Hersheychapter 18

8/9/2019 Hersheychapter 18

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Chapter 18: NeurologyNeurologic Pathways Presenting FeaturesAssessment of Clinical ProblemsTarsal Tunnel Syndrome

Classification of Nerve InjuriesNeuromuscular Causes of Cavus FootTypes of Nerve Surgery


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NEUROLOGYIt is not uncommon for a neurologic illness to affect the feet initially, therebymaking patients seek podiatric consultations first. This chapter will help youunderstand disorders affecting the central and peripheral nervous systemswith emphasis on the lower extremity.

Neurological Pathways

1. Cerebral Cortex: Divided into frontal, parietal, temporal, and occipitallobes2. Descending pathways: Divided into corticospinal (pyramidal) andextrapyramidal3. Thalamus and hypothalamus4. Cerebellum5. Brain Stem6. Spinal Cord7. Nerve Roots8. Peripheral Nerves9. Neuromuscular Junction and Muscle

Presenting Features1. Presenting Problems: Can include pain, numbness, tingling, weakness,unsteadiness, and involuntary movements. Neurologic disorders shouldalways be suspected in patients with:a. A foot deformity (i.e. pes cavus)b. Leg or foot weaknessc. Difficulty in walkingd. 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) Whenwas the child sitting independently? (normal at 6 months) When did the childstart to walk? (normal by 9-15 months) Low or normal birth weight?Any problems at birth?ii. Motor System (Muscle tone/strength): Specific examination ofmuscles includes observation, palpation and strength testing. For muscletone look for atrophy (loss of muscle bulk), fasciculations (brief, fine irregulartwitches), and myotonia (decreased relaxation of muscle following asustained contraction). Sometimes muscle hypertrophy is abnormal To testmuscle strength, the specific muscle must be tested against resistance. It is

graded from zero (no movement), 1 (trace movement), 2 (movement withthe aid of resistance), 3 (movement against gravity), 4 (movement againstresistance supplied by the examiner), and 5 (normal strength).

iii. Stance and gait:There are specific gait patterns associated with specificdiseases.

Abnormalities of MovementFasciculations- visable twitching movements of muscle bundles.Tremors-involuntary rhythmic tremulous movements.Tics- repetitive twitching of muscles often in 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 purposefulmovement.

Athetosis- involuntary movements of the face, extremities that are slower,more twisting and writhing than chorea. They occur at rest or during anypurposeful movement.Myoclonus- involuntary, sudden and rapid unpredictable jerks; faster than

chorea.Asterixis- involuntary and brief loss of muscle tone in the outstretched

Abnormal Gait PatternsSpastic gait- Manifested by internal rotation and adduction of the entire

limb, with hip/knee/ankle in marked flexion. Seen with cerebral palsy,familial spastic diplegia, paraplegia, and hemiplegia.


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iv. Deep tendon reflexes (DTR's): Assesses the afferent nerve, the synapticconnections within the spinal cord, the motor nerves, and the descendingmotor pathways. It is important to note right and left asymmetries and thedegree 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 thecorticospinal thalamic tracts. Hyporeflexia indicates a lesion in the lowermotor 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 strikingthe sole (extention of the great toe), and when present represents an uppermotor 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 abnormalthe 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 pinand an ice cube placed on various dermatomes (See Figure 1).*Vibratory testing (posterior columns) is done with a tuning fork (128cycles/sec) over a bony prominence or joint.*Joint position (posterior columns) is performed by moving the first m.p. jointinto either extension or flexion with the patient's eyes closed.

*Light touch (anterior spinothalamic tracts) is performed using a nylonfilament over various dermatomes.

