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Neurosurgery
Brian G. Ballioe, Habert Lee and Alireza Mansouri, chapter editors Alaina Garbens and Modape Oyewwni, associate editors Adam Gladwish, EBM editor
Neurosurgery NSI
NS2 Neuroaursery
1'oroDio
2011
IBB Func:liaDBI
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Neumaurgery NS3
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Figure 3.
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NS4 Neurosurgery
Disorders of the Spine extradural degenerative: disc herniation, canal stenosis, spondylolisthesis/spondylolysis infection/inflammation: osteomyelitis, discitis ligamentous: ossification of posterior longitudinal ligament (OPLL) trauma: mechanical compression/instability, hematoma tumours (55% of all spinal tumours): lymphoma, metastases (lymphoma, lung, breast, prostate), neurofibroma intradural extramedullary vascular: dural arterio-venous fistula, subdural hematoma (especially if on anticoagulants) tumours (40% of all spinal tumours): meningioma, schwannoma, neurofibroma intradural intramedullary tumours (5% of all spinal tumours): astrocytomas and ependymomas most common; also hemangioblastomas and dermoid syringomyelia (common causes: trauma, congenital, idiopathic) infectious/inflammatory: TB, sarcoid, transverse myelitis vascular: AVM, ischemia
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v- = conslllnt
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INTRACRANIAL PATHOLOGY
ICPmmHg
80
I I 1
100Ll'-. 60
,-
...-I
1
I
ICPNoluma Relationship
adult skull is rigid with a constant intracranial volume contents (CSF, blood, brain) are incompressible increase in one constituent/space-occupying lesion = increase in ICP however, ICP docs not rise initially due to compensatory mechanisms (autoregulation): immediate: displacement of CSF to lumbar theca, blood delayed: displacement of extracellular fluid (ECF) or intracellular fluid (ICF); displacement of brain tissue into compartments under less pressure (herniation) once compensation is exhausted, ICP rises exponentially
Vollda
I
:
I
Wh.n a mass IIICjlllllds withilthe slut compensatury mechanisms initially maintain a nonnaiiCP
Evantualy finl& small inCielllents in voklme produce larger and 1.-ger increments in ICP
Adlpled lrom Unduy llW, lbl9 t NtwtrJ1Jw IIIII Ne!mst6puy 1lu.mrrled. Copyright 2004 with parmilliln
lromB18Viar.
Neurosurgery NSS
ICP Measurement
Acute Monitoring
lumbar puncture (LP) (see sidebar) intraventricular catheter/ventriculostomy/external ventricular drain ("gold standard", permits therapeutic drainage of CSF to decrease ICP)
LDw BP or High ICP Clllllbllll parfusioo prBI$Irll
Chronic Monitoring
fibreoptic monitor (intraventricular, intraparenchymal, subdural), subarachnoid bolt (Richmond screw), and epidural monitor normal ICP <15 mmHg (8-18 em H 20) for adult, 3-7 mmHg (4-9.5 em H 20) for child; varies with patient position moderate elevation: increase in mean pressure >20 mmHg severe elevation: increase in mean pressure >40 mmHg waveform: comprised of respiratory and blood pressure pulsations (Traube-Hering waves); the amplitude increases with ICP beta-waves: coarse, variably increased amplitude, frequency Yz-2/min, often related to respiration plateau waves: elevation ofiCP over 50 mmHg lasting 5-20 min, precursor of further deterioration
.....
,,
Consider Monilllring of ICP in 1lle following Sitllltians 1. Patianll will1an abnoiiTIIII halld CT IJid Glngow Coma Scale {GCSI scors of 3 111 8 llfl8r cardiopulmonary resuscitation.
2. Patianll will11 noiiTIIII hald CT and GCS liCOr& af 3111 8 AND the pra&enCe of two or more of the following: Age over 4C yen Unilabral or billbnll motDr posturing Systulic blood pniSIUI'IIIess than 90mmHg 3. Postoperative monitoring 4. Investigation of normal prenura hydrocsphalus {NPHI
Or
Elevated ICP
Etiology
intracranial space-occupying lesion: tumour
pus
blood [trauma-+ hematoma (most common), subarachnoid hemorrhage] depressed skull fracture foreign body increased intracranial blood volume vasodilatation (increased pC02 /decreased p02/decreased extracellular pH, e.g. hypoventilation) venous outflow obstruction (venous sinus thrombosis, superior vena cava syndrome, space occupying lesion) cranial dependency cerebral edema vasogenic (vessel damage, e.g. hypertensive encephalopathy, tumour) cytotoxic (tissue/cell death, e.g. hypoxia, brain injury) osmotic (acute hyponatremia, hepatic encephalopathy) impaired autroregulation (hypotension, hypertension, brain injury) hydrocephalus (obstructive, non-obstructive) tension pneumocephalus (gas within the cranial cavity) pseudo tumour cerebri status epilepticus (chronic seizure resulting in brain edema)
.....
,,
.....
,,
Clinical Features
1. Acute Blevated ICP headache (HIA) - worse in the morning, aggravated by stooping and bending nausea and vomiting (NN) decreased level of consciousness (LOC) ifiCP =diastolic BP, or midbrain compressed drop in Glasgow Coma Scale (GCS) =best index to monitor progress and predict outcome of acute intracranial process (see Neurotrauma, NS29) papilledema retinal hemorrhages (may take 24-48 hours to develop) abnormal extra-ocular movements (EOM): CN VI palsy: often falsely localizing (causative mass may be remote from nerve} upward gaze palsy (especially in children with obstructive hydrocephalus) herniation syndromes (see Herniation Syndromes, NS6} focal signs/symptoms due to lesion
NS6 Neuroaursery
1'oroDio
2011
2. Chronic Elmated ICP H/A postural: worsened by coughing, straining, bending over morning/evening HIA-+ VIUIOdfiatation due to increased COz with recumbency
visual changes
due to papilledema
enlarged blind spot. ifadvanced-+ eplsodJ.c constrictl.ons ofvisual. fields ('"grey-outs") optic atrophy/blindness differentiate from papillitis (usually unilateral with decreased visual acuity) decreased level ofc:onsd.ousness
Investigations
patients with suspected elevated ICP require an urgent Cf/MRI ICP monitoring where appropriate
Herniation Syndromes
Table1. Hemllllon Syll*ome
Cl1lcal FN1u111
o
DispB;anent ci lesion Small pupila, dilltad. fixed (I'Oitnll clencephalon 11raugh o Diffuse C818b111l tD caudal dataliaration), sapntill flllue of tentDrii!l nab:h o Lata uncal hamimon diancephahn 1111ckla
S.TDRSillr
i 0
: I!
EOt.V
Bninstem IIII!ICIIhaga secondaly 11:1 sh111ring af be&ilar lrtary perfa!Biing VBSS81s) llillblti!S illlipidus (tractiiJI on pillitary d and
end-s!IQI s9'1
Uncus af l8f11)llnll o Llbnl sl4)l'llenblrilllaaion lpslallnii1101H111Ctiva dilll8d pupil(estialt, laba hami1181 down (oflllll'l)ily opanding mast ralllble sign) + ip&i&tlnl EOM pRy$i&. 'llmlgh IIODrial nab:h trauiT'IIIIic lllll'llllamll) plosis (CN II
Contralaleral hemiplegia :!: extensor (upgoRg) plril' response :!: ipsilateral hemiplegia
("Karnallln's natd( -1 fll&a lacelizilg aign re&Uiting from pr8&1lll8 from the adga of 1111 tentorium an 1M cadnllallllll cerrl:nl pedurda)
CerBJellar Willis
hamiates llnugh tentDrii!l inciBIA
o
o
heniation
o
Hydf11C8Phakll !Cinbnllaquecllct Neck stiffness head tilt ftcnsllar. ., Daaaased l.DC (nidbrain
1
Flaccid pnysis
Fltawng LP in praaance al Raapiii1DIV irra(paritiaa.flll)iratrry IIT8IIt intrlcranial mass IB&ian (CIIII)I'IS&ian of macklllaly raspil'llclly centres)
Blood pr111111 illllllility (camii'BIIIian af m&GJIII'f cardDY8SCIB cantras)
calm (sldiiiJ,II:cma
Place .nivParlllylil
ltypemntiltll Bewle head
prevent hypotension with fluid and vasopressor&, dopamine, norepinephrine pm ventilate to nonnocarbia (pCOz 35-40 mmHg) -+ prevents vasodilatation prn to maintain J'02 >60 mmHg -+ prevents hypoxic brain injury
Herniation Syndromet/Hydrocephalus
Neumaurgery NS7
Spec:Hic Mesures
osmolar diuresis (mannitol20% IV solution 1-1.5 glkg. then 0.25 glkg q6h to serum osmolarity of315-320) can give rapidly, acts in 30 minutes, must maintain sBP >90 mmHg sedation \light" e.g. barbiturates/codeine ... "heavy" e.g. fentanyVMgSO.J paralysis with vecuronium -t reduces sympathetic tone, reduces HTN induced by muscle contraction hyperventilate to pCOz 30-35 mmHg use for brief period& only- also resulta in decreased cerebral blood .flow (CBF) drain 3-5 m1 CSF via ventricles. assess each situation independently insert external ventricular drain (lf acute) or shunt corticosteroids ... decrease edema over subsequent days around brain tumour, abscess, blood no prawn value in head injury or stroke hypothennia - cool body tn 34"C no proven value in head injury barbiturate coma induced with pentobarbital to reduce cerebral blood flow and metabolism (10 mglkg aver. 30 min, then 1 mglkg q1b continuous infusion) decreases mortality, but no improvement in neurological outcome decompressive craniectruny is a last resort
Hydrocephalus
Definition
ob&truction to CSF 8ow decreased CSF absorption increased CSF production (rarely) - e.g. choroid plaus papilloma (0.4-1% of intracranial
tumours)
Epidemiology
estimated prevalence 1-1.5%; incidence ofcongenital hydrocephalus -1-2/1000 live births hydrocephalus in children, see Pediatric Neurosurgery, NS37
Classification
Tllllllle 2. Cl&lllllcatlon of Hydrocephalus Ciculllliln blacUd willin (tm.Cimlllllil:llill) Vldricular sy1l8m pmximal to the 8111CI'IIDid IJlftllatiJnS
1. Clloroid plsxu. 2. l..lltalll wntricllll 3. Third venlricle 4. Cerebral aqueduct (Df
5. Four1h vanlrida
Obllrur:linl
Acqund AIJJeduclal stenosis (lllh!sians !GURacticxl, hllllllllhaga) lnlrllv8nlrii:U lnians {lllnaurs e.g. 3nl wnbicle aJIIaid cyst.
hemibms)
Vantriclilr
7. Aracmoid gnmliltions
to lilck
pruxinlll
8. Subal'lll;l'noid
9. Segilllll sinus
par;
1 of
o
iii
Periwnbiclilr hypodensily
Sulcal aflacemllll
mat illo
spacal
....
