Chapter 40 Neuro-surgery

8/10/2019 Chapter 40 Neuro-surgery

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pCHAPTER 40 - Neurosurgery

Julian T. Hoff

Michael F. olan!

GENERAL CONSIDERATIONS

A detailed history and a physical examination are the foundation of neurosurical

dianosis! "eadache# altered consciousness# memory impairment# speech difficulty#

$isual distur%ance# &ea'ness# paresthesia# and incoordination are some symptoms

suesti$e of central ner$ous system disease! "istorical details suest a cause (e!!#

traumatic# neoplastic# $ascular# infectious# deenerati$e# or meta%olic) &hile

neuroloic examination permits anatomic locali*ation of the lesion! +or patients &ith

ner$ous system disorders# an accurate history needs to %e ta'en once# %ut the

examination must %e repeated and recorded often to aue the course of the illness

and to ,ude the urency of other dianostic steps!

Dianostic Studies

Once a differential dianosis is formulated usin the information athered from the

history and the examination# dianostic studies are used to confirm the definiti$e

dianosis! Common studies include plain film radioraphy# myeloraphy#

arterioraphy# computed tomoraphy (CT)# manetic resonance imain (-RI)#

ultrasonoraphy (.SN)# electromyoraphy and ner$e conduction $elocity testin

(E-G/NC0)# e$o'ed potentials ($isual# auditory# and somatosensory)# positron

emission tomoraphy (1ET)# electroencephaloraphy (EEG)# and cere%rospinal fluid

(CS+) analysis!

1lain films# especially of the spine# are useful in trauma and deenerati$e disorders!

-yeloraphy# often com%ined &ith CT# is useful for e$aluatin spinal ner$e roots and

the spinal cord in trauma# tumor# and deenerati$e spine disease! CT and -RI pro$ide

detailed imain of %oth cranial and spinal contents! They are useful in com%ination

for $isuali*ation of %one and soft tissues! Arterioraphy pro$ides detailed information

reardin aneurysms# $ascular malformations# and atherosclerotic disease! It is an

essential tool in the e$aluation of cere%ral hemorrhae# em%olic and throm%otic

stro'e# and preoperati$e plannin for tumor surery! .SN is an important ad,unct in

the operatin room# pro$idin $isuali*ation of tumors# cysts# $ascular malformations#

and conenital anomalies lyin %eneath the exposed surface! .SN is also used to

$isuali*e the %rain and spinal cord in ne&%orns!

E-G/NC0 helps to assess peripheral ner$e and ner$e root lesions! It is also used to

monitor %rachial plexus and peripheral ner$e reco$ery follo&in traumatic in,ury!

0isual and auditory e$o'ed potentials can %e employed in comatose patients to

monitor the se$erity of head in,ury! Auditory potentials are useful in e$aluatin

cranial ner$e and %rainstem function! Somatosensory potentials continually monitor

spinal cord (dorsal column) function and are used often durin surical manipulation

of spinal fractures and tumors! 1ET scans play an important role in epilepsy surery#

preem%oli*ation assessment of s'ull %ase tumors in$ol$in the ca$ernous sinus# and

surically untreata%le $ascular anomalies! EEG helps in delineatin structural and

meta%olic disorders and can %e employed durin cere%ro$ascular surery to monitor


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ade2uacy of cere%ral perfusion! CS+ analysis remains essential for many dianoses#

such as %acterial or $iral meninitis!

S1ECIAL SIT.ATIONS

Sei*ures

Sei*ures are useful clinical sins %ecause the aura# onset# and type of sei*ure and thepostictal state may locali*e the lesion! Sei*ures are particularly common in patients

&ith neoplasms! Repetiti$e sei*ures should %e treated $iorously! 1henytoin

(Dilantin) is the dru of choice3 456 to 7666 m may %e i$en I!0! o$er 7 h as a

loadin dose! Supplemental doses usually consist of 766 m i$en three or four times

a day! 1heno%ar%ital is also useful (89 to :5 m# three or four times a day)# %ut larer

doses may depress consciousness! Dia*epam (0alium) i$en intra$enously in di$ided

doses (76 to 56 m) is hihly effecti$e in the control of status epilepticus %ut is not a

ood lon;term anticon$ulsant!

Raised Intracranial 1ressure

Almost any space;occupyin intracranial lesion can raise intracranial pressure (IC1)!Clinical indications of ele$ated IC1 are headache# stupor# diplopia# nausea# $omitin#

and nec' stiffness! Altered %lood pressure and heart rate are late sins3 typically the

%lood pressure is increased and the heart rate is decreased! Apnea may occur if IC1 is

$ery hih! Raised IC1 may %e pre$ented and treated %y the follo&in measures!

"yper$entilation

The 1aCO 9 should %e monitored and maintained at a%out 85 mm"!


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i$en if the infection is life;threatenin! 0ancomycin (7!6 I!0! e$ery 79 h) and

entamicin (45 m I!0! e$ery ? h) are the drus of choice &hile a&aitin culture

results!

Anti%iotics for pre$ention of CNS infection are rarely indicated! In patients &ith

persistent CS+ lea'ae# a %road;spectrum anti%iotic is sometimes used (ampicillin or acephalosporin)!

+luid


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Coma may %e caused %y poisonin# such as alcohol# %ar%iturate# and narcotic

o$erdose3 cere%ral lesions# such as those caused %y trauma# $ascular accidents#

tumors# infections# and epilepsy3 meta%olic disorders# such as dia%etes mellitus#

hypolycemia# Addison>s disease# uremia# hepatic disease# and eclampsia3 and other

stresses# such as se$ere infection# shoc'# asphyxia# heatstro'e# and hypoxia!

Dianostic features of common types of coma are as follo&s!

Acute Alcoholic Intoxication

A history of alcohol a%use# alcoholic %reath# flushed face# slo& and stertorous

respirations# diminished reflexes# and a %lood alcohol le$el a%o$e =66 m/dL esta%lish

this dianosis!

Narcotic 1oisonin

E$en small doses of narcotics may cause respiratory depression and coma in patients

&ith li$er insufficiency# myxedema# emphysema# or head in,uries and in de%ilitated or

elderly patients! +indins include cold# clammy# cyanotic s'in# pinpoint pupils#

respiratory depression# and a fee%le and often irreular pulse!

Acute toxicity caused %y an o$erdose of a self;administered narcotic occurs

commonly in some localities! The type and purity of the dru are difficult to

determine# althouh a companion or ac2uaintance may 'no& the patient>s dru ha%its!

The examiner should loo' for needle mar's in the arms and les! La%oratory tests are

$alua%le to determine %ar%iturate# alcohol# or narcotic le$els!

Dia%etic Coma

Coma may %e precipitated in a dia%etic patient %y infection or %y failure to reulate

insulin dosae carefully! Dianostic features include the follo&in history of

dia%etes# radual onset# &ith %lurred $ision and thirst# air huner or Bussmaul

respiration# dehydration (soft eye%alls)# acetone %reath (fruity odor on %reath)#

lycosuria# acetonuria# hyperlycemia# 'etonemia# and lo& plasma %icar%onate le$el!

"ypolycemia

"ypolycemic reactions in dia%etics may %e precipitated %y failure to eat# %y $iorous

exercise# or %y insulin o$erdose! -ental confusion and %i*arre %eha$ior precede coma

and con$ulsions! Tachycardia# s&eatin# tremors# and $omitin are other

manifestations! Lo& %lood lucose le$el confirms the dianosis!

-anaementEmerency -easures

Identify and treat any life;threatenin condition immediately! Esta%lish and maintain

an air&ay to pro$ide oxyenation! Insert an endotracheal tu%e if the respiratory rate is

less than 76/min# if the 1aO 9 is %elo& 46 mm"# or if the 1aO 9 is reater than 56

mm" &ith the patient %reathin oxyen throuh a mas'! -onitor arterial %lood

ases fre2uently and treat the patient for shoc'! hen no cause for coma is

immediately o%$ious# o%tain %lood for lucose determination and toxicoloic analysis

and then administer each of the follo&in 56 mL of 56@ dextrose in &ater for

possi%le hypolycemia# 7 mL (6!= m) naloxone for possi%le narcotic o$erdose# and

766 m thiamine I!0! for possi%le ernic'e>s (alcoholic) encephalopathy!

General -easures


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O%ser$e the patient fre2uently# record neuroloic and $ital sins at reular inter$als#

and chane the patient>s position often to a$oid postural pneumonia and decu%itus

ulcers! A lateral and slihtly head;do&n position is %est for patients &ho are li'ely to

$omit! A suction machine and an alert attendant near the %edside are essential!

-aintain $entilation and monitor urinary output throuh an ind&ellin catheter!

-aintain fluid# electrolyte# and caloric inta'e! Nasoastric feedin should %e started ifthe coma lasts more than 9 to 8 days! A$oid administerin narcotics# sedati$es# and

other medications until the dianosis is esta%lished3 aitation can then %e treated %est

%y administration of parenteral dia*epam (9 to 5 m I!0! e$ery 9 h as needed)!