Lower Extremity Dermatomes (Figure 1)L1 and L2 ennervate the anterior thigh. L4 ennervates the lateral thigh, thencrosses the patella to innervate the medial anterior calf and foot (medial sideof the hallux). L5 ennervates the lateral anterior leg and central aspect of thefoot plantarly and dorsally. S1 ennervates the posterior lateral thigh, leg, andlateral border of the foot plantarly and dorsally. S2 ennervates the posteriormedial thigh and leg , and the medial-posterior portion of the heel


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3. Neurologic Diagnostic Procedures:a. Lumbar Puncture: Tapping of the lumbar subarachnoid space between L3and L4 provides important information about intercranial pressure and allowsa diagnostic analysis of the CSF (the CSF count is abnormal if more than 5cells are present).b. CT Scan: Rapid noninvasive imaging for the brain, spinal cord and theirbony enclosures.c. MRI: Provides extraordinary resolution in imaging of the neural structureswithout any known risk to the patient. Helpful in identifying brainstem lesionsand other abnormalities. MRI cannot be used to examine patients withpacemakers, or patients who are pregnant, who have metal prostheses, andwho are dependent on respirators.


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d. Electroencephalography (EEG): Voltage vs. time recordings of electricalcurrents in the brain. Good for detecting epilepsy and metabolic andstructural encephalopathies.e. Electromyography (EMG) and Nerve Conduction Velocities: Whenweakness is clinically difficult to attribute to either nerve, muscle, orneuromuscular junction, electrical studies can establish topographicallywhich nerves and muscles are affected. In EMG, the recording of electricalproperties of muscle is displayed on an oscilloscope during needle insertion.Denervated muscle is recognized by fibrillations and fasciculations on thescreen.In nerve conduction studies the time for an impulse to travel along the nerveis termed the conduction velocity. If there is an increase in this conductionvelocity, there is damage to the particular nerve involved.

Assessment of Clinical ProblemsFinding 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 functiondue to a paroxysmal neuronal discharge in the brain.a. Epilepsy: implies a chronic condition of recurring seizures. Subdivided intotwo typesi. Generalized: Grand mal and petite malii. Partialb. Status epilepticus: recurring seizures, one following another without fullrecovery from the preceding seizure.

c. Etiology: may be metabolic (hypoglycemia), hypocalcemia,phenylketonuria, drug toxicity, drug withdrawal, or a focal abnormality of thebrain 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 tonormal.e. Management: During the seizure administer first aid, preventing thepatient from biting his tongue and keeping the airway open. If the seizure

does not stop within 5 minutes, emergency medical care should beinstituted (IV's w/ D5W/ diazepam/phenytoin PRN). Control should beachieved with as few anticonvulsants as possible.

2. Cerebrovascular Disorders: Cerebral vascular problems usually appeardramatically with sudden onset and often result in permanent loss ofneurologic function. There are two basic typesi. Intracranial hemorrhage: (types) hypertensive, ruptured aneurysm,arteriovenous malformations, traumatic, secondary to brain tumor, and


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secondary to hematologic disordersii. Ischemic stroke: (types) thrombotic and cerebral embolism. The prognosisafter stroke is usually dependent upon the blood vessel involved and itsperfusion territory.

3. Peripheral Neuropathies: In terms of subjective complaints, peripheralneuropathies are the most common causes of foot and toe dysesthesias(burning foot syndrome). In addition patients complain of extremityweakness, muscle atrophy, or both. In addition to motor function, peripheralnerves are responsible for sensory and autonomic function.a. There are three general forms:i. Segmental demyelination: refers to destruction of the myelin segmentswith survival of the myelin segments with survival of axons until late in thecourse of the illness.ii. Axonal degeneration: destruction of the axon.iii. Wallerian degeneration: occurs when the nerve is injured or severed at afocal point, and the distal segment breaks down and is reabsorbed. b.Classification of Neuropathies: Remember the mnemonic "Dang Thrapist"D-DiabeticA-AlcoholicN-NutritionalG-Guillain-Barre

T-ToxicH-HereditaryR-RecurrentA-AmyloidosisP-PorphyriaI-InfectiousS-SystemicT-Tumor

i. Diabetic neuropathy: 2/3 of all diabetics show evidence of peripheralnerve dysfunction (clinically or subclinically), which progresses in the face ofpoor diabetic control. Patients can present with a mononeuropathy,polyneuropathy and can have sensory impairment, or both. At the earlieststage the patient experiences pain, usually worse at night. Symmetric Distal Polyneuropathy: loss of sensation (predominantly)

and motor weakness in a stocking-glove configuration, that occursbilaterally. The distal portion of the longest nerves are affected first andthe feet affected before the hands. Later muscular atrophy can occur withintrinsic muscle wasting.

