Chapter 18: Neurology

Neurologic Pathways Presenting Features

Assessment of Clinical Problems
Tarsal Tunnel Syndrome
Classification of Nerve Injuries
Neuromuscular Causes of Cavus Foot
Types of Nerve Surgery
 NEUROLOGY
It is not uncommon for a neurologic illness to affect the feet initially, thereby
making patients seek podiatric consultations first. This chapter will help you
understand disorders affecting the central and peripheral nervous systems
with emphasis on the lower extremity.
Neurological Pathways
1. Cerebral Cortex: Divided into frontal, parietal, temporal, and occipital
lobes
2. Descending pathways: Divided into corticospinal (pyramidal) and
extrapyramidal
3. Thalamus and hypothalamus
4. Cerebellum
5. Brain Stem
6. Spinal Cord
7. Nerve Roots
8. Peripheral Nerves
9. Neuromuscular Junction and Muscle
Presenting Features
1. Presenting Problems: Can include pain, numbness, tingling, weakness,
unsteadiness, and involuntary movements. Neurologic disorders should
always be suspected in patients with:
a. A foot deformity (i.e. pes cavus)
b. Leg or foot weakness
c. Difficulty in walking
d. Pain or paresthesias in the legs

2. The Physical Examination:

i History: with children get a developmental history which includes questions
such as:
When did the child get head and neck control? (normal at 2 months) When
was the child sitting independently? (normal at 6 months) When did the child
start to walk? (normal by 9-15 months) Low or normal birth weight?
Any problems at birth?
ii. Motor System (Muscle tone/strength): Specific examination of
muscles includes observation, palpation and strength testing. For muscle
tone look for atrophy (loss of muscle bulk), fasciculations (brief, fine irregular
twitches), and myotonia (decreased relaxation of muscle following a
sustained contraction). Sometimes muscle hypertrophy is abnormal To test
muscle strength, the specific muscle must
Abnormalities of be tested against resistance. It is
Movement
graded from zero (no
Fasciculations- movement),
visable twitching1 movements
(trace movement),
of muscle2 (movement
bundles. with
the aid of resistance), 3 (movement against gravity),
Tremors- involuntary rhythmic tremulous movements. 4 (movement against
resistance supplied
Tics- repetitive by the examiner),
twitching of muscles and
often5 in
(normal strength).
the face and upper trunk.
Chorea- involuntary movements of the face and extremities that are rapid,
jerky, and unpredictable. They occur at rest or during any purposeful
iii. Stance and gait: There are specific gait patterns associated with specific
movement.
diseases.
Athetosis- involuntary movements of the face, extremities that are slower,
more twisting and writhing than chorea. They occur at rest or during any
purposeful movement. Abnormal Gait Patterns
Spastic gait- Manifested
Myoclonus- involuntary,by internal
sudden androtation and adductionjerks;
rapid unpredictable of the entire
faster than
limb, with hip/knee/ankle in marked flexion. Seen with cerebral palsy,
chorea.
familial spastic
Asterixis- diplegia, and
involuntary paraplegia, and
brief loss of hemiplegia.
muscle tone in the outstretched
iv. Deep tendon reflexes (DTR's): Assesses the afferent nerve, the synaptic
connections within the spinal cord, the motor nerves, and the descending
motor pathways. It is important to note right and left asymmetries and the
degree of activity, measured from zero to five (zero= no activity, 1=
hypotonia, 2= normal, 3= exaggerated response, 4= multiple contractions,
5= sustained contractions). Hyperreflexia indicates a lesion in the
corticospinal thalamic tracts. Hyporeflexia indicates a lesion in the lower
motor neurons or an intrinsic muscle weakness. The DTR's tested are the:
 Biceps/brachioradialis (C5 and C6)
 Triceps (C7 and C8)
 Patellar (L2, L3, and L4)
 Achilles (S1).
v. The plantar response, or the Babinski reflex is the response to striking
the sole (extention of the great toe), and when present represents an upper
motor neuron lesion of the pyramidal tract.
vi. Rossolimo Sign (reflex): involves flicking the plantar aspects of the toes,
distally. Flexion response occurs in pyramidal tract disease. This same
response may accompany a Babinski reflex.
vi. Rhomberg's sign: assesses balance (cerebellar function) and if abnormal
the patient will not be able to stand with feet together and eyes closed.
Proprioceptive control is lost.
vii. Sensory system testing:
*Pain and temperature (lateral spinothalamic tract) testing is done with a pin
and an ice cube placed on various dermatomes (See Figure 1).
*Vibratory testing (posterior columns) is done with a tuning fork (128
cycles/sec) over a bony prominence or joint.
*Joint position (posterior columns) is performed by moving the first m.p. joint
into either extension or flexion with the patient's eyes closed.
*Light touch (anterior spinothalamic tracts) is performed using a nylon
filament over various dermatomes.