TRA.-A

Trauma is the sinle most common cause of death in children# adolescents# and youn

adults! The ma,ority of accidents in$ol$in motor $ehicles and falls include in,ury to

the %rain# spinal cord# and their supportin structures!

Scalp In,ury

Scalp in,ury may cause hemorrhae and su%se2uent shoc' if not promptly treated!


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Depressed s'ull fractures often re2uire surical treatment to ele$ate the depressed

%one framents! If there are no unto&ard neuroloic sins and the fracture is closed#

repair may %e done electi$ely! Intraoperati$ely# the dura should %e inspected and

repaired!

Open s'ull fractures also re2uire surical inter$ention! Linear or stellate#

nondepressed open fractures can %e treated %y simple closure of the scalp after

thorouh cleansin! Open fractures &ith se$ere comminution of underlyin %one

should %e treated in the operatin room# &here thorouh de%ridement can %e carried

out! The dura should %e inspected to $erify that a laceration has not %een o$erloo'ed!

Dural tears should %e closed either primarily or &ith a fascial patch raft to reduce the

ris' of infection and pre$ent CS+ lea'ae! Depressed# open s'ull fractures should %e

de%rided# ele$ated# and closed in the operatin room after preparations ha$e %een

made for craniotomy# in case %roader exposure of the underlyin dura and/or %rain is

necessary!


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and $eins# allo&in extra$asation of %lood and hematoma formation! Cere%ral edema

occurs in response to $asodilatation and %lood; %rain %arrier disruption! Ischemia

from hypotension or hypoxia can produce cell death and conse2uent cytotoxic edema!

Disruption of CS+ a%sorption %y contamination of CS+ &ith %lood may lead to

hydrocephalus! Inappropriate secretion of antidiuretic hormone or the de$elopment of

dia%etes insipidus can ara$ate cere%ral edema %y alterin fluid and electrolyte%alance! These chanes# either separately or in com%ination# can result in ele$ation of

IC1!

Ele$ated IC1 contri%utes to secondary %rain in,ury %y reducin cere%ral perfusion

pressure (C11)# &hich is defined as the difference %et&een mean arterial %lood

pressure (-A


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"ead ele$ation in the neutral position facilitates $enous drainae3 sedation reduces

posturin and com%ati$e acti$ity# %oth of &hich ele$ate IC13 hyper$entilation to 'eep

1aCO 9 around 85 mm" lo&ers cere%ral %lood $olume and IC13 prophylactic use of

anticon$ulsants pre$ents cere%ral in,ury from sei*ures3 mild dehydration &ith

,udicious sodium replacement and prompt treatment of SIAD" (syndrome of

inappropriate antidiuretic hormone secretion) protects the %rain from insult secondaryto fluid o$erload3 pre$ention of hypotension reduces the extension of ischemic in,ury#

and aressi$e treatment of hypertensi$e episodes reduces cere%ral %lood $olume and

further disruption of the %lood;%rain %arrier3 and treatment of hyperthermia a$oids an

increase in the %rain>s meta%olic demands! All of these manaement principles may %e

re2uired simultaneously to achie$e optimal homeostasis of the %rain!

If IC1 remains ele$ated despite these measures# mannitol (6!5 to 7!6 /' I!0!) and

furosemide (7!6 m/') can %e used to reduce cere%ral edema! Deep sedation &ith

narcotics and the use of paralytic aents such as pancuronium may %e helpful!


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lo $enous epidural hematomas usually form only &hen a depressed s'ull fracture

has stripped the dura from the %one and left a space &here the hematoma can de$elop!

Epidural hematoma classically follo&s a %lo& to the head that fractures the s'ull and

causes a %rief period of unconsciousness! After the patient reains consciousness#

there may %e a lucid inter$al durin &hich there are minimal symptoms or sins!hen the hematoma enlares# hemispheric compression occurs! ith time# the medial

portion of the temporal lo%e is forced o$er the ede of the tentorium# causin

compression of the oculomotor ner$e and dilation of the ipsilateral pupil! Similarly#

compression of the ipsilateral cere%ral peduncle causes contralateral hemiparesis#

&hich may proress to decere%rate posturin! Coma# fixed and dilated pupil(s)# and

decere%ration are a classic triad indicatin transtentorial herniation!

E$en thouh epidural hematomas are cura%le lesions# the mortality rate remains hih

%ecause the se$erity of in,ury is often not reconi*ed early! A patient may %e seen

durin the lucid inter$al and dischared! Later# the patient may %ecome unconscious

%ecause of proressi$e %rain compression %y the expandin hematoma!

s examination sho&s no neuroloic deficit# the patient may %e

dischared! An accompanyin person should %e instructed to a&a'en the patient

fre2uently o$er the next 9= h to %e certain that he or she remains arousa%le! Any

deterioration in consciousness should prompt ree$aluation!

Su%dural "ematoma

Su%dural hematomas may de$elop &hen $eins %ridin the cortex and the dura or

$enous sinuses are torn or &hen an intracere%ral hematoma extends into the su%dural

space! They can %e lare e$en thouh the %leedin is of $enous (lo&;pressure) oriin!

Acute su%dural hematomas are associated &ith se$ere head in,ury and arise from a

com%ination of torn %ridin $eins# disruption of cortical $essels# and laceration of the

cortex! The hematoma is %est seen &ith CT scannin! E$acuation of the clot may lead

to sinificant impro$ement# %ut often a ma,or neuroloic deficit remains %ecause of

the accompanyin &idespread parenchymal in,ury!

Su%acute su%dural hematomas %ecome apparent se$eral days after in,ury and are

associated &ith proressi$e lethary# confusion# hemiparesis# or other hemisphericdeficits! Remo$al of the hematoma usually produces stri'in impro$ement!

Chronic su%dural hematomas arise from tears in %ridin $eins# often after a minor

head in,ury! Initially# the hematoma is small! Later# it %ecomes encased in a fi%rous

mem%rane# li2uefies# then radually enlares! These lesions are more common in

infants and the elderly! Typical presentation includes proressi$e mental status

chanes# &ith or &ithout focal sins (hemiparesis# aphasia# etc!)! 1apilledema may %e

present! The dianosis is confirmed %y CT scannin! Treatment consists of hematoma

drainae %y trephination! Craniotomy may %e necessary if the fluid reaccumulates!

Spinal Cord In,ury


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Traumatic in,ury of the spinal cord may result from $erte%ral fracture#

fracture/su%luxation# hyperextension of the cer$ical spine in the presence of a narro&

spinal canal# herniation of inter$erte%ral disc material into the canal# and penetratin

in,uries such as unshots or sta%%ins! Neuroloic in$ol$ement ranes from mild and

transient to se$ere and permanent! Spinal fracture and cord in,ury should %e suspected

in head;in,ured patients# &ith or &ithout coma# and in those patients &ith multiplein,uries! It is %est to assume that the spine is unsta%le initially and immo%ili*e the

patient on a %ac'%oard &ith a hard cer$ical collar until careful examination and

dianostic testin are done!

Clinical findins of spinal or spinal cord in,ury include spinal tenderness# extremity

&ea'ness# num%ness or paresthesia# respiratory em%arrassment# and hypotension!

Spinal root in$ol$ement accounts for radiculopathy# characteri*ed %y motor and

sensory impairment in the correspondin myotome and dermatome (+i! =6;9)! Spinal

cord in$ol$ement produces myelopathy &ith $aria%le manifestations!

A complete lesion# clinically defined as total loss of motor and sensory function %elo&the le$el of in,ury# is associated &ith anatomic or physioloic transection of the cord!

Acute transections are characteri*ed %y areflexia# flaccidity# anesthesia# and

autonomic paralysis %elo& the le$el of the lesion! Arterial hypotension is in$aria%ly

present &hen the transection is a%o$e T5 %ecause of the loss of sympathetic $ascular

tone! Common spinal cord syndromes are sho&n in +i! =6;8!

Incomplete lesions of the cord may result in the


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efforts cease# accountin for this in,ury>s hih mortality at the scene of the accident!

Althouh spontaneous $entilatory efforts can %e initiated &ith in,uries in$ol$in C=H

C:# tidal $olumes are often insufficient# accountin for proressi$e hypoxia and

car%on dioxide retention! Air&ay o%struction# atelectasis# and pneumonia are common

complications! Assisted $entilation is often re2uired early after in,ury!

Ileus &ith astric distention is common# necessitatin nasoastric drainae! Similarly#

%ladder distention occurs %ecause the %ladder and pel$ic floor muscles are flaccid!


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is reduced# traction should %e maintained! +re2uent follo&;up films are then ta'en to

confirm correct alinment!

Sometimes a cer$ical fracture cannot %e reduced %y traction alone &ithout

,eopardi*in spinal cord function! Open reduction# usually throuh a posterior

approach# com%ined &ith a fusion procedure may %e necessary in those instances!This especially pertains to unilaterally or %ilaterally loc'ed facets!