',
Mall
ID: vanbiclaa -o
CSF prodlad by choroid pillllul. ftOWI of l..uiCI'b (lllll'lll)and MIQardll (medial) ... lblrachnoid spac;e -o ablsofbld by Bl'llchnoid vlflgranuldiona illo ve1111111
lii'IDM.
N...OIIIInl:liR
(er.r...lil:ltilg)
meniVfis, cysticercosis Post-hemonhegic (#2 cause) SAil. MI. tnunatic Dlamid 1)11111111 papilams (rm, c:ausas ilcraased CSF pmcllctian) nannal pi8SSU8 hydracephils
o
CSF production - CSF l'fllbsorptian -sao mVday i'l nonnalld.llll Normal ml (501 spinal, 5D'Io intracl'llnill -o 25 ml idn.VIIItriculllr. 50 mlaubncl'noid)
NPH I'NaNAiol
o
ldiapllhic (50%)
malingitis, 1nlu1111, radiaticDiJcU;ed
D1111entia
NS8 Neurosurgery
Hydrocephalus
Clinical Features (see also Pediatric Neurosurgery, NS36) acute hydrocephalus signs and symptoms of acute raised ICP (see Elevated ICP, NSS) impaired upward gaze ("sunset eyes") and/or CN VI palsy chronic/gradual onset hydrocephalus [i.e. normal pressure hydrocephalus (NPH)] gradual onset of classic triad developing over weeks or months pressure ofventricle on LE motor fibres -+ gait disturbance (ataxia and apraxia usually initial symptoms) pressure on cortical bowc:l/bladder centre -+ urinary incontinence pressure on frontal lobes -+ dementia CSF pressure within clinically "normal" range, but symptoms abate with CSF shunting Investigations CT/MRI periventricular lucency suggests raised CSF pressure ultrasound (through anterior fontanelle in infants) ICP monitoring (e.g. LP) may be used to investigate NPH, test response to shunting (lumbar tap test) radionuclide cisternography can test CSF flow and absorption rate (unreliable) Treatment ventricular drainage surgical removal of obstruction (if possible) or c::xcision of choroid plexus papilloma shunts ventriculoperitoneal (VP) - most common ventriculopleural ventriculo-atrial (VA) - not first choice because of increased infections, shunt emboli lumboperitoneal- for communicating hydrocephalus and pseudotum.our cerebri third ventriculostomy (for obstructive hydrocephalus) via ventriculoscopy LPs [for transient hydrocephalus (e.g. subarachnoid hemorrhage), IVH in premature infants, etc.]
Shunt Compli:ations
Table 3. Shunt Complications
Complication Etiolour Clinical Features lnvestiplians
Obstnlction
(most common)
CT
Radionuclide "shunto!Jlllf"
lnf8c:tion (3-6%)
s. epidermidis
P.ICII8S
S.lMR'fiiRl
Gram-negative bacilli
Fever, NN, anorexia, initabiity CBC Meningitis Blood culture Peritonitis Tap shunt for C&S (LP usualy NOT Signs and symptoms of shunt recommended)
obstruction Shunt naplritis NA shunt)
Ovarsllunting
Slit ventricle synctoma CIYonic or reculring CTIMRI Collapse of ventricles leading headaches often raliavad to occlusion of shunt ports by when lying down ependymal lining ventricles on imaging Seconday crMiosyno510Sis (childran) Subdural hamillumll A&ymptornatic Collapsing brain tears bridging Headaches, wmiting. veins {especially common in somnolence NPH patients) Apposition and overlapping of Abnormal head shape tha cranial sutures in an infllll following decorqnssion of hy!Rcephakls
CT
Clinical
oCT
EEG
Increased inlrllperitonaal hguinal swelling. discomfort results in hernia shunt inserted in inflrlcy) becoming apparent skin breakdown over hardware
U/S
Neumaurgery NS9
Etiology
unknown (majority), but aS&Ociated with: lateral venous sinus thrombosis
habitus/diet: obesity, hyper/hypovitaminosis A endocrine: reprodw:tive age, menstrual irregularities, Addison'&/Cushing's disease, thyroid irregularities hematological: iron deficiency anemia, polycythemia vera drugs: steroid administration or withdrawal, tetracycline, nalidixic acid, etc. risk factors overlap with those ofvenous sinus thrombosis; similar to those for gallstones ('"fat, female, fertile, forties")
Epidemiology
incidence -0.5/100,000 per year usually In 3rd and 4th decade (F>M)
Clinical Features symptoms and signs ofra1secl ICP (HIA in >9096, pulsatile intracranla1 noJse), but NO decreased LOC or diplopia decreased visual acuity. papilledema, visual field defect. optic atrophy (key morbidity) usually self-limited. recurrence is common, chronic In some patientB risk ofblindnes.s is not reliably correlated to symptoms or cl1nica1 course Investigations CT:nonnal CSF studies: normal Treatment
rule out conditions that cause intracranial hypertension
....
,.----------------,
IIRI(:t cantrMt
t.e.ia"' (:t ld11111B. nKro.i,, hsmarrhlgs) Midline shifts 1nd h1111ialians Elfat:oment of ventric:lee and aulei (olbln ipllilatn), batal
Single or mLitijlle mebllbllil) implies
discontinue offending medicatioDS, encourage weight loss, fluid/salt R:5triction CSF production), thiazide diuretic or furosemide pharmacotherapy: acetazolamide ifabove fail: serial LPs, shunt optic nerve sheath decompression (if progressive impairment ofvisual acuity) 2-yea.r follow-up with imaging to nde out occult tumour, ophthalmology follow-up
....
Primary CNS l',mphar.-. npcn11d il 6-201 of HIV inf\lcl8d patienta.
Tumour
Vllllric...r: CGUDid, chomid prDC81S
pepma. apandymoma.
germiloma. tntoma.
...,.._..
LY!l1111ollll
IUOICALDR
QMglioma. lymphoma,
adnma.
piUtaJy
....
MMrySGu- rl
TIIIIIIIIS
lu1g
8r'llql
44lli
10%
(RCC) 7'!1i 0.
Figura 9. Tuaurs
Gl
Mnoma
3%
NSIO Neurosurgery
Tumour
.........................:A
..............
Classification
primaryvs. metastatic, intra-axial (parenchymal) vs. extra-axial, supratentorial vs. infratentorial, adult vs. pediatric benign: non-invasive, but can be devastating due to expansion of mass in fixed volume of skull malignant: implies rapid growth, invasiveness, but rarely extracranial metastasis types of intracranial tumours ( = most common) neuroepithelial glial: astrocytomas, oligodendrogliomas neuronal: ganglion cell tumours, cerebral neurocytomas/neuroblastomas poorly differentiated: glioblastomas, medulloblastomas other: pineal tumours, ependymomas, choroid plexus papillomas meningeal: meningiomas nerve sheath: schwannoma, neurofibroma blood vessels: hemangioblastomas germ cells: genninomas, teratomas pituitary adenomas* craniopharyngiomas cysts: epidermoid/dermoid cysts, colloid cysts local extension: chordomas, glomus jugulare tumours other: primary CNS lymphomas, metastatic tumours
Cwr()lc;d'11X11; 14(41:131-43 Patiantt idan1lJid a hiving !ida lnin ma111ta1is oodelgo llliltmlln11hlt inlilde wide liRin
lll'iuw rJ 1helidlnculnd prldi:u uuidllil8. c.:lllin: Surgicalmilion sllould be consider8d fw IJitiartl wMh pd perfonnlnce IIIU. or no lll'idiiiCI rJ ablcmill cli-.lnd 1 Sllllicdy ICCeslible qe bnlin maiiSIIsis amanllila 1D Becue 1rea1ment il lingle hrail
lldillian tllapy (WIIRij, 111111ical,..ctian and sfnlllctic llldidon..,-, (SRSI. Given 1hlt conllc:ting Mlanctlu beln !Wplflld witli 1l5pacl 1D lhe best IPProacli 1D lilgle brlin rne11st1ses. 1he ..._cologylli.- SiQ Grlql r-r Clf'l Onlllio Progrmn I:Onlb:tld 1 sysllmltic
1llnllll' l'llCU'ItiiC8 fw pl1iants who 11M oodalgont miCii:ln rJ alnilll'lllltiiU. poslupef1live W8I!T should be canlider8d. As an llllmiiM ID up fii8Ction. WBI!Tfollawld lrt SRS boost slwld be CCIIIIidenid lor pa1ien1s wi1h liJ9a llllill mallltlliL Tile Mane& is ildciant 1D lllCDIIIrnendSAS lliorle IS I llilrlpy.
