialneurities/neuroma
Large cervicle rib
Fracture dislocation of
scapula, clavicle or upper
part of humerus
Burner’s or Stringer’s
syndrome
•Vehicular accidents
•Penetrating
wounds
•Stab wounds
Supra clavicular
injury
• Rootsand Trunk
• Follow the
dermatomal and
myotomal
distribution
Infraclavicular Injury
• Cords and Nerves
• Follow the nerve
pattern (Single or
combination)
57.
Preganglionic injury
• Dueto avulsion of the root from the spinal
cord.
• Lesion is proximal to dorsal root ganglion
• Wallerian degeneration doesn’t occur in the
sensory axon as the DRG is saperated from the
spinal cord.
58.
• Conduction velocityin sensory axon – intact
• Conduction velocity in motor axon – lost
• Prognosis poor
59.
Postganglionic injury
• Lesiondistal to DRG.
• DRG is in contact with spinal cord
• Wallerian degenration occurs because DRG is
in contact with the spinal cord but remaining
part of axon is saperated
60.
• Conduction velocityin sensory axon – lost
• Conduction velocity in motor axon – lost
• Good prognosis.
61.
Total plexus injury
•Lesion is very close to the vertebral column.
• Very rare
• All the muscles supplied by brachial plexus are
paralysed
• Loss of sensation c5 to t1 dermatome
• DTR of upper limb - diminished
Causes
– Obstetric injury- forceful separation of the head
and shoulder during difficult delivery most
common cause
– Forceps / Vaccum delivery
– Breech presentation
– Pressure over supra clavicular area
– Post aenesthetic Paralysis
– Injection of foreign vaccines and serum
64.
Signs and Symptoms
•Sensory : Affected over C5-C6 dermatome
– Area of deltoid insertion
– Lateral aspect of forearm and hand
• Deformity :Policeman’s tip or Waiter’s tip
– Shoulder : Extension
Adduction
Internal Rotation
– Elbow : Extention
– Forearm : Pronation
– Wrist and fingers : usually
unaffected
68.
• Reflexes :Biceps and Brachioradialis Jerk
Affected
• Functional Disability : Difficulty in ADLs that
require flexion of shoulder and elbow (eg.
Eating , combing, brushing etc)
69.
Klumpke’s Palsy
• LowerPlexus Lesion
• Injury to C8 -T1 nerve root
• Rare compare to UBP injury
70.
Causes
– Traction andfall on abducted arm
– Breech delivery
– Operation at axilla
– Apical lobe tumor
– Enlarged cervical rib
71.
Signs and Symptoms
•Sensory : Over C8-T1 distribution
– loss of sensation over medial aspect of arm,
forearm, hand, hypothenar eminence
72.
• Motor :Affects the distribution of median
and ulnar nerves
– Weakness and wasting of the small muscles of the
hand and a characteristic claw hand deformity
– Intrinsic muscles of hand (interossei, lumbricles
thenar and hypothenar)
– Wrist flexors (FCU)
– Finger flexors (FDP, ulnar half)
– Forearm pronators (pronator teres)
73.
• Deformity :Claw hand deformity
– Flattening of transverse metacarpal arch and
longitudinal arch
– Forearm supinated
– Wrist extension
– Hyperextension of MCP joint
– Flexion of PIP and DIP
75.
• Horner’s sign:
– Ptosis
– Myosis
– Enophthalmos
– Anhidrosis
• This is because of injury to sympathetic fibers
to the head and neck that leave the spinal cord
through nerve T1.
Common neuropathies ofulnar nerve
• At cervical spine
• At base of neck
• At axilla
• At arm
• At elbow
• At Wrist
Less
Common
82.
Causes
• At cervicalspine :
– PIVD
– Cervical spondylosis
– Rheumatoid disease of cervical spine
• At base of neck :
– Cervical rib
– ToS
83.
• At axilla:
– Crutch palsy
• At arm :
– Tourniquett palsy
– Fracture of supracondylar region of humerus
– Hansen’s disease
84.