1atients &ith thoracic and lum%ar spine fractures are also treated &ith immo%ili*ation

initially! Immo%ili*ation is less strict compared &ith that for cer$ical fractures# %ut the

principles are the same! 1atients are 'ept flat in %ed &ithout traction &hile flexion#

extension# lateral %endin# and rotational mo$ements are a$oided! They typically ha$e

fe&er systemic complications associated &ith their neuroloic in,ury %ut ne$ertheless

re2uire $iilance to pre$ent neuroloic deterioration and pro$ide the %est chance for

neuroloic reco$ery!

Indications for early operation in patients &ith spinal cord in,ury include ina%ility toreduce the fracture/dislocation satisfactorily %y closed methods# neuroloic

deterioration in a patient &ith an incomplete cord lesion initially# se$ere compression

of the spinal cord %y an intraspinal mass sho&n %y myeloraphy or -RI# and a

penetratin in,ury &ith or &ithout a CS+ lea'! Open &ounds# such as those inflicted

%y sta%%ins or unshots# should %e de%rided and closed &hether the cord in,ury is

complete or incomplete! Early operation to sta%ili*e the spine is &arranted %ecause

this translates into early mo%ili*ation and reha%ilitation! Either the anterior or the

posterior approach may %e used# dependin on the nature of the spinal in,ury and the

deree of insta%ility!

If closed reduction is successful and the fracture is sta%le# external immo%ili*ation is

necessary for a minimum of 8 months to ensure proper healin! If surical reduction

and/or fixation is necessary# external immo%ili*ation is still indicated! +or the cer$ical

spine# this in$ol$es a halo $est! Certain exceptions include anterior and posterior

metal platin procedures in &hich a hard cer$ical collar may suffice (+i! =6;:)! The

thoracic and lum%ar spine usually re2uire a plastic %ody ,ac'et or plaster cast for a

minimum# once aain# of 8 months! 1lain films are used to follo& spinal alinment

and the extent of fusion durin the reco$ery period!

If any cord function is preser$ed immediately after in,ury# additional function usually

returns# pro$ided the cord and spine are protected from secondary in,ury! 1atients &ithcomplete in,uries rarely reco$er function %elo& the le$el of the lesion! Reha%ilitation

for them is directed to&ard self; care and $ocational read,ustment! -ost persons &ith

these handicaps can e$entually achie$e independence! Life expectancy is shortened

slihtly in parapleics and sinificantly in 2uadripleics! Lon;term pro%lems

associated &ith s'in care and recurrent urinary tract infections account for the early

mortality rate!

1eripheral Ner$e In,ury

1eripheral ner$e in,uries may %e cateori*ed functionally! Neurapraxia is a temporary

loss of function &ithout axonal in,ury! Structural damae does not occur! The foot that

oes to sleep after crossin the les is an example of functional loss &ithoutpatholoic chane! Axonotmesis is disruption of the axon &ith preser$ation of the


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axon sheath! allerian deeneration of the distal axon frament occurs! Stretch or

proloned compression causes this functional and structural loss! Reeneration of the

proximal axon occurs# %ut functional reco$ery depends on associated in,uries# the

amount of healthy proximal axon remainin after in,ury# and the ae of the patient!

Neurotmesis is disruption of %oth the axon and axon sheath &ith correspondin loss

of function! Transection of a ner$e causes this phenomenon! Reeneration occurs# %utfunction rarely returns to normal!

Clinically# sensory and motor chanes correspond to the peripheral ner$e in$ol$ed! A

detailed history and a precise neuroloic examination can locali*e the site of in,ury

&ith reat accuracy! Sensory findins are usually apparent early and remain so until

reeneration is nearly complete! Compensatory motor function# often seen in the hand

months after in,ury# is rarely seen acutely! A crude %ut clinically helpful sin of

sensory reeneration is Tinel>s sin! 1ercussion of the s'in o$erlyin the lenth of the

in,ured ner$e elicits paresthesias at the site &here reeneration is occurrin!

Radioraphs of the in,ury site are helpful to loo' for fracture or forein %ody!Electromyoraphy (E-G) is not useful &ithin the first 8 &ee's of in,ury# %ut this

dianostic aid %ecomes hihly effecti$e to follo& the state of the

deeneration/reeneration process occurrin later! -anaement decisions are often

made dependin on E-G findins &ee's to months after trauma!

Treatment

Treatment of a lacerated ner$e consists of primary repair &hen the &ound is clean and

uncomplicated# as in sta% &ounds# lacerations from lass# and surical incisions!

Secondary or delayed repair is indicated &hen the &ound is dirty or complicated# as in

unshot &ounds and a$ulsions# &hich disrupt tissue se$erely# ma'in primary repair

less successful! Secondary repair is %est accomplished a fe& &ee's after in,ury# &hen

tissue $ia%ility is o%$ious# the li'elihood of infection is reduced# and dissection planes

are distinct! If end;to;end anastomosis of ner$es is not possi%le %ecause of tissue loss#

ner$e raftin usin autoloous sural ner$e may %e done! Intraoperati$e factors such

as axial orientation of fascicles# proper coaptation# suture material# hemostasis# and

suture line tension determine the outcome!

Ner$e in,uries in continuity (i!e!# resultin from contusion or compression &ithout

laceration) are often explored if they do not impro$e &ithin : &ee's of in,ury#

&hether loss of function is complete or incomplete! Intraneural and extraneural scar

tissue at the site of the lesion may pre$ent axonal rero&th %y its constrictin effect!Neurolysis releases the reeneratin ner$e fi%ers from the impinin scar and may

impro$e functional reco$ery!

1rompt institution of physical therapy is also indicated for impro$ement of muscle

function and maintenance of ,oint motion! It is the %est means of minimi*in the

complications of dener$ation! The dener$ated portion of the lim% is su%,ect to muscle

atrophy and fi%rosis# ,oint stiffness# motor endplate atrophy# and trophic s'in chanes!

The loner the dener$ation persists# the less li'ely &ill ood function result!

Reeneration in a peripheral ner$e occurs at 7 mm/day (rouhly 7 inch per month)# so

impro$ement may not %e o%$ious for many months! +actors that ad$ersely affect thereturn of function include ad$anced ae of the patient# proximal ner$e in,ury#


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extensi$e ner$e tissue loss# associated soft tissue in,ury# and presence of mixed

sensorimotor function deficits! .nfortunately# incomplete neuroloic reco$ery is often

the rule! The use of tendon transfers should %e considered to impro$e functional

outcome if neuroloic function is inade2uate after reco$ery has ceased!

NEO1LAS-SNer$ous system tumors represent almost 76 percent of all neoplasia! Of these# 75 to

96 percent occur in children! Nearly 46 percent of adult tumors are found a%o$e the

tentorium (supratentorial)# &hereas 46 percent of childhood tumors are found %elo&

(infratentorial)! CNS tumors are the most common solid tumors in children! Of all

pediatric cancers# they are second in incidence only to leu'emia!

The incidence of ner$ous system neoplasia decreases in the late teen years and %eins

to pea' aain %y middle ae!


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In eneral# a symptomatic# solitary lesion that is surically accessi%le should %e

remo$ed! Surery# ho&e$er# should not %e underta'en for multiple lesions or in

patients &ho are se$erely afflicted %y their primary disease! Treatment should also

include preoperati$e dexamethasone# as in any %rain or spinal cord tumor# to reduce

ad,acent %rain edema! hole %rain irradiation is almost al&ays indicated! 1ronosis

depends on tumor type# &ith the median sur$i$al ranin from 7 to 9 years! Lon;term sur$i$ors ha$e %een reported &ith surical remo$al of solitary %rain metastases!

uality of life is almost al&ays impro$ed! There is little e$idence that chemotherapy

plays a sinificant treatment role!

Tumor metastasis to the leptomenines (menineal carcinomatosis) is also 2uite

common# particularly in the childhood leu'emias and in adults &ith lymphoma# %reast

and lun cancers# and melanoma! 1atients may present &ith cranial ner$e palsies#

radiculopathies# or o%structi$e hydrocephalus! They often ha$e sins and symptoms

suesti$e of meninitis! Analysis of the CS+ is usually critical# often re$ealin an

increased openin pressure# an ele$ated &hite cell count and protein le$el# and a

decreased lucose le$el! There may or may not %e identifia%le malinant cells# %utcytoloic examination should al&ays %e done!

Treatment of menineal carcinomatosis usually in$ol$es radiation therapy and

intra$entricular chemotherapy! -ethotrexate is a common chemotherapeutic aent!

The outloo' for patients &ith leptomenineal tumor spread is enerally poor# %ut

aain a fe& lon;term sur$i$ors emere!

Spinal Tumors

Spinal tumors constitute approximately 96 percent of all CNS tumors! They are

classified as intradural or extradural! Of the intradural $ariety# ?= percent are outside

the spinal cord (extramedullary) and 7: percent are &ithin it (intramedullary)!

