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NEURO 03-07-13 - CLINICAL CORRELATIONS

THE MUSCLE o A disease may damage the muscle directly


(myopathy), or indirectly by damaging the nerves to cause
Muscles have been classified as RED or WHITE on the basis of neurogenic atrophy
their color o If a muscle loses its innervations because of the
Differentiating type 1 from type 2 muscle fibers lower motor neuron, the muscle fibers fibrillate & atrophy
o In myopathies, the entire muscle fibers
degenerate in a random process affecting muscle fibers of
many motor units (with loss of fibers from all motor units)

DISORDERS OF THE SARCOLEMMA


- Inability to generate action potentials
CHANNELOPATHIES does having inability generating
action potential, ion channels problem (K, Na, Ca problems)
o PERIODIC PARALYSIS altered ionic
conductance in the membrane causes altered resting
potential & loss of action potentials & electric activity,
- Muscles requiring sudden, strong or phasic contractions resulting to weakness of muscle contraction
are made up of type II WHITE or fast-twitch muscle fibers that With triggering factors that would lead to sudden
can function anaerobically paralysis, proximal weakness
for marathon - Other membrane disorders
larger, low oxygen consumption, shorter contraction, o MYOTONIAS there is excessive firing or
fast twitch, irritability of the membrane, excess muscle contraction,
- Muscles requiring steady, continuous contractions are or inability to stop contraction
made up primarily of type I RED, slow twitch muscle fibers that How to elicit? tap the thenar eminence then ask
depend on aerobic metabolism rich in myoglobin, longer the patient to make a fist, after a few seconds, ask the
contraction time, more mitochondria, higher oxygen patient to relax (MYOTONIA unable to stop the
consumption, good blood flow, low fatigability, slow twitch contraction). Tapping triggers or stimulate the
For sprint contraction
- The size of motor units, the innervations ratios, & the
number of motor units in a muscle also are designed to DISORDERS OF THE CONTRACTILE MECHANISM
efficiently perform the appropriate activity - In these disorders, muscle fibers generate normal electrical
MOTOR UNIT 1 axon or 1 nerve fiber innervating activity but do not generate normal force
several muscle fibers (e.g. 1 axon: 5 muscle fibers low - PHOSPHORYLASE DEFICIENCY inability to
innervations ratio or 1 axon: 2000 muscle fibers high generate sufficient energy
innervations ratio) As the muscle runs out of energy, it cramps without
- EXTRAOCULAR MUSCLES low innervations ratio, electrical activation
controlling only 5-10 muscle fibers or muscles of the hand, for
muscles that need fine movements, small group
- In contrast, the GASTROCNEMIUS the innervations
ratio is higher, with each motor neuron controlling as many as
2,000 muscle fibers for muscle that do not require fine
movements
How do you differentiate muscle pathology from neuron disease?
MUSCLE PATHOLOGY: innervations looks normal but the
problem is in the fibers, random abnormality on biopsy
MOTOR NEURON DISEASE only the muscle fibers
belonging to the innervation

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SEQUENCE OF EVENTS LEADING TO MUSCLE WEAKNESS
CONTRACTION & PATHOPHYSIOLOGIC - NERVE symmetrical but distal, gloves & stockings
CORRELATIONS - MUSCLE symmetrical and proximal, arm & thighs
from exctitation to ATROPHY
contraction - NERVE early; dennervated
acetycholine release FASCICULATIONS nerve problem; motor neuron
myasthenia gravis SENSORY LOSS nerve
before you release the Ach AUTONOMIC nerve
vesicles, there is Ca channels CK ENZYMES dennervated at muscle; normal at nerve
involved
Ca should enter for the action DISEASES OF THE MUSCLE
potential of the nerve Inflammatory myopathies polymyositis & dermatomyositis
LEMS problem in the Ca
channel IDIOPATHIC POLYMYOSITIS & DERMATOMYOSITIS
LEMS presynaptic - Common diseases affecting striatal muscles & skin, &
MYASTHENIA GRAVIS post synaptic; Ach has been release sometimes connective tissues
but the problem is the binding of Ach to the receptors - May be associated with CTD (RA, RF, LE, scleroderma,
STEROID MYOPATHY weakness Sjogren, or mixed CTD)

LABORATORY STUDIES POLYMYOSITIS (PM)