Mononeuropathies: both cranial and spinalmononeuropathies can occur which includes femoralmononeuropathy (characterized by pain, motor and sensory loss,and absent knee jerk), peroneal mononeuropathy (characterizedby a sudden foot drop), and tarsal/carpal tunnel syndrome.


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Autonomic Neuropathies: disturbances may be seen in thecardiovascular system, bowel, bladder, and sexual function.Symptoms include, diarrhea, incontinence, impotence,

decreased sweating, and orthostatic hypotension

Neuroarthropathy: foot ulcers occur secondary toneuropathy, microangiopathy, large vessel atherosclerosis, orcombinations of these factors. The Charcot joint seen in thelesser tarsus or tarso-metataral area has an unknown etiology. Itis unfortunately seen after revascularization procedures of theextremities. The most common bony deformities are the medialconvexity, plantar deformity, dorsal midfoot deformity, andplantarflexed metatarsals. A differential diagnosis includes tabesdorsalis, osteomyelitis, leprous neuropathy, and peripheral nerveinjuries. Initial treatment for active arthropathy includes 1-2weeks of bed rest, nonsteroidal anti inflammatory drugs (?), theuse of crutches, and a nonweight-bearing cast or splint until thesoft tissue swelling and erythema subsides. Gradual weight-bearing can be resumed once radiographic evidence of an arrestis visualized. Patients with fractures of the lower 1 /3 of the tibiaare prone to develop ankle arthropathy.

4.

Infectious Diseases:a. Meningitis: Causes symptoms such as fever, neck stiffness, disorders ofconsciousness, and seizures. 80-90% of cases of meningitis are caused byone of three organisms, H. influenzae, N. meningitis, and D. pneumoniae.Diagnosis is confirmed by lumbar puncture (CSF is cloudy, pressureelevated, 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 bymeningitis, and then flaccid paralysis of the limbs and trunk. Herpes zoster

NOTE* The diagnosis of orthostatic hypotension is made by demonstrating adecrease of approximately 25 mm Hg in systolic or 10 mm Hg in diastolicblood pressure after 2 minutes of upright posture without a compensatory

increase in heart rate (treated with fluorocortisone or ephedrine).

Note* Treatment of diabetic neuropathy: For burning pain anddysesthesia (combination of Elavil h.s../ Prolixin t.i.d or Valium t.i.d,Axain topically), lightning-like pain (Tegretol or Dilantin),carpal/tarsal tunnel syndrome (splints/orthotics), itching(diphenhydramine), and diarrhea (codeine).


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(shingles) has a dermatomal distribution of vesicles and demonstratessegmental weakness and pain, sometimes for years.

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

b. Chorea: A variety of neurologic diseases are associated with chorea suchas, childhood rheumatic fever (Sydenham's chorea), systemic disordershyperthyroidism, hypoparathyroidism, and SLE), drugs (oral contraceptives),pregnancy, and hereditary disorders (Huntington's chorea).i. Huntington's chorea: an inherited disease than begins to manifest itselfbetween 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 inabnormal postures of the trunk and extremities, and of more rapid, twistingmovements.i. Dystonia musculorum deformans: a primary hereditary disorder, presentsusually with an equinovarus foot.d. Tremor: Essential tremor is a benign disorder that frequentlyaccompanies 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 ofmultiple neurologic symptoms, including blindness, diplopia, ataxia,nystagmus, spastic weakness, dysesthesia, and difficulty with bladder andbowel function. Electroimmunodiffusion reveals migration of gamma Gimmunoglobulin 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 byprogressive weakness, atrophy, spasticity, hyperreflexia, and fasciculationsoccurring in a widespread distribution. There is a wide variation insymptoms, with some patients showing more atrophy and some showingmore spasticity. Some patients have only cranial nerve involvement. There isno specific therapy. There is an inherited pattern.