Clinical Features
progressive neurological deficit (7096) - usually motor weakness, CN deficits, sensory, cognitive, personality, endocrine deficits (these may localize lesion) H/A (5096) raised ICP (acute or chronic depending on growth rate), H/A classically worse in am but non-specific (likely hypoventilation during sleep causing vasodilatation -+ increased ICP), may worsen with bending forwardlvalsalva N/V (4096) seizures (25%) papilledema, vision changes symptoms suggestive ofTIA (ictal, post-ictal, or ischemic 2 to "steal phenomenonD) rarely presents with hemorrhage familial syndromes associated with CNS tumours von Hippel-Lindau (hemangioma) tuberous sclerosis (astrocytoma) neurofibromatosis type 1 and 2 (astrocytoma, acoustic neuroma respectively) Li-Fraumeni (astrocytoma) Turcot syndrome (glioblastoma multiforme) multiple endocrine neoplasia type 1 (MEN-1) (pituitary adenoma)
Investigations
CT, MRI, stereotactic biopsy (tissue diagnosis), metastatic work-up
Treatment
conservative: serial Hx, Px, imaging for slow growing/benign lesions medical: corticosteroids to reduce cytotoxic cerebral edema, pharmacological (see Pituitary Adenoma, NS13) swgical: total or partial excision (decompressive, palliative), shunt if hydrocephalus radiotherapy: conventional fractionated radiotherapy (XRT), stereotactic radiosurgery (Gamma Knife) chemotherapy: e.g. alkylating agents (temozolomide)
Astrocytoma (all grades) (511%) Craniophlryn.jiorna (2-5%) Others: pineal region tumours, choroid plexus twnours, ganglioglioma, DNET
High IJ!Ide astrocytoma (12-15%. e.g. GBM) Metastasis Metastasis (15-311%, includes infratentorial) Acoustic neuroma (schwannoma) (51II%) Meningioma (15-211%) Hamangiablaslllma {2%) Low IJ!Ide astrocytoma (8%) Pituillry adentma (5-8%) Oligodendroglioma (5%) Othar: CQIIoid cyst. CNS darmoidfepidarmoid cyslll
Tam.our
Neurosursery NSll
Metastatic Tumours
most common brain tumour seen clinically 15-3QlJ6 of cancer patients present with cerebral metastatic twnoUI'!I most common sites = lungs, breast other sites = kidney, thyroid, stomach. prostate, testis, melanoma hematogenous spread most common
Location 80% a.re hemispheric, often at grey-white matter junction or junction of temporal-parietaloccipitallobes (likely emboli spreading to terminal MCA branches) Investigations identify prlmary tumour metastatic work-up (CXR, CT chest/abdo, abdominal U/S, bone scan, mammogram) cr with contrut -+ round, well-drcumscrtbed, often ring enhancing, ++ edema, often multiple MRI more sensitive, especially fur posterior fossa oonsider biopsy in unusual cases. or if no primary identified 1- metubrtic work-up negative -+ brain biopsy 2. metubrtic work-up p011itive biopsy of affi:cted lritc:s other than brain
Treatment
medlcal phenymin for seizure prophylaxis ifpatient presents with seizure dexamethasone to reduce edema given with ranitidine chemotherapy (e.g. small cell lung cancer) radiation stereotactic radiosurgery: for discrete. deep-seatc:dJinoperable tumours multiple lesions: use whole brain radiation therapy (WBRT); consider stereotactl.c radiosurgery If<3lesions post-op WBRT 1.1 commonly used surgical single/solitary lesions: use surgery+ radiation
Prognosis median survival without treatment once symptom.at.k is -1 month, with optimal treatment 6-9 months but varies depending on prlmary tumour type
z
3
1. HIIIBruganoos conlnlllarll.,callllnt Z. 1-deliled bardn(infltraiM) 3. l'lritumaur adarra 4. CantriiiiiCIIISis 5. CamprvAion of vedricla, me shit
AstrDcyiDma 01 CT
Astrocytoma
most common primary intra-uial. brain tumour
'' ,
ICamof*Y lllnlfll c.PIIffGin- 1t1tue Sclll
lldlg Qtlerhl
1- Pilocytic amocytama
('II.I 100
80
70
No compeints; no evidanca of diAbla 111 1:11ny on narmlll activity; minor signs or symptoms of di-
sites: cerebral hemispheres cerebellum. brainstc:m, spinal cord symptoms: recent onset of new/worsening HIA, Ntv; seizure, focal deficits or symptoms of increased ICP
Investigations CT with contrast: va.rl.able appearance depending on grade (see Table 5) tissue biopsy: WHO grade and histology correlates with prognosis, but 25% chance of sampling error due to tumour heterogeneity
80
50
needs
40
30
Disabled; l'llfJJiras .. care and -illance S8VIlnlly -.blld; missicn is indicltad .U.ough
20
10
0
Delli
NS12 Nearomrgery
Tralltment
low grade diffuse astrocytoma close follow-up, radl.ation, chemotherapy, surgery all valid options
radiotherapy alone or post-op pmlongs survival (retrospective evidence) chemotherapy: usually reaerved for tumour progression high grade astrocytomas (anaplastic astrocytoma and GBM)
surgvy
gross total resection: IDIWmal safe resection + fractionated radiation with 2 em margin + concomitant and adjuvant temozolomide - a.cept: enensive dominant lobe GBM. slgnlfica.nt bllatenl involvement, end ofllfe
Meningioma
mostly benign (1-2% anaplastic), slow-growing. extra-axial, drcumsc.ribed (non-iDfiltrative), arise from arachnoid membrane often calcified, cause hyperostosis ofadjacent bone classically see Psammoma bodies on histology
Common Locations parasagittal convexity or falx (70%), sphenoid wing, tuberculum sellae, foramen magnum,
olfactory groove
Clinical Features
1. Homogenous contmt emancement
2. Dui'IIIIIIIBctmmt
middle aged, slight female preponderance (male:female = 2:3), high progesb:rone receptor& (increase in size with pregnancy), symptoms of increased ICP, focal deficits, usually solitmy (10% multiple, likely with lollS ofNF2 gene/22q12 deletion)
3. Dillinc:t margill
cr with contrast: homogeneouB, densely enhancing. along dural border ("dural tall"), well
o
lnvestiglltions
....
,'
angiography most are supplied by extmtal. carotid feeders (meningeal vessel&) also assesses venous sinus Involvement, "tumour blush"' commonly seen (prolonged contrast
image)
Treatment
111r iltoltm
Grade 1: low n.k IJf Grada 2: intamedialll risk of NC.-ce Grade 3: high rilk of recul'l'lnce
conservative .management for non-progressive, asymptomatic le8lons surgeryis treatment ofchoice ifsymptomatic or progression on sequential imaging (curative if complete resection)
stereotactic zadiosurgery (SRS) may be an option for lesions <3 em endovascular embolization to facilitate surgery SRS or XRT for recurrent atypical/malignant meningiomas
Prognosis
>90% 5-year survival. recurrence rate variable (often -10-2096} depends on enent of resection (Simpson's classification)
....
,,
Proglllllive ll'lillltlll'lll or sansorineul'lll '-ing loss - acoustic nauroma ll'1li pmvan lltharwi.
Tam.our
Neurosursery NS13
Futures compression of structures in CPA, often CN VIII (hearing loss 98%, tinnitus, d}'!ICquilibriwn), then V. then VII ataxia and raised ICP are late features
Investigations MRI with gadolinium or T2 FIESTA sequence (>9896 sensitive/specific), CT with contrast 2nd choice
audiogram. bminstem auditory evoked potentials, caloric testll
Treatment
conservative: serlal imaging
radiation: stereotactic radiosurgery is the trea1ment of choice o surgery if: I. lesion >3 em; 2. bn.in8tem compression; 3. edema; 4. hydrocephalus curable ifcomplete resection (almost always possible)
Pituitary Adenoma
primarily from anterior pituitary, 3rd-4th decades, M=F incidence in autopsy studies approximately 20%
classification miaoadenoma <1 em; maaoadenoma 0!:1 em endocrine active (functlonal/seaetory) vs. inactlve (non-functional)
bitemporal hemianopsia (compression of optic chiasm) (see NeuroloBf. N21 for details of visual field deficlt) CN m, IY. V 1, V a. VI palsy (compression of cavernous sinus) o endocrine effects hyperprolactinemla (prolactinoma): lnfe:rtlllty, amenorrhea. galactorrhea, deaeased Ubido ACTI:I production: Cushing's disease, hyperpigmentatln GH production: acromegaly/gigantism panhypopituitarism (hypothyroidism, hypoadrenalism, hypogonadism) associated MEN-I syndrome diabetes insipidus pituitary apoplexy apoplexy (sudden expansion of mass due to hemorrhage or neaosis) abrupt onset HIA, visual disturbances, ophthalmopl.egl.a, reduced mental status, and panhypopltuitarism CSF rhinorrhea and seizures (rare) signs and symptoms ofsubarachnoid hemorrhage (rare) Investigations
formal visual :fi.elda, CN testing endocrine tests (PRL level. TSH. 8 a.m. cortisol. fasting glucose. FSH/LH, IGF-1), electrolytes, urine electrolytes and osmolar.lly imaging (MRI with and without contrast)
o
A co..-ive adenoma in the pilllibrf wil impair honnone produdion in !hit ardar (i.a. GH-I:nllinv calbl ra mDSI S8IISitivrl tD co,..-.ssiDII}.