DTR 0 nerve - Idiopathic, subacute or chronic & symmetrical weakness
Weakness, DTR +2 or +1 muscle of proximal limb & trunk muscles without dermatitis
- ELECTORMYOGRAPHY (EMG) provides - Insidious onset; progressive course (several weeks or
information whether a muscle disease is present, & the type of months)
disease involving the muscle (primary muscle disease, problem in - May develop at any age, either sex; majority are 30 to 60
neuromuscular transmission, or denervation) yrs old; females > males
Can request EMG with NCE (nerve conduction) - Painless weakness of the proximal limbs especially hips &
If requested first may result to false (+) thighs, to a lesser extent shoulder girdle & neck
- NERVE BIOPSY usually tested is the sural nerve - Absence of muscle tenderness; less atrophy
(superficial); do if not sure if nerve or muscle - Other organ systems involved:
- MUSCLE BIOPSY specimens are taken from a muscle o Cardiac muscles (minor ECG changes,
that shows moderate weakness because in severe weakness, there arrhythmias);
may be so much replacement of muscle by fat or connective o Interstitial lung disease
tissue (biceps or quadriceps)
- CK ENZYMES CK-MM; 1st to get first DERMATOMYOSITIS (DM)
CK-MB heart - Skin changes (rash) precede the muscle symptoms
CK-BB brain o Localized or diffused erythema, maculopapular
eruption, scaling eczematoid dermatitis, or exfoliative
CLINICAL CORRELATION dermatitis
o Predilection for extension surfaces (elbows,
knuckles & knees)
o Gottron papule
o HELIOTROPE lilac-colored change in the
skin over the eyelids, bridge of the nose, cheeks & forehead
LUPUS reddish

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PATHOLOGIC CHANGES IN PM & DM SEX LINKED MUSCULAR DYSTROPHIES:
- PM widespread destruction of segments of muscles DUCHENNE & BECKER
(necrosis) with scattered inflammatory reaction - Duchenne muscular dystrophy (DMD) & Becker
(mononuclears, lymphocytes & plasma cells) muscular dystrophy (BMD)
- DM perifascicular muscle atrophy; infiltrates - Mutations in gene for dystrophin at Xp21
predominate in the perimysial connective tissue; - X-linked recessive inheritance (manifest in boys)
microvascular changes - Carriers (girls & women) may have mild symptoms of
high CK
ETIOLOGY & PATHOGENESIS - DUCHENNE more common
- Idiopathic o INCIDENCE: 1 in 3,300 male births
- Autoimmune mechanism (association with other o PREVALENCE: 1 in 18,000 boys
autoimmune disease) - BECKER: 1 in 20,000
- IMMUNOLOGIC DESTRUCTION - DYSTROPHIN a cytoskeletal protein located at
o DM humoral; IgG, IgM, complement (C3) plasma membrane, associated with glycoproteins linking
& membrane-attack complexes (MAC) are cytoskeleton to plasma membrane
deposited in the walls of venules & arterioles) - Mutations in dystrophin gene leads to absence of
o PM cellular; large numbers of activated T dystrophin in DMD; smaller size, reduced levels in BMD
cells mainly CD8; T cells & macrophages o The sarcolemma is unstable in contraction &
enclose nonnecrotic muscle fibers relaxation, liable to breakage, excessive calcium
influx, causing muscle necrosis
DIAGNOSIS & TREATMENT Treatment: genetic counseling
- DIAGNOSTICS CK, EMG, muscle biopsy
- TREATMENT DUCHENNE MUSCULAR DYSTROPHY
o CORTICOSTEROIDS first line; - The most frequent & best known among the early onset
prednisone 1 mg/kg; response is tested by MDs
muscle strength & CK levels - Usually recognized by 3rd year of life, almost always before
o HIGH DOSE METHYLPREDNISOLONE 6 yrs
for acute & severe cases; 1 gm IV infusion - Enlagement of muscles show rubbery feel
for 2 hrs OD x 3-5 days - Pseudohypertrophy
Out patient maintenance for methylprednisone - Proximal weakness with delayed walking; difficulty
o Intravenous immunoglobulin (IV Ig) running, toe-walking, waddling gait
o Plasma exchange (PE) - Progressive to overt symptoms before age 5; difficulty
o Immunosuppressants azathioprine, walking, climbing stairs, rising from chairs
methotrexate - Exaggerated lumbar lordosis, falls, use of arms to push up
on rising from the ground (GOWER SIGN)
PROGNOSIS - ECG is abnormal in most patients
- Generally favorable prognosis (except for those with - Cardiomyopathy with congestive heart failure
malignancy) e.g. polyomyositis with other CTD - Mental retardation in 33%
- CAUSES OF DEATH pulmonary complications, - OTHER POSSIBLE MANIFESTATIONS:
myocarditis Intestinal hypomotility Osteoporosis
Acute gastric dilatation Intellectual impairment