NOTE* Neuroleptics such as chlorpromazine and haloperidol may produce aParkinson-like syndrome. The syndrome stops with withdrawal of the drug.


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c. Friedreich's Ataxia: An autosomal-recessive disorder with cerebellardegeneration. Characteristics include gait changes, decreased position andvibratory sense in the legs, absent DTR's, nystagmus, kyphoscoliosis, pescavus, and hypertrophic cardiomyopathy.

8. Cerebellar Disorders:These patients present with an imbalance and adifficulty with walking.a. Friedreich's ataxiab. Dandy-Walker deformityc. Arnold-Chiari malformationd. Infections

9. Disorders of Muscles and Nerves: Myopathies are disorders of nervescharacterized by progressive weakness. Laboratory tests for diagnosisinclude 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 afrequent mutation rate, which appears with a slowly progressive proximalweakness beginning in the lower extremities and later involving the upperextremities. It is often associated with early toe walking and causes awaddling gait. The gait changes include decreasing cadences, increasinganterior pelvic tilt, increased hip flexion in swing, decreasing ankledorsiflexion, and increased shoulder sway. These patients have a progressivemuscle atrophy and weakness (there is often pseudohypertrophy of the calfmuscles). The serum CPK is markedly elevated in these patients early in thedisease and a muscle biopsy establishes a definitive diagnosis.Pathognomonic for this disease is a positive Gower's sign, where theaffected child rises from a sitting position on the floor by climbing on his ownlegs.ii. Becker's muscular dystrophy: Is a more benign form of X-linked musculardystrophy clinically similar to Duchenne's MD, and is manifested byprogressive proximal limb weakness.iii. Facioscapulohumeral dystrophy (Landouzy-Dejerine): A variant ofmuscular dystrophy with a swing phase drop foot and compensatoryincrease in hip and knee flexion. This disease gives a "Popeye the sailor"forearm appearance.

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 oneof the aforementioned hereditofamilial neurologic diseases.3. Those with isolated, or idiopathic, familial pes cavus with no family historyof hereditofamilial neurologic disease.4. Those with familial pes cavus and lymphedema (very rare syndrome).


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iv. Limb-girdle muscular dystrophy: Mostly autosomal recessive disorderscharacterized by progressive proximal weakness.v. Myotonic muscular dystrophy: An autosomal dominant disorder withsymptoms that involve a combination of weakness and myotonia (myotoniais a delayed relaxation of muscle following contraction and is associated withabnormal EMG discharges).vi. Spinal muscular atrophy: An autosomal recessive condition withprogressive 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 diseaseb. Acquired Myopathies: The following can cause a slow progressive andprominent muscle weakness:i. Endocrine disorders: Hypo/hyperthyroidismii. 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 perinatalinsult (hypoxia) resulting in a pyramidal tract lesion. There are various typesi. Spasticii. Athetoticiii. Ataxiciv. Rigidb. Familial Spastic Diplegia: Has a strong family history of lower limbspasticity, no perinatal insult, and is progressive.

11. Disorders of the Spinal Cord and Nerve Roots:a. Spinal Cord Disorders: Localizing the level of a focal lesion of the spinalcord is easier if one remembers the Brown-Sequard syndrome.

i. Spinal cord dysfunction may be acute or chronic

Acute due to: trauma, compression, inflammation, infarction, vascularmalformation, and hemorrhage.