Lower Extremity Dermatomes (Figure 1)

L1 and L2 ennervate the anterior thigh. L4 ennervates the lateral thigh, then
crosses the patella to innervate the medial anterior calf and foot (medial side
of the hallux). L5 ennervates the lateral anterior leg and central aspect of the
foot plantarly and dorsally. S1 ennervates the posterior lateral thigh, leg, and
lateral border of the foot plantarly and dorsally. S2 ennervates the posterior
medial thigh and leg , and the medial-posterior portion of the heel
3. Neurologic Diagnostic Procedures:
a. Lumbar Puncture: Tapping of the lumbar subarachnoid space between L3
and L4 provides important information about intercranial pressure and allows
a diagnostic analysis of the CSF (the CSF count is abnormal if more than 5
cells are present).
b. CT Scan: Rapid noninvasive imaging for the brain, spinal cord and their
bony enclosures.
c. MRI: Provides extraordinary resolution in imaging of the neural structures
without any known risk to the patient. Helpful in identifying brainstem lesions
and other abnormalities. MRI cannot be used to examine patients with
pacemakers, or patients who are pregnant, who have metal prostheses, and
who are dependent on respirators.
d. Electroencephalography (EEG): Voltage vs. time recordings of electrical
currents in the brain. Good for detecting epilepsy and metabolic and
structural encephalopathies.
e. Electromyography (EMG) and Nerve Conduction Velocities: When
weakness is clinically difficult to attribute to either nerve, muscle, or
neuromuscular junction, electrical studies can establish topographically
which nerves and muscles are affected. In EMG, the recording of electrical
properties of muscle is displayed on an oscilloscope during needle insertion.
Denervated muscle is recognized by fibrillations and fasciculations on the
screen.
In nerve conduction studies the time for an impulse to travel along the nerve
is termed the conduction velocity. If there is an increase in this conduction
velocity, there is damage to the particular nerve involved.

Assessment of Clinical Problems

Finding the site of the lesion is extremely useful in diagnosing the cause.
Once a possible location(s) have been identified, one can review a checklist
of disease processes, such as traumatic, vascular, infectious, metabolic,
immunologic, neoplastic, and inherited problems that may be responsible.

1. Seizure Disorders: A seizure is a sudden disturbance of cerebral function

due to a paroxysmal neuronal discharge in the brain.
a. Epilepsy: implies a chronic condition of recurring seizures. Subdivided into
two types
i. Generalized: Grand mal and petite mal
ii. Partial
b. Status epilepticus: recurring seizures, one following another without full
recovery from the preceding seizure.
c. Etiology: may be metabolic (hypoglycemia), hypocalcemia,
phenylketonuria, drug toxicity, drug withdrawal, or a focal abnormality of the
brain as with trauma or stroke.
d. Time sequence:
1. Prodrome: time preceding the seizure that the patient does not feel well.
ii. Aura: A symptom or sign signaling the beginning of the seizure (visual,
aural or other sensory change)
iii. Postictal period: The period after the seizure while the patient returns to
normal.
e. Management: During the seizure administer first aid, preventing the
patient from biting his tongue and keeping the airway open. If the seizure
does not stop within 5 minutes, emergency medical care should be
instituted (IV's w/ D5W/ diazepam/phenytoin PRN). Control should be
achieved with as few anticonvulsants as possible.

2. Cerebrovascular Disorders: Cerebral vascular problems usually appear

dramatically with sudden onset and often result in permanent loss of
neurologic function. There are two basic types
i. Intracranial hemorrhage: (types) hypertensive, ruptured aneurysm,
arteriovenous malformations, traumatic, secondary to brain tumor, and
secondary to hematologic disorders
ii. Ischemic stroke: (types) thrombotic and cerebral embolism. The prognosis
after stroke is usually dependent upon the blood vessel involved and its
perfusion territory.

3. Peripheral Neuropathies: In terms of subjective complaints, peripheral

neuropathies are the most common causes of foot and toe dysesthesias
(burning foot syndrome). In addition patients complain of extremity
weakness, muscle atrophy, or both. In addition to motor function, peripheral
nerves are responsible for sensory and autonomic function.
a. There are three general forms:
i. Segmental demyelination: refers to destruction of the myelin segments
with survival of the myelin segments with survival of axons until late in the
course of the illness.
ii. Axonal degeneration: destruction of the axon.
iii. Wallerian degeneration: occurs when the nerve is injured or severed at a
focal point, and the distal segment breaks down and is reabsorbed. b.
Classification of Neuropathies: Remember the mnemonic "Dang Thrapist"
D-Diabetic
A-Alcoholic
N-Nutritional
G-Guillain-Barre

T-Toxic
H-Hereditary
R-Recurrent
A-Amyloidosis
P-Porphyria
I-Infectious
S-Systemic
T-Tumor

i. Diabetic neuropathy: 2/3 of all diabetics show evidence of peripheral

nerve dysfunction (clinically or subclinically), which progresses in the face of
poor diabetic control. Patients can present with a mononeuropathy,
polyneuropathy and can have sensory impairment, or both. At the earliest
stage the patient experiences pain, usually worse at night.
 Symmetric Distal Polyneuropathy: loss of sensation (predominantly)
and motor weakness in a stocking-glove configuration, that occurs
bilaterally. The distal portion of the longest nerves are affected first and
the feet affected before the hands. Later muscular atrophy can occur with
intrinsic muscle wasting.
 Mononeuropathies: both cranial and spinal
mononeuropathies can occur which includes femoral
mononeuropathy (characterized by pain, motor and sensory loss,
and absent knee jerk), peroneal mononeuropathy (characterized
by a sudden foot drop), and tarsal/carpal tunnel syndrome.
  Autonomic Neuropathies: disturbances may be seen in the
cardiovascular system, bowel, bladder, and sexual function.
Symptoms include, diarrhea, incontinence, impotence,