Intradural tumors are almost al&ays primary CNS tumors# &hereas the ma,ority of

extradural tumors are either metastatic or primary %one tumors! The ma,ority of

intradural spinal neoplasms are %enin and can often %e excised surically! Tumors

occurrin &ithin the cord (intradural# intramedullary) tend to produce &ea'ness#

spasticity# and sensory loss! Extramedullary lesions present &ith radicular pain from

ner$e root (lo&er motor neuron) compression as &ell as &ith lon tract (upper motor

neuron) sins from cord compression! 1atients &ith lesions in$ol$in the conus

medullaris reion may ha$e early loss of %ladder and %o&el function3 those &ith

lesions in the cauda e2uina present primarily &ith le pain and only later de$elop

sphincter distur%ances!

The definiti$e study for spinal tumors is -RI# althouh a%normalities on plain films

and myelorams may %e dianostic! 1lain films may sho& &idenin of the

interpeduncular distance# %ony erosion# enlarement of neural foramina# or a

paraspinous mass! -yeloraphy helps to determine the tumor>s relationship to the

spinal cord and dura! 1ostmyeloram CT can further define that relationship!

Neurilemoma and Neurofi%roma

Typically %enin# these are the most common spinal cord tumors# comprisin almost

86 percent of the total! They are usually intradural# extramedullary in location! Of

these# 78 percent ha$e extradural extension throuh an ad,acent foramen# producinthe classic dum%%ell shape of the tumor! +ourteen percent are totally extradural! The


16/43

extradural component tends to enlare the in$ol$ed foramen! Treatment is surical

remo$al! -ultiple neurofi%romas are associated &ith $on Rec'linhausen>s

neurofi%romatosis! In these instances# only symptomatic tumors should %e remo$ed!

-eninioma

-eniniomas constitute 9: percent of spinal cord tumors# are %enin# and are usuallyintradural# extramedullary (+i! =6;79)! +ifteen percent occur extradurally! T&o;thirds

arise in the thoracic spine# affectin &omen in their fourth throuh sixth decades in ?6

percent of cases! Surical excision is the treatment of choice!

Ependymoma

Arisin from the ependymal cells of the central canal of the cord# these intramedullary

tumors constitute 78 percent of all spinal cord tumors! They occur more fre2uently in

males! Nearly :6 percent are found in the conus medullaris reion! Ependymomas

should %e surically excised! Their distinct %orders often allo& complete resection3

&hen total remo$al is not possi%le# radiation therapy is usually employed!

Astrocytoma

These lial tumors are deri$ed from astrocytes and are often intramedullary! Their

incidence is a%out the same as that of spinal ependymomas! Total excision is rarely

possi%le due to their infiltrati$e nature! Lo&;rade astrocytomas# if recurrent# are

usually reoperated! Radiation therapy is reser$ed for the malinant astrocytomas# %ut

this is usually only palliati$e! hile the ro&th rate of spinal cord astrocytomas is

slo pronosis is enerally poor!

Lipoma

Lipomas constitute 76 percent of spinal tumors and are often associated &ith spina

%ifida and a su%cutaneous lipoma! Althouh %enin# they tend to %e intert&ined &ith

cord tissue and are usually only partially excised! These do not re2uire radiation# and

the mortality is lo&!

Dermoid

Dermoids are conenital lesions usually found in the lum%osacral area! They often

ha$e an associated sinus tract to the s'in surface and may present &ith infection! The

treatment is surical resection# includin the sinus tract! The resection of the portion

enterin the spinal cord is usually incomplete! The lon;term pronosis is ood!

-etastatic Tumor.p to 95 percent of all spinal neoplasms are metastatic in oriin and most appear in an

extradural location (+i! =6;78)! Common primary sites include %reast# lun# prostate#

and 'idney! If the primary site is not 'no&n or if the neuroloic decline is rapid#

treatment is surical decompression &ith %iopsy! Other&ise# local radiation therapy is

the treatment of choice! Other extradural malinant tumors include lymphoma#

myeloma# plasmacytoma# chordoma# and osteoenic sarcoma! hen sinificant %one

destruction or the surical decompression renders the spine unsta%le# surical

sta%ili*ation throuh an anterior or posterior route is often necessary!

1eripheral Ner$e Tumors

The peripheral ner$ous system includes the peripheral and cranial ner$es# spinal roots#and autonomic ner$ous system! Tumors can arise from any of these elements! The


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The most common cause of stenosis or occlusion of lare $essels is atherosclerosis!

This disease often de$elops extracranially at the oriin of the internal carotid artery in

the nec' %ut may occur in the carotid siphon (that portion of the artery &ithin the

ca$ernous sinus)# the distal internal carotid# or e$en the proximal middle cere%ral

artery (+i! =6;7=)!

Arterial em%oli usually oriinate either from atherosclerotic ulceration in the reion of

the carotid %ifurcation or from sources &ithin the heart! The heart is a common source

of em%oli &hen a mural throm%us forms after a myocardial infarction or as a result of

atrial fi%rillation! Other ris' factors for cere%ral ischemia include hypertension#

dia%etes# hypercholesterolemia# o%esity# smo'in# and family history of stro'e!

Since there is no effecti$e medical or surical therapy for a completed stro'e# the oal

of neurosurical inter$ention is to identify stro'e;prone patients and reduce their ris'

of cere%ral ischemia! These hih;ris' patients are %est identified %y a history of

transient ischemic attac's (TIAs)# &hich ta'e the form of either transient cere%ral

ischemia or amaurosis fuax! Transient cere%ral ischemia in the carotid circulationusually consists of temporary hemianesthesia# hemiparesis# or aphasia! Amaurosis

fuax is transient loss of $ision in one eye! Ischemia in the $erte%ro%asilar system

may cause transient diplopia# di**iness# dysarthria# dysphaia# &ea'ness# num%ness#

loss of $ision# or e$en loss of memory!

-ost ischemic episodes last seconds to minutes and rarely loner than 86 min! As

lon as the neuroloic deficit resol$es &ithin 9= h# the episode is# %y definition# a

TIA! A re$ersi%le ischemic neuroloic deficit (RIND) is one that lasts 9= h to 8

&ee's! Ischemic deficits lastin loner are considered completed stro'es! Careful

2uestionin of indi$iduals &ith completed stro'es re$eals that :6 percent had a prior

history of TIAs# 96 percent presented in a slo step&ise fashion# and only 96 percent

&ere sudden in onset!

1atients &ith TIAs or slo&;onset stro'es are potential candidates for pre$enti$e

surical inter$ention! Surical procedures to pre$ent stro'e are directed to&ard either

remo$al of the source of em%oli or aumentation of %lood flo& to the %rain!

Operations for these conditions include carotid endarterectomy and micro$ascular

%ypass! 1otential candidates enerally undero a CT or -RI scan of the %rain to

e$aluate any deree of cere%ral infarction and to rule out other dianoses such as

tumor# su%dural hematoma# or su%arachnoid hemorrhae! 1atients then undero

anioraphy# includin the aortic arch and the carotid# $erte%ral# and cere%ral arteries!Nonin$asi$e studies of the carotid circulation are less accurate# althouh they are

useful as screenin procedures %ecause of their lo& ris'!

Carotid endarterectomy is indicated &hen ipsilateral symptoms of cere%ral ischemia

or amaurosis fuax exist and anioraphy demonstrates either sinificant stenosis

(usually more than 45 percent) or ulceration in the accessi%le portion of the common

and/or proximal internal carotid arteries (+i! =6;75)! The procedure consists of

openin the affected portion of the carotid artery under systemic heparini*ation and

remo$in the atherosclerotic pla2ue! The mortality from carotid endarterectomy is

a%out 7 percent and the neuroloic mor%idity 5 percent in experienced hands!


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A num%er of patients present &ith cere%ral ischemia ipsilateral to an occluded internal

carotid artery or &ith stenosis of the internal carotid or middle cere%ral artery that is

not surically accessi%le! +or these patients &ith inade2uate collateral cere%ral

circulation# a micro$ascular %ypass procedure is sometimes indicated! The most

common of these is the superficial temporal artery to middle cere%ral artery

anastomosis (STA; -CA)!

"n#racranial Aneurys$Intracranial aneurysms are diseased dilatations of the cere%ral arteries# their &alls

consistin of %allooned;out tunicae intima# media# and ad$entitia &ith a $aria%le

deree of intraluminal or mural throm%us! -ost are conenital in oriin# e$ol$in and

de$elopin durin life! They may %ecome atherosclerotic! Aneurysms are typically

found at the %ifurcation of the ma,or $essels of the circle of illis! .p to 96 percent

of patients &ith aneurysms ha$e multiple aneurysms# and 7 percent demonstrate an

associated arterio$enous malformation (A0-)! If aneurysms are found more

peripherally in the cere%ral $asculature# secondary causation such as trauma or

infection should %e considered!

O$er ?5 percent of cere%ral aneurysms occur in the carotid or anterior circulation!

Approximately 86 percent arise from the intracranial portion of the internal carotid

artery# usually at or near the oriin of the posterior communicatin artery! Another 86

percent occur in the reion of the anterior communicatin artery! A%out 95 percent

arise from the middle cere%ral artery# usually at its first ma,or %ranch point# &hich is

commonly a trifurcation! Aneurysms of the $erte%ro%asilar or posterior circulation

are most fre2uently found at the tip of the %asilar artery %ut may occur more

proximally alon its trun'! The oriin of the posterior inferior cere%ellar artery is the

next most common location!