At elbow
• Cubitaltunnel syndrome (Most common cause)
• Compression of ulnar nerve along cubital
tunnel at medial edge of elbow
• Border of cubital tunnel :
– Medial epicondyle
– Olecranon process
– Tendinous arch joining
two heads of FCU
85.
• Cubitus valgus: In cubitus valgus the floor of cubital
tunnel is already elevated which increases the
compression on the ulnar nerve.
Other causes :
• Ganglia at elbow
• Soft tissue tumor
• Elbow dislocation
• Fracture of medial epicondyle
• Hansens disease
• Typing
86.
• Sensory deficit:
– Parasthesia in palmar and dorsal aspect of little
and ring finger
– No involvement of medial border of forearm
– Aggrevates when elbow is bent
87.
• Motor deficit:
– All muscles supplied by ulnar nerve affected
• FCU
• FDP (3and 4)
• Hypothenar muscles : ADM, ODM, FDM
• Adductor pollicis
• FPB
• Interossei
• Lumbricals ( 3 and 4)
88.
At wrist
• Gayonscanal syndrome
• Compression of the ulnar nerve as it passes through
the canal of gayon.
• Border of Gayons canal
– Medial border - tendon of FCU
and pisiform bone.
– Lateral borber–Hook of hamate
– Floor - flexor retinaculum
– Roof - superficial part of the flexor
retinaculum
89.
Other cause :
•Glass cut injury
• Fracture of the carpal bone
• Tumor
• OA
90.
• Sensory Deficit:
– Parasthesia in little finger and ulnar aspect of ring
finger (Superficial sensory branch)
– Palmar and Dorsal sensory branch not affected
– No involvement of medial border of forearm
91.
• Motor Deficit:
–Weakness of ulnar intrinsic muscles of hand
– FCU and FDP are spared
92.
Deformity
• Classical clawhand : (ulnar claw hand)
– Hyperextension of MCP joint of ring and little
finger 30 degrees
– Flexion of IP joint of little and ring finger
• PIP – 25 degree flexion
• DIP – 10 to 15 degree flexion if lesion at wrist FDP
intact
• Less flexion if proximal lesion due to FDP affected
93.
• Ulnar paradox:
–Lesion at elbow there will be reduced DIP flexion
due to FDP paralysis.
– Hence reduced appearance of deformity.
– “The closer to the Paw worse the claw”
– With reinnervation of the nerve flexion at DIP joint
increase giving appearance of increase deformity
94.
Functional Disability
• Lacklumbrical grip
• Power grip is more affected
– Due to weakness of adductor pollocis
• Lack of Pinch grip
• Lack of spherical grip
– Due to lack of lateralisation of fingers
95.
Trick movements
• Ulnardeviation combined with wrist extension
by ECU
• Wrist flexion combined with radial deviation
by FCR
• Abduction of finger combined with finger
extension by extensor digitorum
• ADM is the first muscle to recover – first sign
of recovery
• Lateral andmedial cord of brachial plexus
(C5-T1)
• Axilla to elbow :
– Pronator teres
– Palmaris longus
– FCR
– FDS
• Anterior interosseous nerve :
– FPL
– FDP (lateral half)
– Pronator quadratus
• Distal to wrist (recurrent branch & palmar digital branch):
– APB
– FPB
– OP
– Lumbricles (1 & 2)
Sensory branch
•Palmar cutaneous Branch
• Digital cutaneous branch
100.
Common neuropathies ofmedian nerve
• Median neuropathy at axilla and arm
• Median neuropathy at elbow and forearm
• Median neuropathy at wrist
101.
Median neuropathy ataxilla and arm
• Cause –
– Axillary aneurysm
– Traction injury
– Penetrating injury
102.
• Sensory –
–Over the distribution of palmar cutaneous and
digital cutaneous branch
– Skin overlying thenar eminence
– Loss of sensation over volar aspect of lateral 3
fingers upto the distal phalanx on dorsal side
103.