Chronic due to: Syringomyelia

Note* The type of spasticity is based on the anatomical areas involved:Diplegia- all four extremities, primarily lowersParaplegia- lower extremities onlyQuadriplegia- all four limbs equally involvedHemiplegia- one side of the body (upper and lower extremities)

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


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b. Radiculopathies:i. A fifth lumbar nerve radiculopathy in addition to back pain, often causesradiating pain down the lateral aspect of the leg with numbness orparesthesias of the lateral calf and the dorsum of the foot.ii. A first sacral nerve radiculopathy characteristically causes radiating paindown the posterior leg with sensory changes on the lateral and plantaraspects 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 reflexdystrophy. This syndrome is characterized by disproportionate pain inintensity, duration, location, often from minor or unapparent trauma to anextremity. Clinical diagnosis is difficult due to the vague subjective data andsubtle objective signs and symptoms. Early diagnosis is important becauseearly treatment gives the best results. The sympathetic nervous system isalways involved and is overactive. Symptoms occur distal to the trauma site.i. Manifestations: (signs and symptoms)

Pain- most prominent characteristic featureQuality of pain: burning, aching or throbbingSeverity of pain: mild to excruciating, usually continuous Paroxysmalaggravations: emotional stress, movement, and touch Localized first thenspreadsNot limited to a dermatome or peripheral nerve distribution

Vasomotor disturbanceVasodilation: warm skin, dry skin, and hypohidrosisVasoconstriction: cyanosis, cool skin, edema of the part, and hyperhidrosis

Delayed return to function Trophic changes- are late changes (atrophy, andosteoporosis)

Involves the skin, appendages, muscle, bone and joints (RSDS arthropathy)

i. There are three grades based upon mode of onset, Intensity, andpreponderance 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 normalresponse and exaggerated response so is often overlooked, usually seenafter surgical procedures

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


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ii. There are three stages of the disease divided as per the time frame - Stage 1 (days to weeks): Characterized byPainHyperesthesiaHyperalgesiaLocalized edemaMuscle spasm and tendernessVasomotor diseaseNo x-ray changesTrophic changes of hair, nails and skin beginIn mild cases (GRADE 3) this stage lasts a few weeks and then subsidesspontaneouslyIn severe cases (GRADE 1) symptoms become progressively worse

Stage 2 (3-6 months):Gradual decrease of painSpread of edema, soft to brawny

Hair scant, nails brittle/cracked and heavily grooved Muscle wastingX-rays reveal spotty osteoporosis (early), and diffuse osteoporosis (late)

Stage 3 (greater than 6 months):Marked trophic changes which eventually become irreversibleSkin is smooth/glassy/drawn/pale or cyanotic with a loss of subcutaneous fatNail changesDigits are thin and pointedMuscle atrophy, especially interosseiLimited ROM of jointsTendon contractions

SubluxationsBone atrophy is diffuse and marked

iii.

Treatment: Neurology consult Psychiatric consult Anesthesiology consult

Sympathectomy (GRADE 1) -Local blocks (GRADE 2 and 3)

Physical therapy

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

NOTE* According to Van Wyngarden and Bleyart in the Journal of FootSurgery, Volume 31- Number 1, their diagnostic test of choice is asympathetic and sensory epidural nerve block. If there is a response,then their treatment of choice is frequent sympathetic blocks(bupivacaine+methylprednisolone), in combination with physicaltherapy, and with oral clonazepam throughout the treatment period.


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Systemic steroids (?) Beta blockers (?) TENS (?) Axain + topical lidocaine (?) Procardia (?) Analgesics (?) Medication to reduce patients' stress

Innervation of the Lower ExtremityLower 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 islocalized to the pelvis), passes through the greater sciatic notch, between thegreater trochanter of the femur and ischial tuberosity, and rests on theposterior surface of the adductor magnus. In the lower third of the thigh, thesciatic 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 thepopliteal 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 vesselsanterior to the ankle joint, where it divides into medial and lateral branches.5. The medial branch of the deep peroneal nerve follows the course ofthe dorsalis pedis artery and stays lateral to it. This nerve splits in the firstinterspace where it supplies the adjacent sides of toes 1 and 2.6. The lateral branch of the deep peroneal nerve passes across thelateral tarsal area where it supplies the extensor digitorum brevis, then splits