BECKER MUSCULAR DYSTROPHY


- 2 DIFFERENCES FROM DUCHENNE
o Age at onset (usually after age 12)
o Rate of progression is slower (walk after age
12, often later)
- Otherwise, the syndrome are nearly identical

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THYROID MYOPATHIES
SEX LINKED MUSCULAR DYSTROPHIES: - Several myopathic diseases are related to alterations in
DUCHENNE & BECKER thyroid function:
- INVESTIGATIONS o Chronic thyrotoxic myopathy
o Serum CK elevated (usually at least 20 times o Exophthalmic ophthalmoplegia (infltrative
the normal) orbital ophthalmopathy)
o DNA test for Xp21 mutation o Myasthenia gravis associated with
o Dystrophin assay by immunoprecipitation of thyrotoxicosis
muscle proteins from biopsy, or immunocytochemistry Myasthenia not actually a muscle problem but
on frozen muscle section the weakness
- MUSCLE BIOPSY o Periodic paralysis associated with
o GENERAL HISTOLOGIC FEATURES OF thyrotoxicosis work up: thyroid (1st), (2nd)
MYOPATHY random variation in fiber potassium, (3rd) adrenals
diameter, with both large & small fibers o Muscle hypertrophy & slow muscle
Fat deposition, Pseudohypertrophy contraction & relaxation associated with
oSome fibers have internal migration of nuclei, myxedema & cretinism
some are splitting or degenerating, & there is
an in connective tissue (Trichome stain; x PATHOGENESIS OF THYROID MYOPATHIES
200) - THYROXINE influences the contractile process but
- DIAGNOSIS does not interfere with the transmission of impulses in the
o Usually evident from clinical features peripheral nerve across the myoneural junction or sarcolemma
o CK values 20 times higher than normal - There is enhancement of the speed of the contractile
o Blood DNA testing usually confirmatory process & reduces its duration fatigability, weakness, loss of
If not, muscle biopsy is performed endurance
- DIFFERENTIAL DIAGNOSIS - The speed of the contractile process is related to the
o Spinal muscular atrophy quantity of the myosin ATPase which is in hyperthyroid
o Conditions causing CK elevation; Xp21 carrier muscle & in hypothyroid
state, idiopathic or symptomatic hyperCKemia,
dysferlinopathies, caveolin-2 mutations CORTICOSTEROID MYOPATHIES
- TREATMENT - CUSHING DISEASE MYOPATHY
o Prednisone therapy beneficial in controlled o Poor correlation between the dose of steroids
trials; limited by side effects of chronic & the severity of weakness
administration (osteoporosis, etc) o Discontinuation or reduction in steroids leads
o Rehabilitation to: to gradual improvement & recovery
Maximize function based on o POSSIBLE PATHOGENESIS there is in
preserved muscle strength the uptake of amino acids & protein synthesis
Prevent contractures by the muscle
o Braces, surgery for spine or limb deformities o EMG is normal or just with mild myopathic
o Social, emotional support, genetic counsel changes; no fibrillations, CK normal
o BIOPSY little or no necrosis, no
inflammatory cells

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- ACUTE STEROID MYOPATHY (Critical Illness oAcute onset of severe muscle cramps &
Myopathy) generalized weakness
o Acute & more severe o CHRONIC ALCOHOLIC MYOPATHY
o Brief periods of high dose steroids e.g. chronic painless weakness & atrophy of
asthma proximal limbs
o There may be critical illness polyneuropathy, - ALCOHOLISM one of the most common causes or
myoglobinuria, renal failure rhabdomyolysis
o Most of the patients recover in 6-12 wks
Stop 1st the steroids before going to extensive CASE 1
procedure - A 58 yr old diabetic female complained of tingling
o EMG fibrillations present sensation (paresthesia) over both feet for the past 6-8 months
o CK elevated - About 3 months ago, she started having numbness &
o BIOPSY varying degrees of necrosis & tingling sensation over the fingers of both hands (gloves &
vacuolation stockings)
- PERTINENT NEUROLOGIC EXAM:
MYOPATHIES CAUSED BY DRUGS & TOXINS o MMT = 5/5 extremities, proximal & distal
FEATURES OF TOXIN-INDUCED MYOPATHIES o DTRs +1 on both lower extremities; +1 to
Statin drugs, colchicines +2 both upper extremities
- SENSORY
NECROTIZING MYOPATHY o 50% deficit as to light touch (using Camel
- RHABDOMYOLYSIS myoglobin & other muscle hair) & vibratory sense over both feet & fingers
proteins enter the bloodstream & appear in the urine (burgundy of both hands
red or brown color) - WHERE WILL YOU LOCALIZE THE LESION?
- MEDICAL CONDITIONS THAT MAY LEAD TO o Muscle
MYOGLOBINURIA crush injury; vascular diseases; repeated o Neuromuscular junction
injury to muscles such as in status epilepticus, generalized tetanus o Nerve
& malignant hyperthermia - GIVE YOUR BASIS
- TREATMENT alkalinization of the urine by ingestion o Sensory signs & symptoms, DTR,
of Na bicarbonate; dieresis; hydration distribution (gloves & stockings)