• Motor
– Weaknessof all the muscles supplied by median nerve
• Pronator teres
• FCR
• Palmaris longus
• FPL
• FDS
• FDP (lateral half)
• Pronator quadratus
• Thenar muscles : APB, FPB, OP
• Lumbricles to digit 2 and 3
104.
Anterior interosseous nervesyndrome
• Sensation – normal
• Motor - weakness of FPL, FDP and PQ
• Pain in forearm and elbow
Median neuropathy atforearm
• Pronator teres syndrome
• Ligament of struthers syndrome
107.
Pronator teres syndrome
–Compression of the
median nerve by the
fibrous band that
connects superficial and
deep head of pronator
teres muscle.
– Less common than ant
interosseous nerve
syndrome and CTS.
108.
Other Causes :
–Compression by bicipital aponeurosis
– Anomalaus fibrous band connecting pronator
teres to tendinous arch of FDS
– Trauma
– Muscle hypertrophy
– VIC
109.
Signs and symptoms-
•Motor :
– Pronator teres is spared.
– Rest all muscles supplied by median nerve are involved.
– The Pronator teres test is an indication of the syndrome
—the patient reports pain when attempting to pronate
the forearm against resistance while extending the
elbow simultaneously.
• Sensory : Loss of sensation over first three fingers
and palm
• Signs andsymptoms –
– Absence of radial pulse on full extention of
forearm
– Weakness of pronator teres + all distal muscles
supplied by median nerve
– Sensory – same as above
Median neuropathy atwrist
• Cause –
– Glass cut injury
– Carpal tunnel syndrome
• RA
• Osteophyte or callus formation
• Ganglion
• Thickening of synovium
• Occupaional
• Pregnancy
• Hypothyrodism
• Myeloma
• DM
• Hereditory pressure palsy
114.
Signs and symptoms–
• Pain –hand and fingers
– Diffuse localised pain that can extend upto elbow
– Nocturnal parasthesia
– Aggravating factors – Extreme flexion and
extension
– Relieving factors- Change in the hand position or
hand shaking
115.
• Sensory :
–Affected over volar aspect of lateral 3 ½ aspect of
fingers upto distal phalanx on dorsal side
– Sometimes the sensation over thenar area
remains intact because palmar cutaneous sensory
branch that arise proximal to carpal tunnel
116.
– 4 patternsof Sensory deficit
• Distal pattern (40%)
• Complete web space pattern
• Half web space pattern
• Distal web space pattern
117.
• Motor:
– Weaknessof OP, FPB and APB
– Weakness of OP and FPB – pinch sign
– Weakness of APB – Bottel sign : The thumb cannot be
adequately abducted and opposed.
Functional Disability
• Difficultyin holding small and big objects.
• Clumsy activity with involved hand
• Can not appreciate the sensation of the object
unless they see the object
121.
Deformity
Depends on siteand extent of lesion
– Pinch sign/ tear drop
– Ape hand deformity
– Partial claw hand
– Pointing index finger
122.
Pinch sign/ teardrop
• Fromet sign
• In anterior interosseous nerve syndrome
• When pt is asked to form tip to tip pinch using
index and thumb there will be pad to pad pinch
• Because of paralysis of
FDP and FPL
• Tear drop appearance
instead of ‘O’
123.
Ape hand deformity
•Monkey hand deformity
• Flattening of thenar eminence
• Lack of oposition of thumb so thumb is held
beside index finger due to over action of
Adductor Pollicis and EPL
124.
Partial claw hand
•Unupposed action of the extensor digitorum
giving rise to hyperextension of MCP joint of
index and middle finger and flexion of IP joint
of these finger.
125.
Pointing Index Finger
•Higher lesion (even common flexors
• When asked to make fist the index finger will
point forward
126.
• This happensbecause when attempt to make
fist the profundus tendon of ring finger will
pull the middle finger into partial flexion
leaving the index finger in extension and
pointing forward
127.
Trick movement
• Radialdeviation combined with wrist
extension by ECR.
• Wrist flexion combined with ulnar deviation by
FCU.