NOTE* The diagnosis of orthostatic hypotension is made by demonstrating a

decrease of approximately 25 mm Hg in systolic or 10 mm Hg in diastolic
blood pressure after 2 minutes of upright posture without a compensatory
increase in heart rate (treated with fluorocortisone or ephedrine).
decreased sweating, and orthostatic hypotension

 Neuroarthropathy: foot ulcers occur secondary to

neuropathy, microangiopathy, large vessel atherosclerosis, or
combinations of these factors. The Charcot joint seen in the
lesser tarsus or tarso-metataral area has an unknown etiology. It
is unfortunately seen after revascularization procedures of the
extremities. The most common bony deformities are the medial
convexity, plantar deformity, dorsal midfoot deformity, and
plantarflexed metatarsals. A differential diagnosis includes tabes
dorsalis, osteomyelitis, leprous neuropathy, and peripheral nerve
injuries. Initial treatment for active arthropathy includes 1-2
weeks of bed rest, nonsteroidal anti inflammatory drugs (?), the
use of crutches, and a nonweight-bearing cast or splint until the
soft tissue swelling and erythema subsides. Gradual weight-
bearing can be resumed once radiographic evidence of an arrest
is visualized. Patients with fractures of the lower 1 /3 of the tibia
are prone to develop ankle arthropathy.

Note* Treatment of diabetic neuropathy: For burning pain and

dysesthesia (combination of Elavil h.s../ Prolixin t.i.d or Valium t.i.d, 4.
Axain topically), lightning-like pain (Tegretol or Dilantin),
carpal/tarsal tunnel syndrome (splints/orthotics), itching
(diphenhydramine), and diarrhea (codeine).
Infectious Diseases:
a. Meningitis: Causes symptoms such as fever, neck stiffness, disorders of
consciousness, and seizures. 80-90% of cases of meningitis are caused by
one of three organisms, H. influenzae, N. meningitis, and D. pneumoniae.
Diagnosis is confirmed by lumbar puncture (CSF is cloudy, pressure
elevated, WBC > 1000/mm3, and positive CBS). Treatment is usually penicillin
G for N. meningitis and D. pneumoniae, and ampicillin for H. influenzae.
Positive Brudzinski and Kernig signs clinically.
b. Tuberculosis: Can result in multiple cranial nerve palsies.
c. Neurosyphilis: Occurs in 25% of patients with syphilis. Diagnosis is by FTA-
ABS test. Penicillin is the treatment of choice.
d. Fungal Infections: Cryptococcus neoformans (most common organism)
which can produce a subacute meningitis.
e. Acute Viral Infections: Poliomyelitis, starts as a flu-like illness, followed by
meningitis, and then flaccid paralysis of the limbs and trunk. Herpes zoster
(shingles) has a dermatomal distribution of vesicles and demonstrates
segmental weakness and pain, sometimes for years.

5. Movement Disorders: Are generally extrapyramidal

a. Parkinson's Disease: Characterized by hypokinesia, tremor, rigidity and
disorders of gait and balance. On examination there is a "pill rolling" tremor
of the hands. The drugs used to treat this disease either act by decreasing
cholinergic activity (trihexyphenidyl) or by increasing dopaminergic activity
(L-dopa usually combined with carbidopa).

NOTE* Neuroleptics such as chlorpromazine and haloperidol may produce a

Parkinson-like syndrome. The syndrome stops with withdrawal of the drug.

b. Chorea: A variety of neurologic diseases are associated with chorea such

as, childhood rheumatic fever (Sydenham's chorea), systemic disorders
hyperthyroidism, hypoparathyroidism, and SLE), drugs (oral contraceptives),
pregnancy, and hereditary disorders (Huntington's chorea).
i. Huntington's chorea: an inherited disease than begins to manifest itself
between the ages of 30-40 with. progression to death within 20 years.
Manifested by the combination of chorea and dementia.
c. Dystonia: Is a movement disorder likely to be seen first by podiatrists,
presenting with a slow sustained contraction of muscle groups, resulting in
abnormal postures of the trunk and extremities, and of more rapid, twisting
movements.
i. Dystonia musculorum deformans: a primary hereditary disorder, presents
usually with an equinovarus foot.
d. Tremor: Essential tremor is a benign disorder that frequently
accompanies other neurologic conditions.