Differential parasellar tumours (e.g. craniopharyngioma. tuberculum sellae meningioma), carotid aneurysm
Treatment
medical for apoplexy: rapid corticosteroid administration surgical decomptession
for prolactinoma: dopamine agonists (e.g. bromocriptlne) for Cushing's: serotonin antagonist (cyproheptadine), inhibition ofcortisol production (ketoconazole) for acromegaly: somatortati.n analogue (octreotide) bromocriptine
endoaine replacement therapy
NS14 Neuroaurgery
1'oroDio
2011
Sources of Pus/Infection
four mutes of microbial access to CNS 1. hematogenous spread (most common): arterial and retrograde venous adults: chest is #l source Oung abscess, bronchiectasis, empyema) children: congenital cyanotic heart disease with R to L shunt immunosuppression (AIDS - tomplasmo!ds) 2. dire<:t implantation: dural disruption due to iatrogenic (e,g, following LP, post-op) congenital defect (e.g. dermal sinus) 3. contiguous spread (adjacent infection): from air sinus, nasa/oropharynx, surgical site (e.g. otitis media, mastoiditis, sinusitis, osteomyelitis, dental abscess) 4. spread from PNS (e.g. viruses: rabies, herpes zoster) common examples epidural abscess: In cran1.al. and spinal epidural space, associated with osteomyelitis treatment: immediate drainage llJld antibiotics, smgical emergency if cord compression subdural empyema: bacteriallfungallnfection, due to contiguous spread from bone or air sinus. progresses rapidly treatment: smg!cal drainage and antibiotics, 20% mortality me:nlngitlB, encephalit:l8 (see lnfectlous Diseases. ID6)
trauma
Brain Allscass on CT
Carabral Abscess
Definition pus in brain substance, surrounded by tissue .reaction (capsule formation) Etiology
modes ofspread (see above): 10-60% of patients have no cause identified pathogens Streptococcus (most common), often anaerobic or microaerophilic Staphylococcus (penetrating injury) Gram-negatives, anaerobes (.Btu:teroides, Fusobacterium) in neonates: Proteus and Citrobat:ter (exclusively) immunocompmmised: fungi and protozoa: Toxoplasma. Noamlia. Candids a1&iams, Listeria monocytogmes, Mycobacterium and Aspergillus
. , . . _ iii4Zpllillll: ll&tn
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I (
Riskflleton; lung abnormalities [infection, AV fistulas; especially Osler-Weber-Rendu syndrome (aka hereditary hemorrhagic telengiectaaia)] congenital coronary heart disease: R-to-L shunt bypasses pulmonary :filtration of
micro-organisms
bacterial endocarditis
dental abcess
Clinical Features
o...:an. ko1e IOOSI- M IDrUwtnnDI Wth!VIIIIiiDicslurlllllllt4Mib. llldmilioa- primlld 11111iens >tS IIIII in
- -dimBIIL!I ,._..:A1ullli llllr:Grnl: 13 !44,411 hid ful _ . , - 42 I2SAI hid rril dRill, 3'l Plliml hid Ill lll:ll:llnl, Hlild il hGIPII!anl13 hldliiiiBD-dllblly, !AJIMrill loil1ic Nllll"iln llhllwld in'fiiNII M:omll ..:illal Mil bqii'IIIIIIIUR Ul, P=O:Im), tmJJ GCS >IZ lOR &.20. P=O.OII), lOR 781 A8. P<D:0011rr l'lllmiiiiMI-'POii!M eocci 1J1M11ian llblcla 1:11lln 111142.3. atlawriiiNspr!Mid ID ba
IIUII:Gn'lrM ....tm:odrGtDihiGII!gCM
HJA.. deaeased LOC; hemiparesis and se:lzures in 5096 mass effect:. increased ICP and sequelae (cnnial enlargement in chlldre:n) hemipareslB llJld seizures in 50% sJg:ns and symptoms ofsystemic Infection (low-grade fever, l.eukocytosls)
Complications
with abscess rupture: ventriculitis, meningitis. venous sinus thrombo!ds CSF obstruction transtentorial herniation
Investigations cr scan often lst test in emergency department MRI imaging of choice apparent diifusion coefficient (ADC) used to differeot:iate abscess (black) from tumour
(white) WBC/ESR may be normal. blood cultures rarely helpful and LP contraindicated iflarge mass CSF: nonspecific (high ICP, high WBC, high protein. normal carbohydratt:), rarely helpful, usually negative culture
llldlll'liliriJ...,.IDflill._u llllirmliii11W11Q1111111.
PwiBlood
Neurosursery NSlS
Treatment aspiration excision and send for Gram stain, acid fast bacillus (AFB), C&S, fu.ngul culture exdsl.on preferable lflocation suitable antibiotics empirically: vancomycin + ceftriaxone + metroniduole or chloramphenl.rol or rifiunpin (6-8 weeks therapy) revise antibiotics when C&S known
anti-convulsants (1-2 years) follow up cr is critical (do weekly initially, more frequent if condition deteriorates)
Prognosis
mortality with appropriate therapy -10%, permanent defidts in -50%
Blood
Tllllla &. Cum)lllrisun uf Epi..........,. EtiDIDIIf Ill lntnn:rasial BIDIIds Tna of EtiDIDar EpidamiCIIDgy Clnical FtlbJIII CT Fllllnl 11..11111111 11.......
fpanllallluma SkYI fraelln c:ausing M. > F111111la (4:1) lucid inllMI bafonl LOC Lanticlilr DIISS
lllllliiiJI!Illenl
11.......
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AQB >50.
Crascen1ic OilS$
HypadaiiiB
CIIRiCBID: lll8iS
Paar
Good
Dopethic, AVMI
m C8888 under
Aae 55-SO
11lnDW's, Raclions.
Aaa >55,
11A-ll8 ..,......,
Epidemiology
young adult, male > female= 4:1; rare before age of2 or after age 60
Clinical Features
signs and symptnms depend on severity but can Include H/A. NJV; amnesia. altered WC, HTN and respiratory distress deterioration can talce hours to days
lnvestigtdions CT without contrast: high density biconvex mass against skull, unlfonn density and sharp margins. usually lim:iJ:ed by suture Unes
in 6096, there is lucid interval of several houn between conCI158ion and coma then, obtundation. hemlpareals, .ip6Jlateral pupillary dilatation
1. Comp1'81Sion of van1ridas
(miclile llhilll
2. Bload
Treatment
admit, observe, bead elevation mannitol pre-op If elevated ICP!brain herniation craniotDmy to evacuate clot, follow up CT
NS16 Neurosurgery
Calcilm antaganisiJ for aneurysmal subaracllloid haemonhage (Review) Cochrane Review 2008; Issue 3. Introduction: This sbJdy looked to review the evidence in regards as to whether calcium antagonists improve the outcome in patients with aneUJysmal subarachnoid haemonhage. Mathods/Papulation: The review included 3361 patients presenting aneurysmal subarachnoid haemorrhage from 16randomised controlled trials comparing treatment with calcium antagonists vs. control from 1980 ID March 2006. Results: The results were based mainly on one large trial of oral nimodipine, which showed aRR of 0.67(95% Cl 0.551D 0.811 and the evidence for other calcium agonists was not statistically significant Con'*sion: The authors endorse the use of oral nimodipine in patients aneurysmal subarachnoid haemonhage.
Blood
Prognosis
good with prompt management, as the brain is often not damaged worse prognosis if bilateral Babinski or decerebration pre-op death is usually due to respiratory arrest from uncal herniation (injury to the midbrain)
Subdural Hematoma
ACUTE SUBDURAL HEMATOMA Etiology
rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, venous sinus) or cerebral laceration
Risk Factors
trauma, anticoagulants, alcohol, cerebral atrophy, infant head trauma (see Pediatrics)
Clinical Features
no lucid period, signs and symptoms can include altered LOC, pupillary irregularity, hemiparesis
CT Density and MRI Appearance of Blood Time Acute (<72hl Subacute 1<4wl Chronic 1>4wl CT Hyper. Iso. Hypo. MRI T1 Grey White Black MRI -T2 Black White Black
Investigations
CT: high density concave mass, "crescentic" usually less uniform, less dense and more diffuse than extradural hematoma
Treatment
craniotomy for clinically symptomatic subdural hemorrhage, or subdurals greater than 1 em; optimal if surgery <4 hrs from onset
Prognosis
poor overall since the brain is often injured (mortality range is over 50%)
Risk Factors
older, alcoholics, patients with CSF shunts, anticoagulants, coagulopathies
Clinical Features
often due to minor injuries or no history of injury may present with minor H/A, confusion, language difficulties, TIA-like symptoms, symptoms of raised ICP seizures, progressive dementia, gait problem obtundation disproportionate to focal deficit; "the great imitator" of dementia, tumours
Investigations
CT: hypodense (liquefied clot), crescentic mass
Treatment
seizure prophylaxis only if posttraumatic seizure reverse coagulopathies burr hole drainage as clot liquefies; craniotomy if recurs more than twice
Prognosis
Figure 16. Subdural Hematoma on CT
good overall as brain usually undamaged, but may require repeat drainage
Cerebrovascular Disease
Neurosurgery NS17
Cerebrovascular Disease
Ischemic Cerebral Infarction (80%)
embolic (heart, carotid artery, aorta) or thrombosis of intracerebral arteries (see Carotid Stenosis, NS21 and Neurology. N45)
---------------------
bleeding into subarachnoid space (intracranial vessel between arachnoid and pia)
Etiology
trauma (most common) spontaneous aneurysms (75-80%) idiopathic (14-22%) AVMs(S%) coagulopathies (iatrogenic or primary), vasculitides, tumours (<5%)
', ,
Grad1 Finding
Normal scan
2 3
4
Epidemiology
-10-28/100,000 population/year peak age 55-60, 20% of cases occur under age 45
Risk Factors
hypertension pregnancy/parturition in patients with pre-existing AVMs, eclampsia oral contraceptive pill substance abuse (cigarette smoking, cocaine, alcohol) conditions associated with high incidence of aneurysms (see Intracranial Aneurysms, NS20)
', ,
Huntlmlllus Grade
Grad1
', ,
World Fedlndion Ill N-ological Surpans Grlllling of SAH
Investigations
non-contrast CT (Figure 17) 98% sensitive within 12h, 93% within 24h; 100% specificity may be negative if small bleed or presentation delayed several days acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible CTA/MRA/ cerebral angiography for localization and treatment planning positive history for SAH with negative CT - MUST do LP to look for blood or xanthochromia (may be negative <12h) lumbar puncture (LP) findings (highly sensitive): elevated opening pressure (> 18 em HzO) bloody initially, xanthochromic supernatant with centrifugation ("yellow") by -12h, lasts 2 weeks RBC count usually> 100,000/mm3 without significant drop from 1st to last tube (in contrast to traumatic tap) elevated protein due to blood breakdown products
WFNS
Grad
GCS
Scare
o
15
2
3
1314 1314
+ +or+or-
7-12
3-6
1nt11ct anltr{sm
NS18 Neuroaurgery
CerebroYascular DJnase
1'oroDio
2011
four vessel cerebral angiography ("gold standard" for aneurysms) demonstrates source of SAH in 80-8596 ofcases "angiogram negative SAH": repeat angiogram in 7-14 days, ifnegative -+ perimesencepbalic SAH" magnetic resonELilce angiography (MRA) and cr angiography sensitivity may be up to 95% for aneurysms
da...