• Rebound phenomena : Thumb DIP joint
flexion by sudden contraction and relaxation
of EPL.
• Cause :
–Carrying heavy weights on the shoulder or by
strapping the shoulder on the operating table.
– Followed immunization
– direct blow
– Thoracic surgery
131.
• Symptoms :
–Shoulder pain
– Inability to raise the arm over the head
– Winging of the medial border of the scapula when
the outstretched arm is pushed forward
• C5-C6
• MuscleSupply : supraspinatus and
infraspinatus muscles.
134.
• Cause :
–Infectious illnesses
– In gymnasts or as a result of local pressure, from carrying
heavy objects on the shoulder (“meat-packer’s”
neuropathy).
• Symptoms :
– Vague dull and achey pain posterior shoulder
– Atrophy of these muscles
– Weakness of the first 15 degrees of abduction
(supraspinatus)
– Pain and weakness on external rotation of the shoulder
joint (infraspinatus). This movement is similar to that
used when reaching backwards to put on a seatbelt in a car.
• This nervearises from the posterior cord of
the brachial plexus (mainly from the C5 root,
with a smaller contribution from C6)
138.
• Muscle supply: teres minor and deltoid muscles
• Cutaneous branch : Supplies sensation to an
area extending from the acromion process to
halfway down the outer aspect of the upper arm.
• Causes of injury :
– Dislocations of the shoulder joint
– Fractures of the neck of the humerus
– Crutches
– Brachial neuritis
139.
• Symptoms :
–Paralysis of abduction of the arm (in testing this
function, the angle between the side of the chest
and the arm must be greater than 15 degrees and
less than 90 degrees)
– As the deltoid atrophies, the rounded contour of
the shoulder is flattened compared to the
uninjured side (Wasting of the deltoid muscle)
– Sensory impairment over the outer aspect of the
shoulder
• C5 C6nerve roots.
• Branch of the lateral cord of the brachial
plexus
• Muscle supply :
– Biceps brachii,
– Brachialis
– coracobrachialis
142.
• Cause :Fracture of the humerus.
• musculocutaneous nerve is rarely injured alone,
but may be damaged by upper brachial plexus
injury
• Symptoms :
– Wasting of these muscles
– Weakness of flexion of the supinated forearm.
– Sensation may be impaired along the radial and volar
aspects of the forearm (lateral cutaneous nerve).
Obturator nerve injury
•Causes :
– Dislocation of hip joint
– Pelvic fracture
– Hernia through obturator foramen
– Prolonged labor
– Compression of the nerve against the wall of
pelvis by mass of tumor or foetus
148.
Signs and Symptoms
SensoryDeficits :
• Sensory alteration over medial
aspect of thigh and knee
– Loss of sensation
– Parasthesia
– Pain
• Pain increases with stretch of
nerve (extension, abduction and
lateral rotation)
149.
Motor Deficits:
• Anteriordivision :
– Adductor longus
– Adductor brevis
– Gracilis
– Pectinius
• Posterior division :
-- Adductor magnus
-- Adductor brevis
• Wasting on the medial side of thigh
• During ambulation thigh is abnormally abducted
and externally rotated results in circumductory and
wide based gait
Causes
• Psoas abcess
•Pelvic anneurysm / neoplasm
• Fracture of pelvis or femur
• Hip dislocation
• Inguinal hernia
• Complication of spinal anesthesia
• Prolapse intervertebral disc
• Lumbar spondylosis or stenosis
• Neuropathy secondary to diabeties mallitus
• Hysterectomy
• Penetrating wounds over lower abdomen
158.
• Sensory Deficit:
– Anterior division : Anterior and medial aspect of
thigh
– Saphenus nerve : Medial aspect of leg and foot
– Loss of sensation, Numbness, tingling, dull ache
159.
• Pain inthe inguinal region That is relieved by
hip flexion and external rotation
160.
• Autonomus zone:
– Small area superior and medial to patella
• Coldness
• Dryness
161.