6. Tumors: Symptoms depend upon the location of the lesion.

7. Demyelinating and Degenerative Diseases:

a. Multiple Sclerosis: characterized by a remitting and exacerbating course of
multiple neurologic symptoms, including blindness, diplopia, ataxia,
nystagmus, spastic weakness, dysesthesia, and difficulty with bladder and
bowel function. Electroimmunodiffusion reveals migration of gamma G
immunoglobulin on discrete bands. There is no specific treatment.
Corticosteroids can shorten the span of an acute attack. Speech is often
explosive.

b. Amyotrophic Lateral Sclerosis: a group of diseases characterized by

progressive weakness, atrophy, spasticity, hyperreflexia, and fasciculations
occurring in a widespread distribution. There is a wide variation in
symptoms, with some patients showing more atrophy and some showing
more spasticity. Some patients have only cranial nerve involvement. There is
no specific therapy. There is an inherited pattern.
c. Friedreich's Ataxia: An autosomal-recessive disorder with cerebellar
degeneration. Characteristics include gait changes, decreased position and
vibratory sense in the legs, absent DTR's, nystagmus, kyphoscoliosis, pes
cavus, and hypertrophic cardiomyopathy.

NOTE* Pes cavus is the major foot type associated with neurologic illness.
Patients with pes cavus can be divided into four groups:
1. Patients with hereditofamilial disease: Friedreich's ataxia and Charcot-
MarieTooth disease.
2. Those who have isolated pes cavus but whose family members have one
of the aforementioned hereditofamilial neurologic diseases.
3. Those with isolated, or idiopathic, familial pes cavus with no family history
of hereditofamilial neurologic disease.
4. Those with familial pes cavus and lymphedema (very rare syndrome).

8. Cerebellar Disorders: These patients present with an imbalance and a

difficulty with walking.
a. Friedreich's ataxia
b. Dandy-Walker deformity
c. Arnold-Chiari malformation
d. Infections

9. Disorders of Muscles and Nerves: Myopathies are disorders of nerves

characterized by progressive weakness. Laboratory tests for diagnosis
include measurement of serum muscle enzymes, creatine phosphokinase
(CPK), electromyography, nerve conduction studies, and muscle biopsy. a.
Muscular Dystrophies:
i. Duchenne's muscular dystrophy: An X-linked recessive disorder with a
frequent mutation rate, which appears with a slowly progressive proximal
weakness beginning in the lower extremities and later involving the upper
extremities. It is often associated with early toe walking and causes a
waddling gait. The gait changes include decreasing cadences, increasing
anterior pelvic tilt, increased hip flexion in swing, decreasing ankle
dorsiflexion, and increased shoulder sway. These patients have a progressive
muscle atrophy and weakness (there is often pseudohypertrophy of the calf
muscles). The serum CPK is markedly elevated in these patients early in the
disease and a muscle biopsy establishes a definitive diagnosis.
Pathognomonic for this disease is a positive Gower's sign, where the
affected child rises from a sitting position on the floor by climbing on his own
legs.
ii. Becker's muscular dystrophy: Is a more benign form of X-linked muscular
dystrophy clinically similar to Duchenne's MD, and is manifested by
progressive proximal limb weakness.
iii. Facioscapulohumeral dystrophy (Landouzy-Dejerine): A variant of
muscular dystrophy with a swing phase drop foot and compensatory
increase in hip and knee flexion. This disease gives a "Popeye the sailor"
forearm appearance.
iv. Limb-girdle muscular dystrophy: Mostly autosomal recessive disorders
characterized by progressive proximal weakness.
v. Myotonic muscular dystrophy: An autosomal dominant disorder with
symptoms that involve a combination of weakness and myotonia (myotonia
is a delayed relaxation of muscle following contraction and is associated with
abnormal EMG discharges).
vi. Spinal muscular atrophy: An autosomal recessive condition with
progressive degeneration of the anterior horn cells. There are three types-
 Group I: Werdnig-Hoffman disease (most severe, diagnosed in infancy
 Group II: intermediate form
 Group III: Kugelberg-Welander disease (mildest form). Also called
WohlfartKugelberg-Welender disease
b. Acquired Myopathies: The following can cause a slow progressive and
prominent muscle weakness:
i. Endocrine disorders: Hypo/hyperthyroidism
ii. Drugs: Corticosteroids, antibiotics, and alcohol.
iii. Collagen vascular diseases: Polymyositis, dermatomyositis, scleroderma,
RA, and SLE.

10. Perinatal or Gestational CNS Damage Disorders:

a. Cerebral Palsy: A nonprogressive brain lesion usually due to a perinatal
insult (hypoxia) resulting in a pyramidal tract lesion. There are various types
i. Spastic
ii. Athetotic
iii. Ataxic
iv. Rigid
b. Familial Spastic Diplegia: Has a strong family history of lower limb
spasticity, no perinatal insult, and is progressive.

Note* The type of spasticity is based on the anatomical areas involved:

Diplegia- all four extremities, primarily lowers
Paraplegia- lower extremities only
Quadriplegia- all four limbs equally involved
Hemiplegia- one side of the body (upper and lower extremities)
11. Disorders of the Spinal Cord and Nerve Roots:
a. Spinal Cord Disorders: Localizing the level of a focal lesion of the spinal
cord is easier if one remembers the Brown-Sequard syndrome.