1atients &ith intracranial aneurysms most commonly present &ith sins and

symptoms of su%arachnoid hemorrhae (SA")! Eihty percent of nontraumatic

su%arachnoid hemorrhaes are caused %y aneurysm rupture! The patient notes a

sudden se$ere headache commonly follo&ed %y nec' stiffness and photopho%ia due to

associated menineal irritation caused %y the su%arachnoid %lood! Transient loss of

consciousness may occur! Some patients may de$elop a focal neuroloic deficit or

%ecome comatose as a result of the acute rise in intracranial pressure! The se$erity of

the SA" can %e raded# as sho&n in Ta%le =6;8! In eneral# the lo&er the rade# the

%etter the outcome!

Not all patients &ith aneurysms present &ith symptoms related to rupture! Throuh

mass effect# an internal carotid artery (ICA) aneurysm may compress the optic (IId)

ner$e (+i! =6;7: A#


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Arterio$enous malformations (A0-s) occur &ithin the central ner$ous system as

conenital a%normalities that allo& %lood to %e shunted directly from arteries to $eins#

%ypassin the normally interconnectin capillary %ed! These malformations may %e

2uite small &ith only a sinle feedin artery# or they may encompass se$eral lo%es of

the %rain and arterial feeders from multiple sources! They may occur in $irtually any

portion of the %rain# includin the cere%ellum and %rainstem! In the cere%ralparenchyma# &here they are most commonly located# the lesion ta'es on a conical

shape# &ith the apex deep# often reachin the lateral $entricle! Rarely# A0-s occur

&ithin the spinal cord# and they may exclusi$ely in$ol$e the dura either intracranially

or &ithin the spinal canal!

1atients &ith A0-s tend to de$elop symptoms %efore ae thirty! The most common

initial presentation is hemorrhae (56 percent of cases and 76 percent of all

intracere%ral hemorrhaes# second only to aneurysms)!


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treatment decision is more difficult in the patient &ho presents &ith sei*ures! If the

patient is youn and the malformation is readily accessi%le# surical resection is

usually recommended# especially &hen the sei*ures are medically refractory!

Operation in$ol$es the microsurical dissection and resection of the entire

malformation# rather than simple liation of feedin arteries! The results of operation

are related to the si*e and location of the malformation! O$erall# the operati$emortality is less than 5 percent and the mor%idity less than 76 percent!

Alternati$e or ad,uncti$e methods of treatment include intraarterial em%oli*ation and

radiation therapy! .sin inter$entional neuroradioloic techni2ues# particulate matter

or lues may %e introduced into A0-s $ia feedin $essels to occlude the $ascular

shunt nidus! It is rarely possi%le to o%literate these lesions completely &ith this

method# ho&e$er! This techni2ue ne$ertheless can reduce flo& throuh the A0- prior

to direct surical inter$ention!

Ioni*in radiation# on the other hand# has the capa%ility of completely o%literatin

selected small; to medium;si*ed A0-s! +ocused amma or proton %eam irradiationhas demonstrated efficacy# and occasional success &ith con$entional irradiation has

%een reported! Ioni*in radiation causes endothelial proliferation and may ta'e :

months to 9 years to o%literate the lesion! +ocused irradiation is recommended for

deep# surically inaccessi%le A0-s!

"n#racere&ral He$orrhage

Spontaneous hemorrhae is most commonly associated &ith systemic hypertension

and occurs in predicta%le locations# includin the putamen# thalamus# cere%ellum# and

pons! "emorrhae can also occur &ithin the $arious lo%es of the %rain!Nonhypertensi$e causes of %rain hemorrhae ha$e %een discussed a%o$e# such as

rupture of A0-s and aneurysms and hemorrhae into areas of ischemia! Additional

causes include induced or endoenous coaulopathies# primary or metastatic %rain

tumors# and rare conditions such as amyloid aniopathy!

Chronic hypertension results in lipohyalinosis of the $essel &all# &hich sets the stae

for either $ascular occlusion or rupture! Occlusion results in infarction# and rupture

produces an intracere%ral hemorrhae! The shorter penetratin arteries of the %rain

appear to %e the most $ulnera%le! The lenticulostriate and thalamoperforatin $essels

are in$ol$ed in putaminal and thalamic hemorrhaes# and affected %asilar %ranches

contri%ute to pontine hemorrhae!

Althouh %rain hemorrhae is often de$astatin# it may %e surprisinly &ell tolerated!

The hematoma tends to dissect alon axonal planes# separatin rather than destroyin

$ital structures! If the resultant mass is tolerated %y the patient# the %lood is slo&ly

resor%ed %y macrophaes alon the periphery# lea$in only a hemosiderin;stained slit

in the %rain! 1atients may &orsen clinically anytime after the initial hemorrhae as a

result of associated edema formation!

"emorrhae into the putamen accounts for the ma,ority of hypertensi$e hematomas!

1resentation is characteri*ed %y the lac' of headache &ith radual de$elopment of

hemiparesis proressin to hemipleia! This may %e associated &ith a hemisensoryloss# aphasia# hemianopia# and/or ipsilateral de$iation of the eyes# dependin on the


23/43

si*e of the hematoma and its direction of dissection! The patient may# of course#

proress into coma if the lesion is lare! Similarly# thalamic hemorrhae presents

initially &ith a hemisensory loss and hemiparesis! Locali*in features include

do&n&ard eye de$iation &ith limitation of $ertical a*e and small# sluish pupils

due to in$ol$ement of the near%y mesencephalon! "eadache is uncommon!

Cere%ellar hemorrhae is sudden in onset and presents &ith headache! 0omitin#

ataxia# and di**iness are accompanyin features! This hemorrhae is extremely

danerous in that it may cause coma and ultimately death due to %rainstem

compression and acute hydrocephalus!


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L5) more medially# ma'in that root more $ulnera%le to disease in$ol$in that disc

(+i! =6;7F)!

Inter$erte%ral Disc Disease

If the nucleus of an inter$erte%ral disc extrudes (herniates) throuh the anulus#

ad,acent neural structures may %e compressed! In the cer$ical and thoracic spine#compression of the spinal cord may result in paraparesis or 2uadriparesis# dependin

on the spinal sement in$ol$ed! At all le$els# compression of a spinal root may cause

&ea'ness and sensory loss in structures inner$ated %y that root! The se$erity of the

clinical syndrome depends on the site and se$erity of compression %y the displaced

disc frament! In some cases the anulus and ad,acent liament hold# pre$entin

complete extrusion of the framented disc! The anulus may only stretch sufficiently to

allo& the disc to %ule into the spinal canal or foramina# accountin for %ac' and le

pain# %ut often &ithout neuroloic deficit!

Often the nucleus does not extrude# %ut simply framents in response to the forces

exerted on the spinal column! This is intensified %y the concomitant dehydration andloss of elasticity of the disc as it aes! The disc space radually narro&s# the ,oint

%ecomes loose# and the cartilainous endplates of the ad,acent $erte%ral %odies a%ut

and &ear more 2uic'ly!


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&hich accompanies cardiac disease! Spinal infections# conenital lesions# and

posttraumatic disorders are other important considerations!

1lain radioraphs typically demonstrate loss of the lordotic cur$e of the cer$ical

spine# &ith narro&in of one or more disc spaces! Osteophyte formation may %e seen!

In cer$ical spondylosis# there is usually radioloic e$idence of osteophytes and discspace narro&in at multiple le$els! In most cases# the anterior;posterior diameter of

the cer$ical spinal canal is narro&ed! -yeloraphy &ith CT is $ery useful in the

dianostic &or'up of ner$e root compression! The use of intrathecal contrast medium

enhances the po&er of CT to delineate the lesion! -RI is suita%le for in$estiatin

myelopathies! In addition to definin the compressi$e lesion# -RI often sho&s

intrinsic cord a%normalities related to compression! Electromyoraphy may confirm

the dianosis and locali*e the lesion more specifically# particularly &hen

myeloraphic defects are multiple!

Treatment

1ainful cer$ical disc disease may %e treated medically as lon as there is no e$idenceof a proressi$e neuroloic deficit (motor loss and %o&el and %ladder dysfunction

%ein most important)! Ade2uate medical therapy includes immo%ili*ation of the nec'

&ith a soft or hard cer$ical collar# analesics# muscle relaxants# and local heat! These

methods# in association &ith a ood physical therapy proram# pro$ide relief under

most circumstances!

.p to 45 percent of patients &ith cer$ical disc disease impro$e follo&in an ade2uate

trial (76 to 7= days) of medical therapy! Some ha$e recurrence of radicular symptoms

on return to full acti$ity! In many cases# these patients can %e manaed for years &ith

intermittent cer$ical traction and a cer$ical collar# %ut some re2uire surical therapy!

+or the 95 percent &ho do not respond to conser$ati$e means# operation is often

helpful!

There are t&o approaches for the surical treatment of cer$ical disc disease!