• Motor Deficit:
– Anterior division : sartorius and pectineus
– Posterior division : rectus femoris, vastus Lateralis,
Vastus medialis and vastus intermedius
– Difficuly in going up and down the stairs. Esp down the
stairs
– Difficulty in walking and knee buckling depending upon
severity of injury
• Reflex : Quadriceps jerk lost
162.
Gait
• Gait :Quadriceps gait
• Hand on knee gait
• Trunk leans in forward flexion to extend knee
at the beginning of the stance phase to lock
the knee when there is quadriceps muscle
weakness
• Use Hands to push knee into extension
Deformity
• Genu recurvatum:
-- Because quadriceps is paralysed the patient
will try to lock the knee into hyperextension to
get the CoG well in Front of knee joint to keep
it stable
• It thenpasses under the inguinal ligament
then into the thigh then divides into two
branches :
– Anterior branch : Anterior and lateral parts of the
thigh to knee.
– Posterior branch : Lateral and posterior surfaces
of the thigh from the level of the greater
trochanter to the middle of the thigh.
Signs and Symptoms
•Pain, Burning and parasthesia on lateral aspect of
thigh
• Worsen on prolonged standing, squatting and
walking
• Hyper sensitivity to heat
• Tenderness over ASIS
• No muscle weakness
• Differentiation from L3 radiculopathy and Femoral
Neuropathy is very important
• Muscular branch:
– Biceps femoris
– Semi tendinosus
– Semi membranosus
– Adductor magnus
• Tibial Nerve
• Common Peroneal
Nerve
• Articular Branch :
– Hip joint
177.
Causes
• Penetrating woundaround pelvis
• Hip arthroplasty
• Trauma
• Fracture of pelvis and femur
• Hip Joint dislocation
• IM injection in gluteal region
• Infection
• Sitting on hard surface
• Compression by Neoplasm, lymphoma or foetal head
• Popliteal cyst
Motor deficit
Weakness/ paralysisof following muscles :
• Biceps femoris
• Semimembranous
• Semi Tendinous
• Hamstring part of adductor magnus
Muscles of tibial nerve – Posterior compartment of
leg
Muscles of common peroneal nerve – Lateral and
anterior compartment of leg and foot
180.
• All themuscles below the knee are paralyzed,
and the weight of the foot causes it to assume
the plantar-flexed position, or Foot Drop.
• Clawing of toes with trophic
ulceration Due to lack of sensation over
foot
181.
Gait
• Steppage gait: (High stepping) gait
abnormality characterised by foot drop due to
loss of dorsiflexion
• The foot hangs with the toes pointing down,
causing the toes to scrape the ground
while walking, requires to lift the
leg higher than normal when walking.
Tarsal Tunnel Syndrome
•Tibial Nerve is entrapped in tarsal tunnel
• Formed by thick ligament flexor retinaculum
covering tarsal bones
194.
• Following structurestravel through the tarsal
tunnel :
– Tibial Nerve
– Tibialis posterior tendon
– Flexor hallucis longus tendon
– Flexor digitorum longus tendon
• In the tunnel, the nerve splits into :
– Medial plantar nerve
– Lateral plantar nerve
195.
Signs and Symptoms
•Sensory deficits :
– Parasthesia and numbness that extend to toes and
sole
• Heel sensation will be spared
as the calcaneal branch
arise proximal to tarsal
tunnel
196.
Pain :
– Perimalleolarpain,
– Increased with Weight bearing
– Pain increases at night
Motor Deficits :
• Involves weakness of the muscles that passes through
tarsal tunnel
• Weakness of intrinsic foot muscles
• Ankle jerk - Normal
Causes
• Compression ofthe nerve by tight plastar or splint
• Fracture of neck of fibula/ head of fibula
• Hansens disease
• Trauma to knee- damage to fibular collateral ligament
• Entrapped by fibrous arch as it winds around the
neck of fibula
• Prolonged immobilisation during which leg rest in ext
rotation
• Habitual crossing of legs
203.