into three interosseous branches that supply the 2nd, 3rd, and 4thinterosseous muscle.7. The superficial peroneal nerve supplies the peroneal muscles, comesdown to the ankle lying between the peroneii and the EDL. It divides into themedial and intermediate (lateral branch) dorsal cutaneous nerves.8.The medial dorsal cutaneous nerve divides in front of the ankle intotwo dorsal digital nerves, the medial and lateral dorsal digital nerves.The medial dorsal digital nerve supplies the medial side of the hallux andthe lateral dorsal digital branch supplies the adjacent sides of the 2ndand 3rd toes.9. The intermediate dorsal cutaneous nerve, the smaller branch of the

superficial nerve, divides into two dorsal digital branches over thedorsolateral aspect of the foot. The more medial branch supplies the adjacentsides of the 3rd and 4th toes. The lateral branch joins with the terminalbranch 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 islocated between the FDL medially and the FHL laterally. It enters the lacinateligament (3rd compartment) and divides into medial and lateral plantar


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nerves to innervate the sole of the foot.11. The medial plantar nerve is the larger branch and its branches. It givesoff a cutaneous branch to the medial side of the hallux, adjacent sides of thehallux and 2nd toe, the adjacent sides of the 2nd and 3rd toes, and theadjacent sides of the 3rd and 4th toes. The 3rd and 4th common digitalnerves communicate in the third interspace and is the site for Morton'sneuromas. The muscular attachments are as per Fig. 4. 12. The lateralplantar nerve supplies the medial and lateral side of the 5th toe and thelateral side of the 4th toe. The muscular attachments are as per Fig. 4.


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Tarsal Tunnel SyndromeIs an entrapment or compression neuropathy of the posterior tibial nerve orone of its three branches, the medial and lateral plantar nerves and/or medialcalcaneal nerve.1. Anatomy: Nerve entrapment occurs either in the porta pedis orlacinate ligamenta. The flexor retinaculum (lacinate ligament) extends from the medialmalleolus to the medial process of the calcaneal tuberosity and the plantaraponeurosis. The deep fibrous septa form four compartments, and convertsbony grooves into canals from anterior-medial to posterior lateral: #1contains tibialis posterior tendon (most superficial), #2 FDL tendon, #3posterior tibial nerve artery and vein, and #4 FHL tendon. Thesecompartments are unyielding spaces.b. The porta pedis is a canal created by the abductor hallucis muscle bellythrough which the medial and lateral plantar nerves pass. c. Division of theposterior tibial nerve into its 3 terminal branches may occur proximal tothe 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 themedial and plantar aspect of the heel. It may arise from either the posteriortibial or lateral plantar nerve.e. The medial plantar nerve gives sensory innervation to the plantaraspect of the hallux, second and third toes, medial half of the fourth toe, andthe medial half of the plantar aspect of the foot. It gives motor innervation tothe abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and thefirst lumbrical.f. The lateral plantar nerve gives sensory innervation to the plantar lateralhalf of the fourth toe, plantar aspect of the fifth toe, and plantar lateralaspect of the foot. Initially it sends motor fibers to the quadratus plantae andabductor digiti quinti before dividing in a superficial and deep branch.Superficial branch supplies motor innervation to the flexor digiti quinti brevisand the dorsal and plantar interossei of the fourth intermetatarsal space. Thedeep branch supplies the remaining intrinsic muscles of the foot.

2. Pathology: Compression of the nerve initially causes only sensoryinvolvement with possibly partial involvement of motor fibers. Continuation ofthe irritation, ischemia, and compression may lead to secondaryhyperactivity of the autonomic nervous system, manifested by coldness andnumbness from the altered sympathetic activity. Eventual structural changes

in the nerve result in the development of muscle wasting, paresis, andobjective sensory loss.

3. Etiology: In the majority of cases no etiology can be found at the time ofsurgical decompression.a. Dilated posterior tibial veins: can also cause severe night discomfort.b. Trauma: Fracture, dislocation, sprain, post-traumatic edema and fibrosis. c.