NOTE* The Brown Sequard syndrome occurs after hemisection of the spinal
cord, which results in an ipsilateral spastic paralysis and loss of postural
sense, and on the opposite side a loss of pain and temperature sensations

i. Spinal cord dysfunction may be acute or chronic

 Acute due to: trauma, compression, inflammation, infarction, vascular
malformation, and hemorrhage.
 Chronic due to: Syringomyelia
b. Radiculopathies:
i. A fifth lumbar nerve radiculopathy in addition to back pain, often causes
radiating pain down the lateral aspect of the leg with numbness or
paresthesias of the lateral calf and the dorsum of the foot.
ii. A first sacral nerve radiculopathy characteristically causes radiating pain
down the posterior leg with sensory changes on the lateral and plantar
aspects of the foot. (absent achilles reflex).

12. Pain Syndromes:

a. Reflex Sympathetic Dystrophy Syndrome: Originally termed
"causalgia". Other variants include Sudek's atrophy and post-traumatic reflex
dystrophy. This syndrome is characterized by disproportionate pain in
intensity, duration, location, often from minor or unapparent trauma to an
extremity. Clinical diagnosis is difficult due to the vague subjective data and
subtle objective signs and symptoms. Early diagnosis is important because
early treatment gives the best results. The sympathetic nervous system is
always involved and is overactive. Symptoms occur distal to the trauma site.
i. Manifestations: (signs and symptoms)
 Pain- most prominent characteristic feature
Quality of pain: burning, aching or throbbing
Severity of pain: mild to excruciating, usually continuous Paroxysmal
aggravations: emotional stress, movement, and touch Localized first then
spreads
Not limited to a dermatome or peripheral nerve distribution

 Vasomotor disturbance
Vasodilation: warm skin, dry skin, and hypohidrosis
Vasoconstriction: cyanosis, cool skin, edema of the part, and hyperhidrosis

 Delayed return to function

 Trophic changes- are late changes (atrophy, and
osteoporosis)
Involves the skin, appendages, muscle, bone and joints (RSDS arthropathy)

NOTE* The striking feature is that while all signs and symptoms are usually
resent, a patient often manifests one out of proportion to all the others.

i. There are three grades based upon mode of onset, Intensity, and
preponderance of symptoms
 Grade 1 (SEVERE): rapid onset, severe burning/knifelike pain, severe
vasomotor disturbance, no mobility, atrophy early.
 Grade 2 (MODERATE): slow onset, dull/throbbing diffuse pain,
aggravated by walking (and relieved with rest and immobilization),
edema, atrophy, and osteoporosis.
 Grade 3 (MILD): most common type, the border zone between normal
response and exaggerated response so is often overlooked, usually seen
after surgical procedures
ii. There are three stages of the disease divided as per the time frame -
 Stage 1 (days to weeks): Characterized by
Pain
Hyperesthesia
Hyperalgesia
Localized edema
Muscle spasm and tenderness
Vasomotor disease
No x-ray changes
Trophic changes of hair, nails and skin begin
In mild cases (GRADE 3) this stage lasts a few weeks and then subsides
spontaneously
In severe cases (GRADE 1) symptoms become progressively worse

 Stage 2 (3-6 months):

Gradual decrease of pain
Spread of edema, soft to brawny
Hair scant, nails brittle/cracked and heavily grooved Muscle wasting
X-rays reveal spotty osteoporosis (early), and diffuse osteoporosis (late)

 Stage 3 (greater than 6 months):

Marked trophic changes which eventually become irreversible
Skin is smooth/glassy/drawn/pale or cyanotic with a loss of subcutaneous fat
Nail changes
Digits are thin and pointed
Muscle atrophy, especially interossei
Limited ROM of joints
Tendon contractions
Subluxations
Bone atrophy is diffuse and marked

NOTE* The goal is to restore functional and anatomical integrity ASAP and
break the sympathetic response.

NOTE* According to Van Wyngarden and Bleyart in the Journal of Foot

Surgery, Volume 31- Number 1, their diagnostic test of choice is a iii.
sympathetic and sensory epidural nerve block. If there is a response,
then their treatment of choice is frequent sympathetic blocks
(bupivacaine+methylprednisolone), in combination with physical
therapy, and with oral clonazepam throughout the treatment period.
Treatment:
 Neurology consult
 Psychiatric consult
 Anesthesiology consult
 Sympathectomy (GRADE 1) -Local blocks (GRADE 2 and 3)
 Physical therapy
 Systemic steroids (?)
 Beta blockers (?)
 TENS (?)
 Axain + topical lidocaine (?)
 Procardia (?)
 Analgesics (?)
 Medication to reduce patients' stress