Anteriorly# ner$e roots# spinal cord# or %oth may %e decompressed throuh discectomy

&ith or &ithout %one raft fusion! The other approach is posteriorly throuh a

laminectomy and/or foraminotomy! The choice of operati$e direction is %ased on

consideration of the patient>s anatomic lesion! Impro$ement follo&s operati$e

treatment of symptomatic cer$ical disc disease %y either approach in approximately

?6 percent of patients &ho fail to respond to medical treatment! Surical treatment of

cer$ical spondylotic myelopathy results in impro$ement in most cases! Arrest of theproressi$e myelopathic deficit usually occurs!

Lum%ar Disc Disease

"erniated lum%ar discs often produce some deree of ner$e root compression! The

se$erity of the syndrome depends on the deree of root compression! Occasionally#

the entire cauda e2uina may %e in$ol$ed# resultin in loss of motor and sensory

function# includin %o&el and %ladder sphincter control! Sometimes disc rupture may

occur in the midline# compressin centrally positioned sacral roots preferentially#

&ithout in$ol$ement of laterally placed lum%ar roots!

+ramentation of a lum%ar disc may occur &ithout extrusion of the nucleus pulposusas descri%ed a%o$e for cer$ical disc disease!


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disc# mo%ility of the inter$erte%ral ,oint is increased! The anulus fi%rosus may simply

%ule &ithout tearin! ith time# osteophytes may form around the deenerated disc

and encroach on the spinal canal and neural foramina! This deenerati$e hypertrophy

in$ol$es the liamentous structures as &ell! Stenosis of the lum%ar spinal canal is the

e$entual result# a spondylotic condition common in the elderly!

In the lum%ar spine# o$er F6 percent of clinical pro%lems arise from the L=HL5 and

L5HS7 inter$erte%ral discs! 1ain is usually chronic# %ut its onset may %e acute &hen

associated &ith fran' herniation! There may %e %ac' pain# le pain# or %oth! Radiation

of lo& %ac' pain into the %uttoc'# posterior thih# and calf is usually the same &ith

disease at the L=HL5 and L5HS7 le$els! This radiatin pain may %e exacer%ated %y

couhin# snee*in# or strainin!


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similar fashion# often successfully! Surical treatment is reser$ed for the patient &ith

an acute or proressi$e neuroloic deficit# chronic disa%lin pain# or %oth! The acute

onset of &ea'ness or sphincter distur%ance constitutes an emerency# demandin

prompt dianosis and early operation!

Operation usually entails a unilateral laminotomy &ith remo$al of the offendin discframent! +oraminotomy may %e necessary in the presence of osteophyte formation!

ith lum%ar stenosis# multile$el laminectomy is curati$e! Should plain films

demonstrate any insta%ility preoperati$ely# com%inin the laminectomy &ith posterior

fusion# either &ith or &ithout instrumentation# is enerally indicated! If the imain

studies demonstrate an extruded disc frament that accounts for the clinical sins and

symptoms# ?5 to F6 percent of patients reco$er &ith surical treatment! If the

syndrome is atypical# the myeloram e2ui$ocal# and the patient poorly moti$ated#

operation is less effecti$e! Emotional factors# psycholoic distur%ances# litiation# and

industrial in,ury play an important role in the e$entual outcome# &hether the treatment

is medical or surical! Alternati$es to the laminotomy approach include percutaneous

discectomy done %y endoscopic excision of the pro%lematic nucleus pulposus!Clinical results for the alternati$e approaches are less predicta%le!

IN+ECTIONS

The central ner$ous system may %e infected %y $iruses# %acteria# funi# and parasites!

De$elopment of infection depends on the host>s resistance (i!e!# immune defenses) and

on the infectin aent>s $irulence!


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and anaero%ic streptococci! Occasionally# ram;neati$e oranisms and funi are

responsi%le! Treatment consists of drainae# de%ridement of infected %one# and

appropriate anti%iotics for a proloned period# usually : &ee's!

Epidural A%scess

Spinal epidural a%scess is much more common than intracranial epidural a%scess! It ischaracteri*ed %y fe$er# local spinal tenderness# and rapid proression of neuroloic

deficits# often constitutin a medical and surical emerency! Radicular pain and

impairment of cord function# &ith early motor and sensory deficits includin sphincter

distur%ances# occur &ithin a fe& days! -ost epidural a%scesses are caused %y local

extension of osteomyelitis or %y hematoenous spread from a distant suppurati$e

focus! The dianosis is suested %y the clinical presentation! The CS+ often has a

mar'edly ele$ated protein le$el &ith mild pleocytosis! -RI defines the extent of the

epidural mass! If the dura is intact# infection rarely extends across it!

The most common causati$e oranisms are Staphylococcus aureus and the

streptococci! Treatment should %e immediate# %einnin &ith %road anti%ioticco$erae until the offendin aent is identified! Specific anti%iotic therapy should %e

continued for a proloned period# often up to : &ee's! Surical drainae is necessary

&hen neuroloic deficits proress despite aressi$e medical therapy! Corticosteroids

in the perioperati$e period are %eneficial in reducin locali*ed edema# althouh

proloned use can reduce the host immune response to the infection! Reco$ery of

neuroloic function is directly related to the duration and se$erity of impairment

%efore treatment!

Su%dural Empyema

Su%dural empyema is a purulent infection of the su%dural space! It accounts for

approximately 95 percent of all intracranial infections and is usually a complication of

sinusitis# meninitis# or open contamination of the su%dural space at operation or after

trauma!

ith sinusitis# infection can spread intracranially %y transcranial emissary $ein

throm%ophle%itis! Staphylococci# streptococci# and anaero%ic cocci are commonly

responsi%le! Once the su%dural space is $iolated# infection can spread o$er the

con$exity of the %rain! The accumulation of purulent material may %e sufficient to

produce an intracranial mass# pro$o'in ad,acent %rain s&ellin! The clinical result is

rapid neuroloic deterioration# often &ith laterali*in sins# coma# and death!

Treatment includes craniotomy &ith de%ridement# drainae# and intra$enousanti%iotics! The source of the infection must %e treated aressi$ely! A sinus or

mastoid drainae procedure is often re2uired if this is the source! -ortality from acute

fulminant su%dural empyema from a paranasal source remains a%out 95 percent!

The dianosis of intracranial su%dural empyema is made readily %y CT or -RI scan#

%ut it may %e difficult to distinuish from su%acute or chronic su%dural hematoma!

The mass itself may %e isodense# necessitatin the administration of intra$enous

contrast! Includin the sinuses on the scan may demonstrate the source of infection!

Lum%ar puncture to o%tain CS+ for analysis ris's transtentorial herniation3 thus L1

should %e a$oided if the scan sho&s sinificant mass effect!


30/43

Spinal su%dural empyema is rare! It usually de$elops from local extension

transdurally or throuh the arachnoid in the presence of meninitis! Spinal cord

compression and trans$erse myelitis may de$elop! Treatment is emerent# consistin

of surical drainae and proloned anti%iotic administration!

-eninitis


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Complications of %acterial meninitis include communicatin hydrocephalus# %rain

a%scess# su%dural empyema# and su%dural effusions# particularly after "! influen*ae

meninitis in infants! The ris' of complications is sinificantly reduced %y prompt#

early treatment!

rain A&scess


32/43


33/43

infestation! Anticon$ulsants# CS+ shuntin# and occasional remo$al of symptomatic

cysts are additional treatment options!

Echinococcosis"ydatid disease is caused %y Echinococcus ranulosus# the do tape&orm! It ispre$alent in southern South America# northern and eastern Europe# Australia# Africa#

China# and the -iddle East! "umans may ser$e as intermediate hosts %y inestin the

lar$ae! The li$er and luns are preferentially in$ol$ed throuh hematoenous

dissemination &ith su%se2uent formation of hydatid cysts! hen the CNS is in$ol$ed#

cysts are usually solitary# lare# and confined to &hite matter! There is a nelii%le

inflammatory response!

-ost cysts produce sins and symptoms related to their mass effect! Dianosis of the

infection is made seroloically! CT and -RI of the %rain and ultrasonoraphy of the

li$er and spleen may %e definiti$e! Chest x;ray often sho&s calcified pulmonary cysts!Treatment consists of patient isolation from the source and surical remo$al of

symptomatic cysts! Care must %e ta'en to remo$e the intact cyst to a$oid seedin &ith

$ia%le lar$ae! "ydatid disease of the CNS is disa%lin# %ut rarely fatal# pro$ided cysts

are remo$ed &hen they %ecome symptomatic!

C+N(EN"TA, AN' 'E)E,+PMENTA, AN+RMA,"T"E*Approximately 9 percent of ne&%orns possess some type of conenital a%normality!

Sixty percent of these in$ol$e the central ner$ous system# and o$er half of those are

related to defecti$e de$elopment or closure of the dorsal midline structures! -any

ha$e associated hydrocephalus! The commonly encountered neuroloic

malformations are listed in Ta%le =6;5!

Spinal Dysraphism


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epithelium! The accompanyin neuroloic deficit usually consists of complete

a%sence of motor and sensory function %elo& the le$el of spinal cord in$ol$ement!