NOTE* Reflexes are unaffected


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Systemic disease: Gouty arthritis with urate deposits, rheumatoid arthritis,diabetes mellitus, and myxedema.d. Space occupying lesions: Ganglions, neurofibromas, neurilemmomas, andsynovial cysts.e. Hypertrophy of abductor hallucis muscle belly.f. Biomechanical: excessive pronation

4. Clinical Symptoms: Symptoms can be either distal to the metatarsalarea, or the medial and lateral heel depending on the branch involved. a.Early:i. Intermittent burning pain, numbness and paresthesias over the medial sideof 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 paresthesiasb. History of traumac. History of systemic diseased. Hoffman-Tinel's sign: A tingling in region of the distribution of the involvednerve with light percussion, results in paresthesias distal to the site ofpercussion.e. Valleix Phenomena: A nerve trunk tenderness above and below the pointof compression, with paresthesias proximal and distal to the point ofpercussion.f. Turk's test: Application of a venous tourniquet to the lower extremity willelicit positive symptoms on the affected side, by producing a venousocclusion.g. Forced eversion of the foot.h. Positive radiographic evidence of previous injuryi. Positive lab studies for any specific diseasej. EMG's and nerve conduction studies are only useful for late stage disease.

6. Treatment: Conservativea. Local blocks: Posterior tibial nerve blocks with steroids

Note* EMG may show fibrillation potentials which indicate denervation ofmuscle. 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 malleolus3. Recording electrode (for conduction of the medial plantar nerve) throughthe abductor hallucis ms. belly.4. Recording electrode (for the lateral plantar nerve) through the abductordigiti quinti muscle belly.


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b. Unna boot: can be combined with nerve blocksc. Support hose: for varicositiesd. Functional orthoses

7. Treatment: Surgical Decompression (positive EMG's and nerveconduction studies mandate surgical decompression). Involves the completeexploration of the tarsal tunnel with release of the flexor retinaculum and itsfibrous 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 tothe medial malleolus by 1 cm.b. The subcutaneous tissue is incised and the superficial vessels are ligatedas 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 itsterminal 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 yougo.g. The nerve(s) is followed distally to the point where the medial and lateralplantar nerves pass through the fibrous canals superior to the abductorhallucis ms. belly.h. The abductor hallucis ms. is examined for any abnormality, and anyhypertrophy 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 reapproximatedl. Sterile compression dressing and a non-weight-bearing BK cast applied for3 weeks.

8. Complications:a. Recurrence: due to fibrosisb. Severing the PT artery : if done then tie off and prepare patient formicrovascular repair later.c. Severing a nerved. Tenosynovitise. Hematomaf. Wound dehiscence

Classification of Nerve Injuries1. Seddon and Sunderland classified nerve injuries:a.Seddon's classificationi. Neuropraxia: (first degree injuries) a conduction disturbance with completerecoveryii. Axonotmesis: (second and third degree injuries) an incomplete division ofsupportive tissues of the nerveiii. Neurotmesis: (fourth and fifth degree injuries) a complete division of a


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nerveb. Sunderland's classificationi. First degree: only local changes to the myelinii. Second degree: injury to the axons that is incompleteiii. Third degree: leads to more severe axonal injury with fibrosisiv. Fourth degree: severe neuronal injury with the axons in completedisarray (no complete neuronal separation)v. Fifth degree: complete transection of the nerve (dismal prognosis)

Neuromuscular Causes of the Cavus FootThe cavus foot is classified according to the level of the CNS that is affected1. Cerebral Cortex: Hysteria2. Pyramidal and Extrapyramidal: C.P.,athetosis, dystonia musculorumdeformans3. Spinocerebellar Tracts: Friedreich's ataxia, Roussy-Levy syndrome4. Spinal Cord Level: Polio, myelomeningocele, diastematomyelia, cordtumor