BP
l.OC
.-ent I CTicen
mic7ie
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puncture
DIC heme
f"IJIFI 18. Appraacii1D SAH
Treatment admit to ICU or NICU oxygenlventilation pm NPO, bed rest, elevute head ofbed 30D, minimal external stimulation, neurological vitals qlh aim to maintain sBP =120-150 (balance of vasospasm prophylaxis, risk of re-bleed, risk of hypotension since CBF autoregulation impaired by SAH)
Foley pm, strict monitoring of ins and outs IV NS with 20 mmol KClJL at 125-150 cclb. phenytoin ifseizure or temporal lobe clot mild sedation pm nimodipine fur vasospum neuroprotection for 21 day5; may discontinue earlier ifpatient is clinkally well
Cerebrovascular Disease
Neurosurgery NSHI
Complications vasospasm - vessel constriction in response to extravascular blood irritation clinical features: confusion, decreased focal deficit (speech or motor) onset 4-14 days post-SAH (deterioration within first 3 days is NOT caused by vasospasm) risk factors: large amount of blood on CT (high Fisher grade), smoking, increased age, HTN "symptomatic vasospasm in 20-3096 ofSAH patients "radiographic" vasospasm in 30-70% of arteriograms performed 7 days following SAH (peak incidence) diagnosed clinically, and/or with transcranial Doppler (increased velocity of blood flow) risk of cerebral infarct and death treatment "triple W therapy using fluids and pressors (examples: norepinenphrine, phenylephrine) angioplasty for refractory cases hydrocephalus (15-20%} - due to blood obstructing CSF drainage can be acute or chronic, requires extraventricular drain (EVD) or shunt, respectively neurogenic pulmonary edema hyponatremia - SIADH, cerebral salt wasting diabetes insipidus cardiac- arrhythmia (>50% have ECG changes), MI, CHF
we.
Hyparllnsion
Hypervolemia
H1111odilution
Prognosis 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 weeks) 30% of survivors have moderate to severe disability a major cause of mortality is rebleeding, for aneurysms: risk of rebleed: 4% on first day, 15-20% within 2 weeks, 5096 by 6 months if no rebleed by 6 months, risk decreases to same incidence as unruptured aneurysm (296) only prevention is early clipping or coiling of"cold" aneurysm rebleed risk for "perimesencephalic SAH" is approximately same as for general population
----------------------------
Definition hemorrhage within brain parenchyma, accounts for -10% of strokes can dissect into ventricular system (IVH) or through cortical surface (SAH) Etiology hypertension (usually causes bleeds at putamen, thalamus, pons and cerebellum) hemorrhagic transformation (reperfusion post stroke, surgery, strenuous exercise, etc.) vascular anomalies aneurysm, AVMs and other vascular malformations (see Vascular Malformations, NS22) venous sinus thrombosis arteriopathies (cerebral amyloid angiopathy, lipohyalinosis, vasculitis) tumours (1%}- often malignant (e.g. GBM,lymphoma, metastases) drugs (amphetamines, cocaine, alcohol, anticoagulants, etc.) coagulopathy (iatrogenic, leukemia, TTP, aplastic anemia) CNS infections (fungal, granulomas, herpes simplex encephalitis) post trauma (immediate or delayed, frontal and temporal lobes most commonly injured via coup/contre-coup mechanism) eclampsia post-operative (post-carotid endarterectomy cerebral reperfusion, craniotomy) idiopathic Epidemiology 12-15 cases/100,000 population/year
Risk Factors
increasing age (mainly >55 years) male gender hypertension Black/Asian > Caucasian previous CVA of any type (23x risk) both acute and chronic heavy alcohol use; cocaine, amphetamines liver disease anticoagulants
NS20 Neurosurgery
Cerebrovascular Disease
Clinical Features TIA-like symptoms often precede ICH, can localize to site of impending hemorrhage location: basal ganglia/internal capsule (50%), thalamus (15%), cerebral white matter (15%), cerebellumlbrainstem- usually pons {15%} gradual onset of symptoms over minutes-hours, usually during activity HJA, NN and decreased WC are common specific symptoms/deficits depend on location ofiCH Investigations hyperdense blood on noncontrast cr Treatment medical decrease BP to pre-morbid level or by -20%; check PTT/INR, and correct coagulopathy (stop anticoagulation for 1-2 weeks) control raised ICP (see Intracranial Pressure Dynamics section, NS4) phenytoin for seizure prophylaxis follow electrolytes (SIADH common) angiogram to r/o vascular lesion unless >45 yrs, known HTN, and putamen/thalamid posterior fossa ICH (yield - 0%) surgical craniotomy with evacuation of clot. treatment of source of ICH {i.e. AVM, tumour, cavernoma), ventriculostomy to treat hydrocephalus indications symptoms of raised ICP or mass effect rapid deterioration (especially if signs ofbrainstem compression) favourable location, e.g. cerebellar, non-dominant hemisphere young patient (<50 yrs) if tumour, AVM, aneurysm, or cavernoma suspected (resection or clip to decrease risk of rebleed) contraindication& small bleed: minimal symptoms, GCS >10 poor prognosis: massive hemorrhage (especially dominant lobe), low GCS/coma, lost brainstem function medical reasons [e.g. very elderly, severe coagulopathy, difficult location (e.g. basal ganglia, thalamus)] Prognosis 30-day mortality rate 44%, mostly due to cerebral herniation rebleed rate 2-6%, higher if liTN poorly controlled
Intracranial Aneurysms
Epidemiology prevalence 1-4% (20% have multiple) female > male; age 35-65 years Risk Factors autosomal dominant polycystic kidney disease ( 15%) fibromuscular dysplasia (7-21 %)
AVMB
connective tissue diseases (Ehlers-Danlos, Marfan's) family history bacterial endocarditis Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia) atherosclerosis and HTN trauma
Types (Figure 4, NS3) saccular (berry) most common type located at branch points of major cerebral arteries (Circle of Willis) 85-95% in carotid system, 5-15% in vertebrobasilar circulation fusiform atherosclerotic more common in vertebrobasilar system, rarely rupture mycotic secondary to any infection of vessel walL 20% multiple 60% Streptococcus and Staphylococcus 3-15% of patients with SBE
Cerebrovascular Disease
Neurosurgery NS21
Table 7. 5-year Cumulative Rupture Risk in Unruptured Aneurysms Based on Size and Location
Cmlmo111 Cuolid
<7 mm 7-12mm 13-24mm <!:24 rnn 0% 0%
3%
ACJMCIIC
0% 2.6% 14.5% 40%
V.llllbmbuillrJPC./PCIIIIIII
2.5% 14.5% 18.4% 50%
6.4%
n.y; MC- middle c8lllbnll nry; K:- inllrnll ci!Oiid llllllry; PC- pnrior cnbmlllllllry; Ff.omm - po6Q
1111 t.at2003;362:10J.IO
Clinical Presentation rupture (90%), most often SAH, but 30% ICH, 20% IVH, 3% subdural bleed sentinel hemorrhage ("thunderclap HIN) -+ requires urgent clipping/coiling to prevent catastrophic bleed mass effect (giant aneurysms) internal carotid or anterior communicating aneurysm may compress: the pituitary stalk or hypothalamus causing hypopituitarism the optic nerve or chiasm producing a visual field defect basilar artery aneurysm may compress midbrain, pons (limb weakness), or CN III posterior communicating artery aneurysm may produce CN III palsy intracavemous aneurysms (CN III, IY, V1, V2, VI) distal embolization (e.g. amaurosis fugax) seizures headache (without hemorrhage) incidental CT or angiography finding (asymptomatic) Investigations CT angiogram (CTA), magnetic resonance angiography (MRA), angiogram Treatment ruptured aneurysms overall trend towards better outcome with early surgery or coiling (48-96 hours after SAH) treatment options: surgical placement of clip across aneurysm neck, trapping (clipping of proximal and distal vessels), thrombosing using Gugliemi detachable coils (coiling), wrapping (last resort) choice of surgery vs. coiling not yet well defined, consider location, size, shape, and tortuosity ofthe aneurysm, patient comorbidities, age, and neurological condition. In general: coiling: posterior> anterior circulation, deep/eloquent location, basilar artery bifurcation/apex, older age, presence of comorbidities, presence of vasospasm clipping: superficial > deep, broad aneurysmal base, branching arteries at the aneurysm base, tortuosity/atherosclerosis of afferent vessels, dissection, hematoma, acute brainstem compression unruptured aneurysms average 1% annual risk of rupture: risk dependent on size and location of aneurysm no clear evidence on when to operate: need to weigh life expectancy risk of morbidity/mortality of SAH (20%/50%) vs. surgical risk (2%/5%) generally treat unruptured aneurysms > 10 mm consider treating when aneurysm 7-9 mm in middle-aged, younger patients or patients with a family history of aneurysms follow smaller aneurysms with serial angiography
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1'IUOIIIViCII clppilg.