The most se$ere form of spinal dysraphism is myeloschisis# &hich is much less

common than myelomeninocele! The spinal cord is unfused and presents directly on

the surface of the %ac' &ithout o$erlyin menines or epithelium! It usually occurs atthe thoracolum%ar reion and is $irtually al&ays associated &ith parapleia and

a%sence of %ladder function!


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"ydrocephalus

The term hydrocephalus implies an increase in the amount of CS+ &ithin the

$entricular system (+i! =6;9=)! This is almost al&ays due to a decrease in the

a%sorption of fluid# althouh there are rare cases of choroid plexus papillomas causin

hydrocephalus %y an increase in CS+ production! "ydrocephalus is traditionallyclassified as communicatin and noncommunicatin! In the former# the $entricular

system continues to communicate &ith the su%arachnoid spaces outside the %rain

throuh the fourth $entricular foramina of Lusch'a and -aendie! In the

noncommunicatin $ariety (often termed o%structi$e)# it does not! The common

causes of hydrocephalus $ary &ith ae and are listed in Ta%le =6; :!

Infantile "ydrocephalus

"ydrocephalus occurs most fre2uently %et&een %irth and 9 years of ae and is most

commonly due to conenital a%normalities of the %rain! These a%normalities typically

produce noncommunicatin hydrocephalus! Stenosis of the cere%ral a2ueduct is one

such common conenital anomaly! Another is the Arnold;Chiari malformation#descri%ed earlier! The Dandy;al'er malformation produces a mar'edly enlared

fourth $entricle as a result of conenital o%struction of CS+ outflo& from the fourth

$entricle# &ith resultant hydrocephalus! Other# less common conenital lesions

include arachnoid cysts# $ascular anomalies# and conenital tumors!

Ac2uired hydrocephalus in the infant is often the result of meninitis or intracranial

hemorrhae# %oth potentially causin o%struction of either the CS+ a%sorpti$e

mechanism or the intra$entricular path&ays! A2ueductal stenosis may de$elop &ell

after %irth %ecause of infection or hemorrhae and thus %e considered ac2uired!

Tumors may also o%struct the outflo& of CS+# resultin in noncommunicatin

hydrocephalus!

Infants &ith hydrocephalus usually# %ut not in$aria%ly# present &ith an enlarin head

circumference! They often ha$e a tense# %ulin anterior fontanelle &ith distended

scalp $eins and split cranial sutures! They may appear to ha$e sun settin of the

eyes# &ith only the tops of the irises $isi%le (1arinaud>s syndrome)! The head may

transilluminate %ecause of a lac' of cere%ral su%stance! "ydrocephalus usually does

not impair the infant initially %ecause the open cranial sutures allo& for cranial $ault

expansion! In the more chronic forms# or in older infants &ith closed sutures#

papilledema# optic atrophy# and 0Ith ner$e palsies may %e seen!

Childhood "ydrocephalus

"ydrocephalus in children o$er 9 years of ae may ha$e a more acute presentation

%ecause of the decreased a%ility of the more mature %rain and s'ull to accommodate

the increase in CS+! Conse2uently# raised intracranial pressure may cause headache#

nausea# $omitin# lethary# coma# and e$en death! Slo&er onset may result in

decreased mentation# %eha$ioral chanes# diminished performance in school# 0Ith

ner$e palsies# optic atrophy# paralysis of up&ard a*e# spastic le &ea'ness# and

endocrine (hypothalamic) disorders! Causes of hydrocephalus in this ae roup

include tumors# meninitis# intracranial hemorrhae (%oth spontaneous and

traumatic)# and a2ueductal stenosis! 0entricular shunt malfunction can cause acute

hydrocephalus in the shunt;dependent patient# reardless of the patient>s ae or theunderlyin cause of the hydrocephalus!


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Adult "ydrocephalus

"ydrocephalus in adults may also result from o%structi$e tumors# meninitis# and

intracranial hemorrhae# %ut it may also %e more insidious in onset! An entity called

normal pressure hydrocephalus occurs in the older population# in$ol$in a

communicatin hydrocephalus &ith relati$ely normal intra$entricular pressure! Thecause remains un'no&n %ut is thouht to %e due to su%clinical hemorrhae or

infection in the patient>s remote past and mala%sorption of CS+! The classic symptom

triad of ataxia# urinary incontinence# and failin mentation suests the dianosis!

Treatment is %y $entricular fluid shuntin!

Reardless of the cause# the treatment of hydrocephalus is essentially the same! Either

the cause must %e remo$ed (e!!# tumor) or a shuntin procedure must %e performed

to di$ert accumulated CS+! Sometimes %oth measures are necessary! The most

commonly used procedure is a lateral $entricle to peritoneal ca$ity shunt &ith a one;

&ay pressure;reulatin $al$e in the system! If the peritoneal ca$ity is not suita%le for

shuntin# the distal catheter may %e placed in the riht atrium of the heart or in thepleural ca$ity! In selected cases of communicatin hydrocephalus# a lum%ar

su%arachnoid to peritoneal shunt may %e used! Common complications of ind&ellin

shunts include shunt o%struction and infection!

Craniosynostosis

Craniosynostosis is the premature closure of one or more cranial sutures# typically

manifested &ithin the first : months of life! Since the %rain dou%les in si*e durin the

first : months of life and ro&s another 56 percent %y ae t&o# the cranial sutures

must remain open to allo& for s'ull expansion to accommodate this ro&th! .sually#

&hen one suture fuses prematurely# the %rain is not compressed sinificantly# %ut the

s'ull &ill then de$elop in a distinctly a%normal shape! If more than one suture is

fused# %rain ro&th may %e restricted!

The saittal suture fuses prematurely most often! The s'ull then de$elops an elonated

shape &ith a narro& %iparietal diameter# often referred to as scaphocephaly! The

supraor%ital ride may %e s2uare;shaped due to o$erexpansion of the open metopic

suture! Associated conenital anomalies are rare!

The next most common suture to %e in$ol$ed is the coronal# &hich may close

prematurely on one or %oth sides! .nilateral in$ol$ement produces an asymmetrically

shaped forehead &ith flattenin on the affected side and compensatory enlarementon the opposite side! This is called plaiocephaly and is not usually associated &ith

other a%normalities! s disease and Apert>s and Carpenter>s

syndromes!

Less common forms of craniosynostosis include premature closure of the lam%doid

suture or the metopic suture! ith unilateral synostosis of the lam%doid suture# the

s'ull appears flattened in the affected occipital area# &hich may %e confused &ith

%irth moldin! ith premature closure of the metopic suture# the forehead assumes a


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Chronic pain that de$elops in chest# flan'# or a%dominal incisions may &arrant an

a%lati$e procedure! Since these reions do not contain critical sensory areas# unilateral

dorsal ner$e roots may %e sectioned to depri$e the in$ol$ed area of sensation! It is

necessary to a%late at least three ad,acent le$els in order to dener$ate one dermatome

ade2uately %ecause of o$erlappin sensory distri%ution! Dorsal rhi*otomy may %e

carried out openly throuh a laminectomy or percutaneously throuh radiofre2uencythermocoaulation! 1ain relief from rhi*otomy is ood initially# then less so as time

passes!

Intrathecal morphine can %e i$en temporarily or permanently %y infusion of small

%ut effecti$e doses! This ne&er method of pain control is particularly effecti$e in

de%ilitated patients &ith terminal illnesses! The procedure in$ol$es the su%cutaneous

implantation of a constant infusion pump that can %e rechared periodically!

In chronic painful states of nonmalinant spinal oriin# such as lo& %ac' and/or le

pain# a nona%lati$e neuromodulation techni2ue may play a role in therapy! This

in$ol$es transcutaneous excitatory ner$e stimulation (TENS)# &hich %loc's ner$econduction of pain impulses! It is simple# safe# and relati$ely inexpensi$e! Electrodes

are taped to the s'in# usually o$er the reion of the pain or directly o$er the affected

ma,or ner$e# and then connected to a small# porta%le stimulatin de$ice! The de$ice

has a $aria%le pulse &idth# fre2uency# and amplitude# &hich the patient can ad,ust in

order to achie$e maximum pain relief! .se of this de$ice for a %rief time often

pro$ides lon;lastin relief &ith no unto&ard side effects! Direct stimulation of the

spinal cord %y surically implanted electrodes com%ined &ith percutaneous telemetry

can also pro$ide relief from chronic pain!

Peripheral Ner%e1ain from a partial or complete ner$e in,ury usually in$ol$es the ner$e>s sensorydistri%ution %ut may include the &hole extremity! Chronic pain de$elopin after an

amputation may %e present in the remainin portion of the lim% at the site of the

amputation (stump pain) or in the nonexistent amputated portion (phantom pain)!

The causation of the pain may %e related to the sensory component of the ner$e or to

its associated sympathetic ner$e supply!

ith partial or complete peripheral ner$e transection# a painful neuroma may form!

The usual treatment is excision of the neuroma# &ith pre$ention of recurrent

formation %y %uryin the ner$e end in %one or muscle or &rappin it in tantalum or

Silastic! Neuromodulation techni2ues may also %e applied in cases of painfulneuromas!