5. Peripheral Nerve or Spinal Nerve Root: C.M.T.,polyneuritis-Sotas6. Muscle: Muscular dystrophy

Types of Nerve Surgery1. Neurolysis: Frees the nerve from adhesions or scar tissue that obstructthe growth of regenerating axons or block the conduction of nerve impulses.Immature nerve fibers may suffer temporary conduction block withneurolysis. If the entrapped nerve and branches are found in dense scartissue, the nerve may be rerouted to a more favorable bed which minimizesthe risk of subsequent compressiona. It is indicated in a complicated first degree injury in which scarring or

adhesions have interrupted conductionb. In a second degree injury, the nerve is intact and normal in appearance,but the interfunicular tissue is scarred. Internal neurolysis may be necessaryto split the, sheath and release the bundles from the interfunicular scar tissue(difficult)

2. Neurorrhaphy: Nerve repair is justified when conservative care fails andnerve function deteriorates. When it is determined that a traumatizednerve is partially or completely severed neurorrhaphy can be attempted.


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Neurons retain for several years the capacity to regenerate a new axon. Theregenerative process of the nerve remains intact, and the new axons enterthe endoneurial tubes in the stump distal to the trauma. The earlier the

reinnervation, the better the prognosisa. If a small nerve is partially or virtually severed, repair of the severedsection by partial sutures or resect the damaged segment, mobilize the nerveproximally and distally to gain the added length, and perform an end to endanastomosisb. 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 anastomosisc. Whenever a nerve is transected, it retracts approximately 4% of its normallength between excision points

3. Neuroma (Morton's):a. Definition: A neuroma represents hyperplasia of Schwann cells, axonalelements and fibroblasts in an area where proximal elements cannot relocateto their distal pathwaysb. Histopathology: The term neuroma refers only to nodules that are formedby hyperplasia of axons and Schwann cells. This process is characterized byendoneural and neural edema (early stages); perineural, epineural, andendoneural fibrosis (late stages); and eventually demyelination. It is areactive lesion, not a tumor. The term 'Morton's Neuroma' refers to a lesion inthe third intermetatarsal space only.

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

dissecans (Freiberg's), localized vasculitis, ischemia, tarsal tunnel, nerve rootcompression syndromes, peripheral neuropathy (especially diabetic

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

NOTE* Endoneural edema, fibrosis and demyelination are diagnostMorton's neuroma and other types


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neuropathy), and intermetatarsal bursitisf. Etiology: Compression trauma, and stretching of the interdigital nerve, withmicro-tears of axonsg. Treatment:i. Conservative: Injections, padding, strapping, orthoses, and wider shoesii. Surgery:

Surgical approach is either dorsal longitudinal, web splitting, plantarlongitudinal, and plantar transverse

Other surgical option is decompression of intermetataralneuroma via cutting the transmetatarsal ligament. Can be doneopen or endoscopically (E.D.I.N., as described by Steven Barret,D.P.M.)

h. Complications:The most annoying complication is the formation of astump or amputation neuroma. The pain perceived is more proximal plantarlyon the foot than with the pre-existing neuroma. There is a positive Tinel'ssign. This complication does not usually respond to conservative care, andmust be surgically resected. The operation should be done under general or

spinal anesthesia, with a longitudinal plantar incision. The nerve should becut back proximally, bathed in steroid, and finally buried in a muscle bellywith a non-absorbable suture. Additionally, nerve caps, and vein grafts havebeen used successfully.

NOTE* It is important to do the following when doing this procedurea. Achieve meticulous hemostasisb. Identify the digital branches before completing the resectionc. Remove the neuroma without damaging the intermetatarsal artery oflumbricald. Cut the nerve proximal enough to avoid stump neuroma and if possible,bury the cut end in local musclee. Close the dead space

NOTE* Local inflammatory reactions (intermetatarsally) may producesymptoms and signs reminscent of neuroma. These may be chronic,leading to surgical intervention with a clinical impression ofneuroma. Histologic studies may reveal vascular fibrofatty tissuewith inflammation, but no neuroma

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