STATIN INDUCED MYOPATHY more common CASE 2


- SYMPTOMS from mild muscle aches to potentially - A 32 yr old male was brought to the ER because of
fatal rhabdomyolysis flu, myalgia progressive weakness of the lower extremities over a period of 3
- FIRST GENERATION STATINS (Pravastatin, days
Simvastatin) not frequently toxic especially when combined - The weakness was described to have ascending pattern
with gemfibrozil - 2 weeks prior, there were fever & diarrhea; no consult
- MECHANISM OF DAMAGE chronic use of statins done
reduce levels of both ubiquinone & small GTP-binding proteins - PERTINENT NEURO EXAM
- TREATMENT discontinuation o Both Lower Ext = 1/5
o DTRs 0 in all extremities
ALCOHOLIC TOXIC MYOPATHY o No Babinski sign
- Several forms of muscle weakness acute or chronic - NERVE
o Painless, predominantly proximal weakness - GBS ascending
associated with severe hypokalemia (<2 meq/L)
o ACUTE ALCOHOLIC MYOPATHY
occurs acutely at the height of prolonged drinking,
severe pain, tenderness, edema of the muscles of the
limbs & trunk; with renal damage

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THE SPINAL LEVEL - Flexion of the spinal cord or traction on a peripheral
Start of the spinal cord FORAMEN MAGNUM nerve (e.g. disc herniation or tumor) can stretch & irritate a
No gross differentiation of the medulla & the spinal cord spinal nerve & cause pain RADICULAR PAIN
Similarity of the lower medulla & upper spinal cord - GENERAL GUIDELINES FOR LOCATING THE
LEVEL OF A SPINAL CORD INJURY WITH RESPECT
SPECIAL PHYSIOLOGIC & ANATOMIC FEATURES OF TO THE VERTEBRAE:
THE SPINAL CORD o Between T1 & T10, add 2 to the number of
- Prominent function in sensorimotor conduction & the vertebral spine to determine the spinal cord
relatively primitive reflex activity segment at same location
- Its long, cylindrical shape with 2 enlargements EXAMPLE: gunshot wound at T2 T4 (add 2)
cylindrical & lumbar Spinothalamic ascend 2 levels before crossing
- Its small cross-sectional size o The lumbar segments of the cord are
- Its tight envelopment by the meninges approximately at the level of the spinous
- The peripheral location of myelinated fibers next to the processes of T11 & T12
pia o Sacral & coccygeal segments are at the level of
- The special arrangement of its blood vessels the L1 spinous process
- The relationship to the vertebral column o There are 8 cervical segments & only 7 cervical
vertebrae, so that the cervical enlargement at
REVIEW OF ANATOMY C7 cord segment is centered at the C7
- INTERVERTEBRAL FORAMEN the bony canal vertebral level
formed by 2 adjacent vertebrae
- From the foramen magnum up to the lower border of the DERMATOMES
1st lumbar vertebra - Each spinal nerve is distributed to a well-defined area of
- Cylindrical/conical in shape with 2 enlargements, the skin called DERMATOME
cervical (brachial plexus) & the lumbar (lumbosacral plexus) T4 - nipple
- Caudal end is called CONUS MEDULLARIS T10 umbilicus
From the conus medullaris, there is a long ligament plus the T7 xiphoid process
spinal nerve roots coming from the lumbar & sacral level L1 inguinal
CAUDA EQUINA L2 or L1 spinal nerve root
- 31 Spinal Nerves Umbilicus or going up spinal cord
(8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal) - Dermatomes of adjacent spinal nerves overlap. This
INTERVERTEBRAL FORAMEN formed from 2 adjacent overlap accounts for the variation in sensory loss seen in
vertebra; patients with spinal nerve lesions
TRANSVERSE FORAMEN where vertebral arteries will
pass thru BLOOD SUPPLY
- Because the nerve is surrounded by bony structure, it is - 1 anterior (2/3) & 2 posterolateral arteries (1/3)
particularly vulnerable to local compression by a tumor, Anterior more common to stroke
herniated disc or arthritic changes in the bones - The spinal arteries receive their supply from the vertebral
- Because there are only 7 cervical vertebrae, C1 to C7 arteries & from the intercostal, lumbar, & sacral arteries through
nerves exit above the vertebra while the C8 exit between C7 & 6-8 radicular arteries, the largest usually entering at the lower
T1 for localization thoracic or upper lumbar region of the cord
C2 exits at between C1 & C2
C7 exits between C6 & C7 INTERNAL MORPHOLOGY
- Below T1 spinal nerves exit below the vertebrae of same - WHITE MATTER Outer
number o Longitudinally arranged myelinated &
- Nerve roots are anchored in the intervertebral foramina by unmyelinated nerve fibers, with an abundance of
the DENTICULATE LIGAMENT myelin that gives it a glistening white appearance