Innervation of the Lower Extremity

Lower extremity innervation is supplied by branches of the sciatic nerve.
1. The sciatic nerve is the interconnection of spinal nerves from L1, L2, L3,
L4, L5, S1, S2, and S3 (S2, S3, and S4 make up the pudendal nerve which is
localized to the pelvis), passes through the greater sciatic notch, between the
greater trochanter of the femur and ischial tuberosity, and rests on the
posterior surface of the adductor magnus. In the lower third of the thigh, the
sciatic nerve splits into the tibial nerve and common peroneal nerve.
2. The common peroneal splits into the deep peroneal, superficial
peroneal and gives off a branch called the lateral sural cutaneous in the
popliteal fossa.
3. The lateral sural cutaneous meets with a branch of the tibial nerve
(medial sural cutaneous) to form the sural nerve.
4. The deep peroneal nerve (anterior tibial) descends with the vessels
anterior to the ankle joint, where it divides into medial and lateral branches.
5. The medial branch of the deep peroneal nerve follows the course of
the dorsalis pedis artery and stays lateral to it. This nerve splits in the first
interspace where it supplies the adjacent sides of toes 1 and 2.
6. The lateral branch of the deep peroneal nerve passes across the
lateral tarsal area where it supplies the extensor digitorum brevis, then splits
into three interosseous branches that supply the 2nd, 3rd, and 4th
interosseous muscle.
7. The superficial peroneal nerve supplies the peroneal muscles, comes
down to the ankle lying between the peroneii and the EDL. It divides into the
medial and intermediate (lateral branch) dorsal cutaneous nerves.
8. The medial dorsal cutaneous nerve divides in front of the ankle into
two dorsal digital nerves, the medial and lateral dorsal digital nerves.
The medial dorsal digital nerve supplies the medial side of the hallux and
the lateral dorsal digital branch supplies the adjacent sides of the 2nd
and 3rd toes.
9. The intermediate dorsal cutaneous nerve, the smaller branch of the
superficial nerve, divides into two dorsal digital branches over the
dorsolateral aspect of the foot. The more medial branch supplies the adjacent
sides of the 3rd and 4th toes. The lateral branch joins with the terminal
branch of the sural nerve to form the lateral dorsal cutaneous nerve.
10. The tibial nerve descends at the back of the thigh to the popliteal fossa,
where it passes with the popliteal artery beneath the soleus muscle,
and descends to the back of the leg with the posterior tibial vessels. It is
located between the FDL medially and the FHL laterally. It enters the lacinate
ligament (3rd compartment) and divides into medial and lateral plantar
nerves to innervate the sole of the foot.
11. The medial plantar nerve is the larger branch and its branches. It gives
off a cutaneous branch to the medial side of the hallux, adjacent sides of the
hallux and 2nd toe, the adjacent sides of the 2nd and 3rd toes, and the
adjacent sides of the 3rd and 4th toes. The 3rd and 4th common digital
nerves communicate in the third interspace and is the site for Morton's
neuromas. The muscular attachments are as per Fig. 4. 12. The lateral
plantar nerve supplies the medial and lateral side of the 5th toe and the
lateral side of the 4th toe. The muscular attachments are as per Fig. 4.
Tarsal Tunnel Syndrome
Is an entrapment or compression neuropathy of the posterior tibial nerve or
one of its three branches, the medial and lateral plantar nerves and/or medial
calcaneal nerve.
1. Anatomy: Nerve entrapment occurs either in the porta pedis or
lacinate ligament
a. The flexor retinaculum (lacinate ligament) extends from the medial
malleolus to the medial process of the calcaneal tuberosity and the plantar
aponeurosis. The deep fibrous septa form four compartments, and converts
bony grooves into canals from anterior-medial to posterior lateral: #1
contains tibialis posterior tendon (most superficial), #2 FDL tendon, #3
posterior tibial nerve artery and vein, and #4 FHL tendon. These
compartments are unyielding spaces.
b. The porta pedis is a canal created by the abductor hallucis muscle belly
through which the medial and lateral plantar nerves pass. c. Division of the
posterior tibial nerve into its 3 terminal branches may occur proximal to
the lacinate ligament, which is most common; within the lacinate ligament,
as described in most texts; or distal to the lacinate ligament, which is rare.
d. The medial calcaneal nerve is entirely sensory, and innervates the
medial and plantar aspect of the heel. It may arise from either the posterior
tibial or lateral plantar nerve.
e. The medial plantar nerve gives sensory innervation to the plantar
aspect of the hallux, second and third toes, medial half of the fourth toe, and
the medial half of the plantar aspect of the foot. It gives motor innervation to
the abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the
first lumbrical.
f. The lateral plantar nerve gives sensory innervation to the plantar lateral
half of the fourth toe, plantar aspect of the fifth toe, and plantar lateral
aspect of the foot. Initially it sends motor fibers to the quadratus plantae and
abductor digiti quinti before dividing in a superficial and deep branch.
Superficial branch supplies motor innervation to the flexor digiti quinti brevis
and the dorsal and plantar interossei of the fourth intermetatarsal space. The
deep branch supplies the remaining intrinsic muscles of the foot.

2. Pathology: Compression of the nerve initially causes only sensory

involvement with possibly partial involvement of motor fibers. Continuation of
the irritation, ischemia, and compression may lead to secondary
hyperactivity of the autonomic nervous system, manifested by coldness and
numbness from the altered sympathetic activity. Eventual structural changes
in the nerve result in the development of muscle wasting, paresis, and
objective sensory loss.