Carotid Stenosis
Definition narrowing of the internal carotid artery lumen due to atherosclerotic plaque formation, usually near common carotid bifurcation into internal and external carotids Risk Factors for atherosclerosis: HTN, smoking, DM, CVD or CAD, dyslipidemia Clinical Features may be asymptomatic symptomatic stenosis may present as TIA, reversible ischemic neurologic deficit (RIND), or stroke retinal insufficiency or infarct permanently or temporarily (amaurosis fugax), (see Neuroloi}'> N47 and OP37) middle cerebral artery (MCA) occlusive symptoms
NS22 Neurosurgery
,..__of!IIQqllldFIIII._IIJ
Sui:CIIIful Clnlid &IIIIIIIII:IDIIJ ill'dlnll MhlltRICIIIINUIIagi:ll lluilonUid C.allll Trill
Investigations
CBC, PTT/INR (hypercoagulable states) fundoscopy: cholesterol emboli in retinal vessels (Hollenhorst plaques) auscultation over carotid bifurcation for bruits carotid duplex Doppler ultrasound: determines size oflumen and blood flow velocity, safest but least accurate, unable to scan above mandible but invasive and 1/200 risk of stroke (not for screening) angiogram: "gold MRA: safer than angiogram, may overestimate stenosis
Llnc:et2004; 363:1491-1502
Slllly: AlympiDnwlic Carotid Sllgary Trill {ACST), a lilldomized, controlled 1rial will 5)WTI. l'llilnll: 3120 asymplomllic pl1ients NUl
111lllllr blllwlan immllilll carotid andulnclmny (CEA) UJ1 indafuitB dafumll ri CEA IIIII \'MII followad for up 1D 5years {maan 3.4 yBIIII. Mlil Oldaml: flirt stroke (incliding flllll or dillblinglc.:llli: In pi!ien1swilh CIIII CI!Qiid QlyQno5ia. immdlbl CfA Nduced the stroke riskflom lllout 1D llbaullft.. lid rltlis5-yalr bnlit iMMd dillbling or fllal Slnla
Treatment
control ofHTN,lipids, diabetes antiplatelet agents (ASA dipyridamole, clopidogrel) -25% relative risk reduction carotid endarterectomy (generally if symptomatic and >70% stenosis, see Tables 8 and 9) endovascular angioplasty stenting
nets..,.
Prognosis
Table 8. Symptomltic Carotid Stenosis: North American Symptomatic Carotid Endarterectomy Trial (NASCET)
%Stun on Angiogr111
Medal Rx
70-99% 50-6!1%
Medal + Sllf1liCII Rx
!1% over 2years
<50%
Table 9. Asymptomltic Carotid Stenosis: Asymptomltic Carotic Atllerosclerosis Study (ACAS) and Asymptomatic Carotid Surgery Trial (Acsn
%S1anosis on Angiogr111 MadicaiRx
60-9!1% 70-9!1%
Vascular Malformations
Types
arteriovenous malformations (AVMs) cavernous malformations (cavernoma, cavernous hemangioma/angioma) venous angioma capillary telangiectasias arterio-venous fistula (AVF) (carotid-cavernous fistula, dural AVF, vein of Galen aneurysm) "angiographically occult vascular malfonnations" (any type:, 10% of malformations) clinical significance: AVMs and cavernous malformations produce intracranial hemorrhages and scizu.rcs
, ..----------------.
Sc:ere
1 2
Definition
tangle of abnormal vessels/arteriovenous shunts, with no intervening capillary beds or brain parenchyma congenital
Size
0-3cm
Epidemiology
3
0 1 0 1
3.1-6.0 em >6cm
Location Noneloquent Eloquent
prevalence -0.14%, male:female = 2:1, average age at diagnosis= 33 years 15-20% of patients with hereditary hemorrhagic telengiectasia (OslerWeber Rendu syndrome) will have cerebral AVMs
Clinical Features
hemorrhage (40-60%) - small AVMs are more likely to bleed due to direct high pressure AV connections seizures (50%) - more common with larger AVMs mass effect focal neurological signs secondary to ischemia (high :O.ow -+ "steal localized headache:, increased ICP bruit (especially with dural AVMs) may be asymptomatic ("silenn
Present
A'iM gl'llla8 Clbilbld tr;" addirQ tlla 3 inllvidull Spallllr-MI11in Scala -.s 11om Ilia abova table. E.g. A2em 1llnDur in nonaloq.lllnt bcaliDn wilhout daap wnoiJI chinaga Gradel.
Neurosursery NS23
Investigations
MRI (Bow void), MRA angiography (7% will also have one or more associated aneurysms)
Tnatment decreases risk offuture hemorrhage and seizure surgical excision is treatment of choice stereotactic radiosurgery (SRS) is preferred for small {<3 em) or very deep lesions endavascular emboliza.tion (glue. balloon) am facilitate surgery or SRS for larger lesions conservative (e.g. palliative embolization, seizure control ifnecessary) Prognosis
10% mortality, 3D-50% morbidity (serious neurological defidt) per bleed
Cavernous Malformations
Definition
benign Vl!llcular hamartoma consisting of irregular sinUIIoidal vucular channels located within the brain without intervening neural tissue or associated large arteries/veins
Epidemiology
0.1-0.2%, both sporadic and hereditary forms described several genes now described: CCMI, CCM2, CCM3
Clinical Features
seizures (60%), progressive neurological deficit (5096), hemorrhage {20%), HIA often an incidental finding hemorrhage risk less than AVM, usually minor bleeds
T2WI MRI (non-enhancing); gradient echo sequencing {best for diagnosis) usually not seen with angiography or cr
Treatment
surgical acision
Investigations
only appropriate for symptomatic lesions that are surgically accessible (supratentorial lesions are less likely to bleed than lnfratentorialleaions)
Prognosis
good with surgicallnterventlon
Mlllfennallon
A. T2 weighted imaging MRI B. Gradient Echo aaquancing MRI
NS24 Neuro1urgery
1'oroDio
2011
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..... ,
C5 - Sho!Mir abductioNellow fllllion Cl - Wrist IXIInsors C7 - Bbow IDdlnlion ca - Squ- hand T1 - Abduct fiiG'ers 12-8 -lntlrcolllal (Abdominal n&.l Tt-1 0 - Upperlbclomillll
Tll-12 -I.Jiwar abdominall l2-Fiax.hip
Mvnnl
L3 - Hip addulrtion
L4- Knaa IDIIIInlliDIIand BJtla
L5
i ...
(t
1, 2 tia my shoe -> S1-2 Anlda jerk 3. 4 kidt lhe door-> LJ-4 ICMe 5, I pick up sticks -o C5-l Bicaps/ Brac:lioradilli 7, Slay!hem *-ight -> C7-8 Triclpl
IIIIIIIDa
Extradural Lesions
Root Compression
Differential Diagnosis herniated disk neoplasm (neurofibroma, schWllllllOinll) synovial c:}'!t. abscess
.......,
fYI'I1P1DmL
hypertrophic bone/spur
c.....-.nfrlcb,.
Epidemiology
Bowel/lllddar ll'llllltion or
BACK PAIN
most common levels C6-C7 (C7 root) > C5-C6 (C6 root)
Clinical Features
pain down arm in nerve root distribution, worse with neck extension, ipsilateral rotation and lateral flexion (all compress the ipsilateral neural foramen)
LMN signs and symptoms central cervical disc protrusion causes myelopathy as well as nerve root deficits
NIUIIIIIotDr dlficihl
Investigations
Ifred flags: C-splne x-ray, CT, MRI (imaging of choice) consider EMG, nerve conduction studies Ifdiagnosis uncertain
JW:radural Leal.ODI
Neurosursery NS25
Treatment conservative no bedrest: unless severe radicular symptoms activity modiftcation, patient education (reduce sitting, lifting) phys1otherapy. exerd8e programs analgesl.cs, collar, tractl.on may help surgical indications in:tnu:table pain despite adequate conservative treatment for >3 months progreMM: neurological deficit llll12rior cervical discectomy is usual ru.rgical choice
"',.--------------. ,
.
Disc hamidions lnpinga tha 111M root
It thaiMI below the illtnpaca (i.e.