Chronic pain resultin from peripheral ner$e in,ury may %e sinificantly altered %y

interruption of the sympathetic ner$e supply to the affected extremity! The classic

example of this dysautonomic state is ma,or causalia! This term implies a partial

in,ury to a ma,or ner$e in an extremity! -inor causalia is reser$ed for an in,ury to a

more distal minor sensory ner$e# &hich may also %ecome a source of sinificant pain!

It is also &ell reconi*ed that a dysautonomic state may %e created %y ma,or or minor

trauma to an extremity that does not in$ol$e a peripheral ner$e! This has %een termed

ma,or or minor traumatic dystrophy! The entire collection of causalias and traumatic

dystrophies ma'es up a syndrome called reflex sympathetic dystrophy!


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-a,or causalia is most commonly related to partial in,ury of the sciatic or the median

ner$e! Typically# symptoms %ein in the affected ner$e>s distri%ution %ut may proress

to in$ol$e the &hole extremity! The extremity first %ecomes s&ollen# &arm#

erythematous# and 2uite sensiti$e to touch! ith time# it %ecomes cool and pale!

"yperhidrosis (excessi$e s&eatin) may follo&! Due to lac' of ,oint motion# the

normal flexion and extension creases disappear and the s'in %ecomes smooth and flat!1lain radioraphs may demonstrate osteoporosis! E$entually the extremity may

%ecome completely useless! A constant# %urnin pain de$elops and persists throuhout

these $arious staes! It may %e exacer%ated %y touchin or mo$in the extremity!

E$en temperature chanes and emotional stress can trier &orsenin of pain! -inor

causalia and the traumatic dystrophies may %e accompanied %y similar# %ut less

se$ere symptoms!

The treatment of these dysautonomic states is complex! They may %e helped %y

disruption of the sympathetic ner$e supply to the extremity! Sympathetic dener$ation

may %e extremely re&ardin in ma,or causalia %ut is less so in minor causalia and

the traumatic dystrophies!

Less se$ere and more easily treated pain may arise from chronic compression of

selected peripheral ner$es! The most common are compression of the median ner$e at

the &rist (carpal tunnel syndrome) and compression of the ulnar ner$e at the el%o&!

Chronic compression may result in pain# paresthesias# num%ness# and e$entually

&ea'ness and atrophy of muscles in the distri%ution of the affected ner$e! These

compression syndromes are dianosed clinically and confirmed %y findin

dener$ation and slo&ed ner$e conduction on electromyoraphy and ner$e conduction

$elocity testin! Treatment is surical decompression of the in$ol$ed ner$e# &ith

prompt and lon;lastin relief in most cases!

EP",EP* AN' M+)EMENT '"*+R'ER*

Epilepsy

That remo$al of specific areas of the %rain can cure epilepsy has %een 'no&n for

many years! Inade2uate dianostic tools and poorly defined indications for surery#

ho&e$er# precluded &idespread use of surery to treat the disease! A%out 9 million

people in the .nited States ha$e epilepsy# and most undero treatment for it! -ost

$arieties of epilepsy can %e cateori*ed into either enerali*ed (rand mal) sei*ures

characteri*ed %y loss of consciousness &ith tonic/clonic mo$ements# or partial

sei*ures manifested %y in$oluntary mo$ements %ut no loss of consciousness! Epilepsy

can %e controlled fairly &ell %y a$aila%le medications in a%out ?6 percent of patients!Of the remainin 96 percent# nearly 766#666 may %enefit from a$aila%le surical

procedures! Interest in surical manaement of epilepsy has increased sinificantly in

recent years %ecause of the a$aila%ility of accurate physioloic locali*ation of sei*ure

foci and hih; 2uality imain of the %rain %y CT# -RI# and 1ET scannin!

Epilepsy has many etioloies! Conenital anomalies of the %rain are relati$ely

common causes in the pediatric ae roup!


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1atients can %e tested effecti$ely in order to select those &ho can clearly %enefit from

surery! Electroencephaloraphy and -RI are initial monitorin tools! -ore in$asi$e

monitorin in$ol$es recordins from depth electrodes placed stereotactically and

su%dural electrodes placed %y open craniotomy! Specific foci can %e identified &ith

proloned monitorin usin $ideo recordin coupled &ith continuous EEGmonitorin! Areas of %rain that ser$e specific functions such as speech and

motor/sensory functions can also %e identified %y specific tests# includin 1ET

scannin and functional -RI!

Operation is planned once a focus has %een identified that is amena%le to surical

resection &ithout undue ris'! Often sei*ure surery is performed &ith the patient

under local anesthesia! Electrocorticoraphy# &hich is similar to

electroencephaloraphy except that it is performed directly from %rain cortex# can

further identify the focus of sei*ures at the time of operation! Stimulation of %rain is

also used to map the cortex and to identify reions that su%ser$e speech# $ision# and

sensory/motor functions!

Outcomes of sei*ure surery today are often ratifyin! -any patients &ith

uncontrolled epilepsy are not a%le to function in society %ecause of their sei*ures!

A%out half of those &ho ha$e uncontrolled sei*ures can %e made sei*ure;free %y

surical techni2ues! Another one;2uarter can ha$e sinificant reduction in %oth

sei*ure fre2uency and sei*ure intensity %y surical therapy!

-o$ement disorders

-o$ement disorders result from a $ariety of central ner$ous system diseases and are

manifested %y a%normal $olitional mo$ement! Typical examples are the restin (or

pill;rollin) tremor of 1ar'inson>s disease and the intention tremor that accompanies

$olitional mo$ement as a conse2uence of cere%ellar disorders! -any treatments ha$e

%een used since these conditions &ere first reconi*ed# %ut most ha$e %een

ineffecti$e!


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Stereotactic methods# particularly pallidotomy# ha$e %ecome popular %ecause medical

therapy has not remained effecti$e in many patients o$er the lon term! Escalatin

doses of medication ha$e often %een necessary to control par'insonism# resultin in

&idely fluctuatin symptoms and sins! 1atients &ho ha$e restin tremor &ithout

%rady'inesia are considered for thalamotomy# and those &ith riidity# %rady'inesia#

and a*e and %alance difficulties are candidates for pallidotomy!

Other mo$ement disorders that respond to a%lati$e lesions in the %asal anlia include

essential tremor# intention tremor of multiple sclerosis# and the choreiform

mo$ements of "untinton>s disease! "emi%allismus and hereditary dystonia can also

%e treated %y stereotactic lesions in the %asal anlia!

RA'"+*R(ERRadiosurery is a hihly focused ioni*in radiation deri$ed from an external source

deli$ered to a stereotactically defined intracranial taret! Treatment of lesions in the

depths of the %rain %y focused radiosurery %ean a%out 96 years ao! The techni2ue#usin the so;called amma 'nife# allo&s deli$ery of radiation to a specific taret

from a $ariety of sources# a%latin the taret &ithout sinificant ad$erse effects on

tissue surroundin it! In some instances# the techni2ue is deli$ered %y fixed co%alt

sources deli$erin photon radiation to the taret# aided %y a stereotactic frame

attached to the patient>s head and a computer proram couplin the radiation source to

the frame on the patient! Identification of the intracranial taret is made %y CT or -RI

scannin# usin a computer to relate the taret to the stereotactic frame and the patient

&ithin it! Other systems in$ol$e a similar principle# %ut the radiation source# deli$ered

%y linear accelerator# mo$es around a fixed taret!

Currently radiosurery is i$en in a sinle dose re2uirin little or no time in thehospital! +ractionated treatments usin radiosurery are %ein de$eloped# reducin the

ris' of treatment and increasin its effecti$eness! Radiosurery is used for a $ariety of

conditions# includin arterio$enous malformations and neoplasms# and is particularly

adapta%le to deep intracere%ral lesions! It causes sclerosis of $ascular structures#

resultin in proressi$e occlusion of arteries# such as those &ithin arterio$enous

malformations# and cell necrosis in tumors! Radiosurery can radually a%late small

to medium;si*ed arterio$enous malformations &ith ?5 percent efficacy o$er a 9; to 8;

year follo&;up period!

Radiosurery is also used to treat neoplasms# includin intracranial sch&annomas and

meniniomas! In %oth instances the taret is usually &ell defined and ad,acent %rain isnot in$ol$ed! A tumoricidal dose can %e deli$ered in a sinle shot &ithout sinificant

ad$erse affects on surroundin tissue! Collimation of the %eam allo&s it to %e shaped

to fit the anatomic dimensions of the taret lesion!

The role of radiosurery in other tumors# such as metastatic tumors and liomas# is

uncertain at this time! It is pro%a%le that metastatic intracere%ral lesions &ill %e treated

more %y this techni2ue in the future %ecause it is relati$ely nonin$asi$e# and it is

pro%a%ly as effecti$e as surery for small lesions! Larer lesions are less &ell suited to

radiosurery %ecause they &ould re2uire radiation doses larer than can %e deli$ered

safely!


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Documents

Chapter 40 Neuro-surgery