NOTE* Reflexes are unaffected

3. Etiology: In the majority of cases no etiology can be found at the time of

surgical decompression.
a. Dilated posterior tibial veins: can also cause severe night discomfort.
b. Trauma: Fracture, dislocation, sprain, post-traumatic edema and fibrosis. c.
Systemic disease: Gouty arthritis with urate deposits, rheumatoid arthritis,
diabetes mellitus, and myxedema.
d. Space occupying lesions: Ganglions, neurofibromas, neurilemmomas, and
synovial cysts.
e. Hypertrophy of abductor hallucis muscle belly.
f. Biomechanical: excessive pronation

4. Clinical Symptoms: Symptoms can be either distal to the metatarsal

area, or the medial and lateral heel depending on the branch involved. a.
Early:
i. Intermittent burning pain, numbness and paresthesias over the medial side
of the heel, the toes, and the plantar aspect of the foot. b. Late:
i. A paresis that will develop into paralysis of the pedal intrinsic muscles.
ii. Proximal radiations of pain may develop in the posterior calf.
iii. Pain that is proportional to the amount of activity during the day.
iv. May develop some sensory loss

5. Diagnosis: Not always easy, as the signs are not always definitive a.
History of paresthesias
b. History of trauma
c. History of systemic disease
d. Hoffman-Tinel's sign: A tingling in region of the distribution of the involved
nerve with light percussion, results in paresthesias distal to the site of
percussion.
e. Valleix Phenomena: A nerve trunk tenderness above and below the point
of compression, with paresthesias proximal and distal to the point of
percussion.
f. Turk's test: Application of a venous tourniquet to the lower extremity will
elicit positive symptoms on the affected side, by producing a venous
occlusion.
g. Forced eversion of the foot.
h. Positive radiographic evidence of previous injury
i. Positive lab studies for any specific disease
j. EMG's and nerve conduction studies are only useful for late stage disease.

Note* EMG may show fibrillation potentials which indicate denervation of

muscle. Nerve conduction studies may reveal an increased distal latency.
Placement of nerve conduction study surface electrodes are as follows:
1. Proximal stimulation point: distal aspect of popliteal fossa
2. Distal stimulation point: behind the medial malleolus
3. Recording electrode (for conduction of the medial plantar nerve) through
the abductor hallucis ms. belly.
4. Recording electrode (for the lateral plantar nerve) through the abductor
digiti quinti muscle belly.

6. Treatment: Conservative
a. Local blocks: Posterior tibial nerve blocks with steroids
b. Unna boot: can be combined with nerve blocks
c. Support hose: for varicosities
d. Functional orthoses

7. Treatment: Surgical Decompression (positive EMG's and nerve

conduction studies mandate surgical decompression). Involves the complete
exploration of the tarsal tunnel with release of the flexor retinaculum and its
fibrous bands, and resection and ligation of any dilated veins in the area.
The surgical technique is as follows:
a. Without a tourniquet, a curvilinear incision is made posterior and inferior to
the medial malleolus by 1 cm.
b. The subcutaneous tissue is incised and the superficial vessels are ligated
as necessary.
c. The neurovascular structures superior to the retinaculum are identified,
preserved, and retracted (especially the medial calcaneal branch).
d. The flexor retinaculum is incised and the posterior tibial nerve or its
terminal branches are identified and mobilized.
e. The nerve(s) is retracted with a penrose drain.
f. The nerve(s) is followed proximally, incising the flexor retinaculum as you
go.
g. The nerve(s) is followed distally to the point where the medial and lateral
plantar nerves pass through the fibrous canals superior to the abductor
hallucis ms. belly.
h. The abductor hallucis ms. is examined for any abnormality, and any
hypertrophy is excised.
i. If there are any posterior tibial vein varicosities, they should be ligated.
j. The retinaculum is not reapproximated and no deep closure is done.
k. The superficial fascia is reapproximated and the skin reapproximated
l. Sterile compression dressing and a non-weight-bearing BK cast applied for
3 weeks.

8. Complications:
a. Recurrence: due to fibrosis
b. Severing the PT artery : if done then tie off and prepare patient for
microvascular repair later.
c. Severing a nerve
d. Tenosynovitis
e. Hematoma
f. Wound dehiscence

Classification of Nerve Injuries

1. Seddon and Sunderland classified nerve injuries:
a. Seddon's classification
i. Neuropraxia: (first degree injuries) a conduction disturbance with complete
recovery
ii. Axonotmesis: (second and third degree injuries) an incomplete division of
supportive tissues of the nerve
iii. Neurotmesis: (fourth and fifth degree injuries) a complete division of a
nerve
b. Sunderland's classification
i. First degree: only local changes to the myelin
ii. Second degree: injury to the axons that is incomplete
iii. Third degree: leads to more severe axonal injury with fibrosis
iv. Fourth degree: severe neuronal injury with the axons in complete
disarray (no complete neuronal separation)
v. Fifth degree: complete transection of the nerve (dismal prognosis)

Neuromuscular Causes of the Cavus Foot

The cavus foot is classified according to the level of the CNS that is affected
1. Cerebral Cortex: Hysteria
2. Pyramidal and Extrapyramidal: C.P., athetosis, dystonia musculorum
deformans
3. Spinocerebellar Tracts: Friedreich's ataxia, Roussy-Levy syndrome
4. Spinal Cord Level: Polio, myelomeningocele, diastematomyelia, cord
tumor
5. Peripheral Nerve or Spinal Nerve Root: C.M.T., polyneuritis-Sotas
6. Muscle: Muscular dystrophy