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- GRAY MATTER inner if a patient has weakness or numbness (legs first) ascending
o A longitudinally continuous matrix of neuronal compression is coming from the outside
cell bodies, dendrites, myelinated & unmyelinated if a patients presentation is at the arm first, then gradually
nerve fibers, with an abundance of myelin that gives involving the legs medially
it a glistening white appearance Intramedullary spared initially the sacral (sacral sparing)
o Divided into dorsal horns, intermediate gray & Extramedullary roots may be compressed (e.g. herniated disc),
ventral horns prominent pain (radicular pain)
o 2 MAIN TYPES OF NEURONS are
Projectional neurons & Interneurons OVERVIEW
- 2 DISTINCT PATTERNS OF ABNORMALITY
INTERNEURONS OCCUR:
- Interneurons have axonal projections that remain in the o SEGMENTAL: produces signs localized in a
spinal cord & constitute the bulk of spinal neurons single segment of the body horizontal
- Interneurons integrate segmentally & intersegmentally, Flaccid weakness, atrophy, loss of
both ipsilaterally & contralaterally reflexes, loss of sensation
o LONGITUDINAL: produces deficit for all
REXED LAMINAE functions below the level of the lesion vertical
- LAMINA II SUBSTANTIA GELATINOSA Weakness (spastic type), no atrophy
o Receives input from unmyelinated nociceptive initially, reflexes, presence of Babinski signs, loss
C fibers (carrying pain & temperature) of sensation, autonomic disturbances (bowel,
- LAMINA IV Contains the Clarkes column bladder, sexual dysfunctions)
proprioception C6 carry the biceps, brachioradialis
The cells are tract cells that sends axons to the
o
cerebellum via the dorsal spinocerebellar tracts THE SYNDROME OF ACUTE PARAPLEGIA OR
- LAMINA IX Contains the motor neurons (alpha) QUADRIPLEGIA CAUSED BY TRAUMATIC & OTHER
anterior motor neurons PHYSICAL FACTORS (TRANSVERSE MYELOPATHY)
- LAMINA X Surrounds the central canal
I. TRAUMA TO THE SPINE & SPINAL CORD
SPINAL CORD LAMINATION OF TRACTS A. MECHANISMS OF SPINE & SPINAL CORD
major ascending (blue) - USEFUL CLASSIFICATION fractures-dislocations,
& descending (red) pure fractures, pure dislocations (3:1:1) more common
tracts of the spinal cord - Most injuries are the result of force applied at a distance
white matter. C, - FLEXION INJURY the head is bent forward when the
cervical; L, lumbar; Th, force is applied; the adjacent cervical vertebrae are forced
thoracic; S, sacral together at the level of maximum stress; the posterior part of the
fractured vertebral body is displaced backward & compresses the
spinothalamic pain going up, carrying pain & temperature spinal cord
- fibers from the sacral, lumbar (from the legs) are laterally - HYPEREXTENSION INJURIES the head is in an
located extended position when the force is applied; stress is mainly on
- fibers from the upper extremities, arm, cervical fibers are the posterior elements of the midcervical vertebrae (C4-C6)
medially located which may be fractured; spinal cord damage is caused by sudden
same on motor going down inward bulge of the ligamentum flavum (vertebral column;
- fibers going to the upper extremities medially located posterior ligament; intersegmental)
- fibers from the legs (lumbosacral) for the strength, motor
laterally located
only different is the dorsal column or the posterior column