C5-ti dise
Prognosis
95% improve spontaneously in 4-8 weeks
C5 2\
C&
C8 10%
Rilg fing 5th finger
Digillll flexors, nmsics
SIIJuldar
Delblid, biceps, tuplllpinlltul
FascicuUI gl'lcilirlcunllllul: joint po.ition. fine txlueh, villnltion Spiullhlllamil: lnll:l: Pain 11'11
rrFibras
tampemn
No clwlga
llicapl. Bnlclial'lldillis
Triceps
resultant syndromes include mechanical neck pain. radiculopathy (root compreasion), myelopathy (spinal cord compression) and combinations
Epidemiology
typically begins at age 40-50, men >women, most commonly at the C5-C6 > C6-C7levels
Pathogenesis
with neck atenslon. the c:ervical. cord is pinched. With neck flalon. the canal dimensions increase slightly to relieve pressure on the cervical cord
Fetdures
insidiOUII onset of mechanical neck pain exa.cerbated by excess vertebral motion (particularly rotation and lateral bending with a vertical compressive force - Spurling's test). Pain is worse with neck extension. relieved with flenon
Figu111 Z1 A. AliiaI uctian Df Cervical Spine with Vascr Wid Functional Terltlclrlll
ocdpltal headache is common radiculopathy may Involve 1 or more roots, and symptoms include neck. shoul&W" and arm pain, paresthesias and numbness cervical myelopathy may be characterized by weakness (upper > lower extremity), decreased derterity and sensory changa. UMN findings such as hyperreflexia, clonw and Babinslri reflex may be present 1he most worrisome cmnplaint is lawex extremity weakneM (corticospinal tracts) myelopathy may be associated with funicular paiD. characterized by burning and stingiDg Lhermitte's sign (lightning-like sensation down the back with neck flexion)
lnvutlgatlona
x-ray of cervical spine flmOD!emnslon or oblique views (studied for changes in LU8chka and fe.cet: joints, osteophytes and disc space narrowing), MRI, cr, EMG Treatment NSAIDS, moist heat. strengthening and range of motion exercises, analgesics. cervical collar, cervical traction surgical indications: myelopathy with motor impairment, progressive neurologl.c impairment. intractable pa.ln
FlgUI'II 21 B. Axial secllon of Tbonlcic Spine wilfl Vaacul end fiiiCiional TarritDria
NS26 Neuroaurgery
1'oroDio
2011
Clinical Fntures
limited back movement (especially forward flexion) due to pain motor weakness. dermatomalsensory changes, reflex changes exacerbation with coughing. sneezing or straining. Relief with flexing the knee or thigh nerve root tension signs straight leg raise (SLR: Lasegue's test) or aossed SLR (pain should occur at less than 60 degrees) suggests LS, Sl root ilivolvement femoral stretch test suggests L2, L3 or L4 root involvement
Investigations x-ray spine (only to rule out other lesions), Cf, MRI myelogram and post-myelogram cr (only ifMRI ls contraindicated) Treatment conserwtive (same as cervical disc disease) surgical indications same as cervical disc + cauda equina syndrome Prognosis 9596 improve spontaneously within 4 to 8 weeks
Tablu11. Lllt:Dral Llnbar Disc Syu*a..us Figure 21 D. AKial semion of S111:111l Spine wltll Ya&cular aad
Functloaal Terrllerlea
Root .......
llcidaiC8
L4
<10% flllllllllpattam Madill leg Tibillislllllerior (dorlillsxion)
Klwejerk
L5
451.
Sciatic patllm
S1
45%
Sciatic palbln
.....,.
Ptin
l..a1inll !oat
Gntrocnemius, ealu (pllmr fl&Xian)
MaiDr
Raila.
AM!ejerk
IDllal unilateral
symmallic
legs,IB:k. or bladder
Sadcle; no sensiiY dissociation; may be unilllarll end asymmetric AsyrrmaiJE; pnsi& IWJI9 mar1cld; lllqlby may be llf8Sid; fascil:ulatians nn
Autonomic dysfunction,
Extradural Lesions
Neurosurgery NS27
---------------------------------------
Etiology compression or irritation oflumbosacral nerve roots below conus medullaris (below L2level) decreased space in the vertebral canal below 1.2 common causes: herniated disk spinal stenosis, vertebral fracture and tumour
Clinical Features usually acute (develops in less than 24 hours); rarely subacute or chronic motor (LMN signs) weakness/paraparesis in multiple root distribution reduced deep tendon reflexes (knee or ankle) autonomic urinary retention (or overflow incontinence) and/or fecal incontinence due to loss of anal sphincter tone sensory low back pain radiating to legs (sciatica) aggravated by Valsalva maneuver and by sitting; relieved by lying down bilateral sensory loss or pain: depends on the level affected saddle area (S2-S5) anesthesia sexual dysfunction (late finding)
Treatment urgent investigation and decompression (<48 hrs) to preserve bowel, bladder and sexual function and/or to prevent progression to paraplegia Prognosis markedly improves with surgical decompression recovery correlates with function at initial presentation: if patient is ambulatory, likely to continue to be ambulatory; if unable to walk, unlikely to walk after surgery
Investigations spine x-ray, cr, MRI, myelogram Treatment conservative - NSAIDs, analgesia surgical-laminectomy with root decompression
Neurogenic Claudication
----------------------------------
Etiology ischemia oflumbosacral nerve roots secondary to vascular compromise and increased demand from exertion, often associated with lumbar stenosis
Clinical Features dermatomal pain/paresthesia/weakness of buttock, hip, thigh, or leg initiated by standing or walking slow relief with postural changes (sitting >30 min), NOT simply exertion cessation induced by variable degrees of exercise or standing may be elicited with lumbar extension, but may not have any other neurological findings, no signs of vascular compromise (e.g. ulcers, poor capillary refill, etc.)
....
,,
v-1u CIMit:don
Claudlclltian: denmrtolllll distribution with positional relief accurrilg over minutes. Vacular CIMit:don: sclarotomll distribution with relief accurrilg with
rest owr s1condl.
Investigations bicycle test may help distinguish neurogenic claudication (NC) from vascular claudication (the waist-flexed individuals on the bicycle with NC can last longer) Treatment same as for lumbar spinal stenosis
NS28 Neuro1urgery
1'oroDio
2011
Definition
tumour
Clinical Features nonspecific features for any intramedullary spin81 oord pathology: sensory loss similar to central cord syndrome pain and temperature loss with preserved touch and joint position sense in a cape-like distribution at level ofcervical syrinx dysesthetic pain often occurs in the distrlbution of the &eDllory l.o&a LMN arm/hand weakness or wasting painless arthropathles (Charcot's joints), especially in the shoulder and neck due to loss of pain and temperature sensation (seen in less than 5%)
Flg1re Z3. T1 WelgMid IIIRI of
SyringDmyalil
Investigations
....... ,
Compartmentalize spillll cord lllllomil:lllv by loaation.
Complete Spinal Cord Lesion bilateral loss of motor/sensory and autonomic function at :M segments below lesion/injury, with
UMNsigns about 396 of patients with complete in:jurie& will develop some recovery within 24 hours, beyond
II
'1i!
any residual function at :2:4 segments below lesion signs include sensory/motor function in lower li.mbs and "sacral sparing" (perianal sensation, voluntary rectal sphincter contraction)
Tble13. CDmJMriiOn b8tween IIICGIIIplete Spinal Card l..eiiDn Syndrom11
Hemiseetion of card lpsilatinl Lt.lll weakness at tha l11im lpsilatanll UMN waakness bllaw lha l11ian BilatemllMN weakness at the lesioo Bilateml UMN 'ltoelkness belaw the lesion Urillry 1'818nti111 Ipsilateral loss of vibration and pra!Jiacaptian Cormlataralloss of pail111d ta'npnure PmiMIII lii#Jtlauch
Presi!M!d vlnlion and proprioceplion Bilteralloss d pain and lefl1llnlure Presi!M!d lii#Jt tuul:h
.B
A111H Canl
Sytivlmytlia_ tlmaur&, BiiUDI mlltlr Wlllkna&s: spinal Uppa' 1mb W8lkna&s (l.llfi lesion) iniiiY (J8Itsr 1Im LDwer liiD waalcness (UMN lasianl Urillry llllantian
IU!arir. spinal allay
Vllilbla blldsi'IIIIU&pal1dad slll&aly loa Loss d pain and tsiJ'C)III'Era 1han lass of vibl'llian and
P'allllriar Cord
PmiMIII
infarction. 'lnUIII
Peripheral Nerves/Neurotrauma
Neurosurgery NS29
Peripheral Nerves
see Neurology; N30
Investigations
neurological exam (power, sensation, reflexes), localization via Tinel's sign (paresthesia& elicited by tapping along the course of a nerve} electrophysiological studies (EMG, nerve conduction study) may be helpful in assessing nerve integrity and monitoring recovery; not helpful unti12-3 weeks post-injury labs: bloodwork, CSF imaging: C-spine, chest/bone x-rays, myelogram, CT, MRI "neurography" to rule out cerebral/ spinal cord lesions, identify etiology angiogram if vascular damage is suspected
Treatment
early neurosurgical consultation if injury is suspected entrapment conservative: prevent repeated stress/injury, physiotherapy, NSAIDs, local anaesthesia! steroid injection surgical: nerve decompression transposition for progressive deficits, muscle weakness/ atrophy, failure of medical management stretch/ contusion follow-up clinically for recovery; exploration if no recovery in 3 months axonotmesis if no evidence of recovery, resect damaged segment prompt physical therapy and rehabilitation to increase muscle function, maintain joint range of motion, and maximize return of useful function recovery usually incomplete neurotmesis surgical repair of nerve sheath unless known to be intact [suture nerve sheaths directly if ends approximate or nerve graft (usually sural nerve)] clean laceration: early exploration and repair contamination or associated injuries: tag initially with nonabsorbable suture, reapproach within 10 days
Complications
neuropathic pain: with neuroma formation complex regional pain syndrome: with sympathetic nervous system involvement
SPECIALTY TOPICS
Neurotrauma
Trauma Management (see also Indications for Intubation in Trauma
1. depressed WC (patient cannot protect airway): usually GCS 2. need for hyperventilation 3. severe maxillofacial trauma: patency of airway is doubtful 4. need for pharmacologic paralysis for evaluation or management ifbasal skull fracture suspected, use orotracheal instead of nasotracheal intubation note: intubation prevents patient's ability to verbalize for determining GCS
Medicine, ER7}
NS30 Neurosurgery
Neurotrauma
Trauma Assessment
.....
,
5orinlld
400lhslil
INITIAL MANAGEMENT ABC's of Trauma Management see Emeri!=DQ" Medicine. ER8 NEUROLOGICAL ASSESSMENT Mini-History
period of LOC, post traumatic amnesia, loss of sensation/function, type of injury/accident
3lelionl0poil ... pa!UiiQ 2lllllm0110poil
....
, .. ,......
, ........
ln1-
-.