Sensory Deficits
• Sensaorydeficit is seen over the cutaneous
distribution of following nerve
– Lateral sural cutaneous nerve
– Superficial peroneal nerve
– Deep peroneal nerve
204.
• Deep peronealnerve palsy
– Web space between great toe
and second toe
• Superficial peroneal nerve
palsy
– Anterior and lateral aspect of
leg
– Dorsum of foot and toe except
the web space area between
great toe and second toe
Deformity
• Equino VarusDeformity
– Due to over activity of posterior comartment of
muscles and invertors
– Plantarflexed and Inverted
– Foot Drop Deformity
207.
Gait
• Steppage gait
•Slapping gait (each step makes a slapping
noise)
• High stepping Gait
• Toes drag while walking
#3 Somatic : part of peripheral nerves that is associated with skeletal muscle and voluntary movement of body and reflexes
Spinal nerves
Cranial nerves
Autonomic : regulates the function of internal body organs such as stomach, intestine and heart
Regulated by hypothalamus
Two type : Sympathatic and parasympathatic
sympathatic from T1 to l1-2
Parasypathatic brainstem (CN 3,7,9,10) and sacral cord (s2-4)
#6 Each nerve is formed by many bundles or groups of nerve fibers. Each bundle of nerve fibers is called a fasciculus.
Coverings of Nerve
The whole nerve is covered by tubular sheath, which is formed by a areolar membrane. This sheath is called epineurium.
Each fasciculus is covered by perineurium
Each nerve fiber (axon) is covered by endoneurium
#8 Mononeuropathy is a type of neuropathy that only affects a single nerve.[5] Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection.
The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause mononeuropathy.
motor neuropathy may cause impaired balance and coordination or, most commonly, muscle weakness; sensory neuropathy may cause numbness to touch and vibration, reduced position sense causing poorer coordination and balance, reduced sensitivity to temperature change and pain, spontaneous tingling or burning pain, or skin allodynia (severe pain from normally nonpainful stimuli, such as light touch); and autonomic neuropathy may produce diverse symptoms, depending on the affected glands and organs, but common symptoms are poor bladder control, abnormal blood pressure or heart rate, and reduced ability to sweat normally.[1][2][3]
#9 Mononeurities multiplex: leprosy (common peroneal and ulnar nerve), hepatities
#42 Arcade of Frohse called the supinator arch,[1] is the most superior part of the superficial layer of the supinator muscle, and is a fibrous arch over the posterior interosseous nerve.
The arcade of Frohse is a site of radial nerve entrapment,[2] and is believed to play a role in causing progressive paralysis of the posterior interosseous nerve, both with and without injury. Sensory loss will not present because PIN is purely motor.
The arcade of Frohse was named after German anatomist, Fritz Frohse
#48 Wrist - 45 of palmar flexion due to overactivity of wrist flexors unopposed by extensors
Thumb – Palmar abduction and slight flexion due to unopposed action of short flexors and abductors
MP joints – 30 flexion die to ED paralysis and unopposed lumbricles
#67 Flexors :-- Deltoid, biceps
Abduction Deltoid
Lateral rotation Supraspinatus, infra spinatus and teres minor
Elbow flexors biceps, bracioradialis
Forearm supinators supinator
#73 Lumbricles flex the metacarpophalangeal joints while extending both interphalangeal joints of the digit on which it inserts. The lumbricals are used during an upstroke in writing.
Interrocei flex the metacarpophalangeal joints while extending both interphalangeal joints of the digit on which it inserts
#76 Enophthalmos is the posterior displacement of the eyeball within the orbit
Ptosis is a drooping or falling of the upper eyelid
Myosis excessive constriction of the pupil of the eye.
Anhidrosis is the inability to sweat normally.
#93 Hyperextension of MCP joint of ring and little finger 30 degrees due to over action of EDM and ED and lumbricle paralysis
Flexion of IP joint of little and ring finger lumbricle paralysis
#106 FPL and Flexor profundus of index finger do not work resulting in extension at DIP
#125 Paralysis of first two lumbricle and over activity of extensor digitorum