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WHIPLASH INJURY (TRAUMATIC CERVICAL II. STAGE OF HEIGHTENED REFLEX ACTIVITY
DISTORTION) o Babinski sign
- WHIPLASH OR RECOIL INJURY most often due o Return of DTR hyperreflexia
to vehicular accidents, sudden forward flexion of the neck o Withdrawal reflexes flexor spasms
followed by retroflexion, the occipitonuchal & the o Reflex defecation & urination (automatic
sternocleidomastoids are affected much more often than the emptying of the bladder)
spinal cord or roots o AUTONOMIC DYSREFLEXIA occurs in
response to a certain stimulus such as
B. PATHOLOGY OF TRAUMATIC SPINAL CORD distended bladder; composed of hypertension,
INJURY reflex bradycardia, cutaneous flushing,
- Squeezing or shearing of the spinal cord destruction of headaches; secondary to release of adrenaline
gray & white matter; hemorrhage (traumatic necrosis) from adrenal medulla & norepinephrine from
hematomyelia (nu surgery) disinhibited sympathetic terminals
intramedullary
- Maximal at the level of injury & at 1 or 2 segments above TRANSIENT CORD INJURY (SPINAL CORD
& below CONCUSSION)
- As the lesions heals, it leaves a gliotic focus or cavitation - Recovery within minutes or hours but may persist in
progressive cavitation (traumatic syringomyelia) mild form for days or longer
develops after few months or years - Transient symptoms such as bibrachial weakness,
- In most traumatic lesions, the central part of the cord quadriparesis, paresthesias & dysesthesias
suffers the most - Usually observed in some sports such as football, hockey
& rugby
C. CLINICAL EFFECTS OF SPINAL CORD INJURY
- THREE DISORDERS OF FUNCTION: MANAGEMENT OF SPINAL INJURY
1. Immediate loss of all voluntary movements below - Immobilization of the spine
the lesion - High dose methylprednisolone bolus of 30 mg/kg
2. Sensation below the level of the lesion is abolished followed by 5.4 mg/kg every hour, beginning within 8
3. Reflex functions in segments of the isolated spinal hr of injury & continued for 23 hrs
cord are suspended (spinal shock) deep tendon - Radiologic examinations
reflexes & autonomic reflexes - MRI to see the cord & the nerves
- If with vertebral dislocation, neck traction for
SPINAL SHOCK immobilization & maintain spine alignment use of
- VARIABLE DURATION 1-6 wks or even longer halo brace (4-6 weeks)
1. STAGE OF SPINAL SHOCK - SPINE SURGERY most delay the operations or
o Loss of motor function (quadri- or para- operating only in those with compound wounds or with
plegia), flaccidity progression of neurologic deficits
o Immediate atonic paralysis of the bladder & - The greatest risks to the patient occurs in the 1st 10 days
bowel (gastric dilatation, ileus, shock, infections)
o Gastric atony - Management of bowel & bladder dysfunction
o Loss of sensation below the level of lesion - Prevention of complications of prolonged
o Almost complete suppression of all spinal immobilization such as pulmonary embolism, bed sores
segmental reflexes - Nutrition
o Hypotension - Pain management
o Due to sudden interruption of suprasegmental - Control of spasticity baclofen, diazepam
descending fibers

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III. RADIATION INJURY OF THE SPINAL CORD
- TRANSIENT RADIATION MYELOPATHY
o 3-6 months after radiopathy
o Spontaneous, uncomfortable sensations in the
extremities; may be provoked by neck flexion
- DELAYED PROGRESSIVE RADIATION
MYELOPATHY
o 6 months or more after the radiotherapy
(usually 12-15 months)
o Insidious onset of sensory symptoms
(paresthesias, dysesthesias) followed by
weakness of both legs

IV. SPINAL CORD INJURY CAUSED BY ELECTRIC


CURRENTS & LIGHTNING
- Immediate effects due to direct heating of the nervous
tissue
- Delayed effects may be due to vascular occlusive changes
induced by the electric current
- Temporary effects of the anesthesia on cauda equina
- Transient & asymmetric paraparesis numbness
- More serious & permanent injury of the conus medullaris
is affected immediate ipsilateral leg weakness & numbness
LP: Hit at L3 or L4/L4 or L5
Conus medullaris lower border of L1

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