Types of Nerve Surgery

1. Neurolysis: Frees the nerve from adhesions or scar tissue that obstruct
the growth of regenerating axons or block the conduction of nerve impulses.
Immature nerve fibers may suffer temporary conduction block with
neurolysis. If the entrapped nerve and branches are found in dense scar
tissue, the nerve may be rerouted to a more favorable bed which minimizes
the risk of subsequent compression
a. It is indicated in a complicated first degree injury in which scarring or
adhesions have interrupted conduction
b. In a second degree injury, the nerve is intact and normal in appearance,
but the interfunicular tissue is scarred. Internal neurolysis may be necessary
to split the, sheath and release the bundles from the interfunicular scar tissue
(difficult)

2. Neurorrhaphy: Nerve repair is justified when conservative care fails and

nerve function deteriorates. When it is determined that a traumatized
nerve is partially or completely severed neurorrhaphy can be attempted.
Neurons retain for several years the capacity to regenerate a new axon. The
regenerative process of the nerve remains intact, and the new axons enter
the endoneurial tubes in the stump distal to the trauma. The earlier the
reinnervation, the better the prognosis
a. If a small nerve is partially or virtually severed, repair of the severed
section by partial sutures or resect the damaged segment, mobilize the nerve
proximally and distally to gain the added length, and perform an end to end
anastomosis
b. In a large nerve, if one half is disrupted, partial neurorrhaphy is advisable,
and if a neuroma is encountered, resect back to normal tissue and do an end-
to-end anastomosis
c. Whenever a nerve is transected, it retracts approximately 4% of its normal
length between excision points

3. Neuroma (Morton's):
a. Definition: A neuroma represents hyperplasia of Schwann cells, axonal
elements and fibroblasts in an area where proximal elements cannot relocate
to their distal pathways
b. Histopathology: The term neuroma refers only to nodules that are formed
by hyperplasia of axons and Schwann cells. This process is characterized by
endoneural and neural edema (early stages); perineural, epineural, and
endoneural fibrosis (late stages); and eventually demyelination. It is a
reactive lesion, not a tumor. The term 'Morton's Neuroma' refers to a lesion in
the third intermetatarsal space only.

NOTE* Endoneural edema, fibrosis and demyelination are diagnostic for

c. Anatomy: Morton's neuroma and other types
lies in the 3rd
intermetatarsal space, plantar to the transverse intermetatarsal ligament,
where the communicating branch of the lateral plantar nerve joins the
communicating branch of the medial plantar nerve
d. Signs and symptoms: Burning, radiating, lacinating pain and paresthesia.
Can cause calf and heel pain. Palpation can produce pain upon squeezing the
intermetatarsal space, and often a "click" is felt upon lateral pressure
(Mulder's sign)
e. Differential Diagnosis: Metatarsal stress fractures, RA, osteochondritis

The above diagrams A,B, and C show the technique of partial neurorrhaphy.
Diagram D shows the exposed nerve with orientation sutures, the ends
mobilized, bulbous distal segments removed (E) and epineural sutures
inserted circumfrentially (G,H,I) to repair the nerve

dissecans (Freiberg's), localized vasculitis, ischemia, tarsal tunnel, nerve root

compression syndromes, peripheral neuropathy (especially diabetic
neuropathy), and intermetatarsal bursitis
f. Etiology: Compression trauma, and stretching of the interdigital nerve, with
micro-tears of axons
g. Treatment:
i. Conservative: Injections, padding, strapping, orthoses, and wider shoes
ii. Surgery:
 Surgical approach is either dorsal longitudinal, web splitting, plantar
longitudinal, and plantar transverse

NOTE* It is important to do the following when doing this procedure

a. Achieve meticulous hemostasis
b. Identify the digital branches before completing the resection
c. Remove the neuroma without damaging the intermetatarsal artery of
lumbrical
d. Cut the nerve proximal enough to avoid stump neuroma and if possible,
bury the cut end in local muscle
e. Close the dead space

 Other surgical option is decompression of intermetataral

neuroma via cutting the transmetatarsal ligament. Can be done
open or endoscopically (E.D.I.N., as described by Steven Barret,
D.P.M.)
h. Complications: The most annoying complication is the formation of a
stump or amputation neuroma. The pain perceived is more proximal plantarly
on the foot than with the pre-existing neuroma. There is a positive Tinel's
sign. This complication does not usually respond to conservative care, and
must be surgically resected. The operation should be done under general or
spinal anesthesia, with a longitudinal plantar incision. The nerve should be
cut back proximally, bathed in steroid, and finally buried in a muscle belly
with a non-absorbable suture. Additionally, nerve caps, and vein grafts have
been used successfully.

NOTE* Local inflammatory reactions (intermetatarsally) may produce

symptoms and signs reminscent of neuroma. These may be chronic,
leading to surgical intervention with a clinical impression of
neuroma. Histologic studies may reveal vascular fibrofatty tissue
with inflammation, but no neuroma