Neurological Exam
Glasgow Coma Scale (GCS) head and neck (lacerations, bruises, basal skull fracture signs, facial fractures, foreign bodies) spine (palpable deformity, midline pain/tenderness) eyes (pupillary size and reactivity) brainstem (breathing pattern, CN palsies) cranial nerve exam motor exam, sensory exam (only if GCS is 15), reflexes sphincter tone record and repeat neurological exam at regular intervals
It'
IPII'IIAtlittll vilwl
Investigations
spinal injury precautions (cervical collar) are continued until c-spine is cleared C,T,L-spine x-rays AP,lateral, odontoid views for C-spine (must see from Cl to T1 (swimmer's view if necessary) or CT rarely done: oblique views looking for pars interarticularis fracture ("Scottie dog" sign) CT head and upper C-spine (whole C-spine if patient unconscious) look for fractures, loss of mastoid or sinus air spaces, blood in cisterns, pneumocephalus cross and type, ABG, CBC, drug screen (especially alcohol) chest and pelvic x-ray as indicated
ABCDS Al9mlent (Columns: lllllerior v.n.bnlllin1, portarior vtlrtablllllinl, spinolaminar line, posterior spinou5 tine) IIane (vartebral bodies, facets, spinous
proce5Ses) Cartilqa
Softtissun
Treatment for Severe Head lniury (GCS s8) clear airway and ensure breathing (if GCS sa, intubate)
secure C-spine maintain adequate BP monitor to detect complications (GCS, CT, ICP) monitor and manage increased ICP if present (see Herniation Syndromes, NS6)
skull fracture indirect signs of basal skull fracture confusion, impaired consciousness focal neurological signs extreme headache, vomiting seizures concussion with >5 minutes amnesia unstable spine use of alcohol poor social support (i.e. no friend/relative to monitor for next 24 hours) if there is any doubt, especially with children
KEY POINTS never do lumbar puncture in head injury unless increased ICP has been ruled out
all patients with head injury have C-spine injury until proven otherwise alcohol may not be the cause of coma - there may also be a hematoma low BP after head injury means injury elsewhere must clear spine both radiologically AND clinically (will require re-assessment if/when patient improves clinically)
Neurotrauma
Neurosurgery NS31
Head Injury
Epidemiology male to female: 2-3:1
-------------------------------------------------
Pathogenesis acceleration/deceleration: contusions, subdural hematoma. axon and vessel shearing/ mesencephalic hematoma impact: skull fracture, concussion, epidural hematoma penetrating: worse with high velocity and/or high missile mass low velocity: highest damage to structures on entry/exit path high velocity: highest damage away from missile tract Scalp Injury rich blood supply considerable blood loss (vessels contract poorly when ruptured) minimal risk of infection due to rich vascularity Skull Fractures depressed fractures: double density on skull x-ray (outer table of depressed segment below inner table of skull), CT with bone windows is gold standard simple fractures (closed injury): no need for antibiotics, no surgery compound fractures (open injury}: increased risk of infection, surgical debridement within 24 hours is necessary internal fractures into sinus may lead to meningitis, pneumocephalus risk of operative bleed may limit treatment to antibiotics basal skull fractures: not readily seen on x-ray, rely on clinical signs retroauricular ecchymoses (Battle's sign) periorbital ecchymoses (raccoon eyes) hemotympanum CSF rhinorrhea. otorrhea (suspect CSF ifhalo or target sign present); suspect with Lefort II/ III midface fracture Cranial Nerve Injury most traumatic causes of cranial nerve injury do not warrant surgical intervention surgical intervention CN II -local eye/orbit injury CN III, IY, VI- if herniation secondary to mass CN VIII - repair of ossicles CN injuries that improve CN I - recovery may occur in a few months; most do not improve CN III, IY, VI - majority recover CN VII - recovery with delayed lesions CN VIII - vestibular symptoms improve over weeks, deafness usually permanent (except when resulting from hemotympanum) Arterial Injury e.g. carotid-cavernous (C-C) fistula. carotid/vertebral artery dissection Intracranial Bleeding (see Blood, NS15 and Cerebrovascular Disease, NS17)
....
,, ,,
Etioloaill
....
U,.rsllf Sclllp
SCALP
Brain Injury
Primary Impact InJury mechanism of injury determines pathology: penetrating injuries, direct impact low velocity: local damage high velocity: distant damage possible (due to wave of compression), concussion concu,.ion: a trauma-induced alteration in mental status American Academy of Neurology (AAN) Classification (see sidebar) no parenchymal abnormalities on CT coup (damage at site ofblow) contre-coup (damage at opposite site ofblow) acute decompression causes cavitation followed by a wave of acute compression
..... ,
...----------------.
AAN Clulliflc:nan Grade I : altered lllllltll status < 15 min Grade 2: altered lllllltll status > 15 min Grad 3: any loss of consciousn111
NS32 Neuro1urgery
Neurotrauma
1'oroDio
2011
'' ,
Exa'ni1115 nin for .,..ill IIIII a1N symptar.-. IIJblm Ia nonnaiii:IMty H lynrml willin 15 nn lllrncrw fnlm activity far
contusion (hemorrhagic} high density areas on CT mass effect commonly occurs with brain impact on bony prominences (inferior frontal lobe, pole of temporal lobe) diffuse axonal injury/shearing
wide variety of damage results
may tear blood vesscll (hemorrhagic foci) often the cause of decreased LOC ifno space occupying lesion on cr
Secondary Pathologic Processes same subsequent biochemical pathways for each traumatic etiology
delayed and progressive injury to the brain due to high glutamate release -+ NMDA -+ cytotoxic cascade cerebral edema intraaanial. hemorrhages ischemia/infarction
raised ICP,lntracranial. HTN
1day, 1hlln - -
hydrocephalus
Extracranial Conditions
hypoxemia
slllus
due to trauma to the chest, upper airway, bra.instem extremely damaging to vulnerable brain cells leads to ischemia. raised ICP hypercubia leads to raised ICP (secondary to vasodilation)
systemic hypotension caused by blood loss (e.g. ruptured spleen)
II:IMtv .nv
wilhaul
2..,..
hyperpyraia
leads to increased brain metabolic demands -+ ischemia fluid and electrolyte imbalance iatrogenic (most common)
SIADH caused by head injury diabetes lnslpidus (DI) from head injury may lead to cerebral edema and raised ICP coagulopathy
Direction Df Fun:a
Intracranial Conditions
raised ICP due to traumatic cerebral edema OR traumatic intracmnial hemorrhage
Brain InJury Outcomes mJl.dl.y traumatic (GCS 13-15): post-concus&l.ve symptoms: HIA. fatlgu.e, dizzine88 nausea, blurred vision, diploplia, memory impairment, tinnitus, irritability, low concentration; 5096 at 6 weeks, 1496 at 1 ytm moderately traumatic (GCS 9-12): proportional to age (>40) and CT findings; 6096 good recovery, 2696 moderately disabled. 796 severely disabled. 796 vegetative/dead severe (GCS S8): difficult to predict. correlates with post-reSU&dtation GCS (espedally motor) and age
Figure ZS. CT Showing Ceep-Contr.Coup InJury
-----
inddence related to severity and location of injury (increased with local brain damage or intracranial hemorrhage) post-traumatic seizure may be immediate, early, or late presence ofearly (within first week) post-traumatic seizure raises incidence oflate seizures meningitis: associated with CSF leak from nose or ear hydrocephalus: acute hydrocephalus or delayed normal preiSUre hydrocephalw (NPH)
Neurotrauma
Neurosurgery NS33
Neurogenic and Spinal Shock 1. neurogenic shock: hypotension that follows SCI (SBP usually S:80 mmHg) caused by
interruption of sympathetics (unopposed parasympathetics) below the level of injury loss of muscle tone due to skeletal muscle paralysis below level of injury -+ venous pooling (relative hypovolemia) blood loss from associated wounds (true hypovolemia) 2. spinal shock: transient loss of all neurologic function below the level of the spinal cord injury, causing flaccid paralysis and areflexia for variable periods
Spiii/CII'II2004; lllrodadon: T1'il study YlliS liNd II illllrmning l'lllellierneudogi:IIIM:omewu improved will early 1<24 houll) lliial WV8'Y as C1J1111111Bd 1D lither ID 1>24 hou,.j 11111111V cr
-mMI m-uanart.
37lllicl.
Whiplash-Associated Disorders
definition: traumatic injury to the soft tissue structures in the region of the cervical spine due to hyperfle.xion, hyperextension or rotational injury to the neck
1683 eligibl& plli8rQ ltnioomic spinal iljuy), 919 lWii irid 764 lWii"" IIIIIIUDgicll dlficit lkill:on wu dltllriied bv' cak:ulltiig the percenblge al pllieniJ Mil senSOIY or molD! r..ction irnprMrnentiiCCOI'ding 1D the FninQI'1 ale. buill: &II;' daCIJII1IIIRion I1UIBd in imp!Md wtcoma COII1llll1d 10 hotllllltand COIII8MtM
tni.......
lulll"'
inPv IP<O.DDIIIdi
slides 11Milled .... pllie!O illdQJing nrlv lor incomplll inPv wu homogenous lp>O.IP.iL howeveull iilhar .. lwtaraganaity. Can&bln: Allilllglllllti!ti:lt{ jll1illilirQ. Mil .... lick of pllianl bomOQIIIIIity il T8C8i1l sbilial, tlil anll riCGIIIIiliidaliJn isilatMiugical decompression be considnl as "" optional priCtica liii!JMrG 1l'lllnllic spilllll Cllld ....
......,..,,...had ......
............ hllmnliiiCIDipi..
. . . . dnugllt
7lit Spiil.lrunl/2006; 6:335-343 lllrodlllliln: BIQng in lhlla 70's irid tliraugb1DU.eerly ID's tlil Nltilll'lll Awtl Spinll CGnl ..jlly SWes INASCISI were Clllluclld in tlir8e llrgt lliidomillld conlrolled trilll,liid lium tiiCIIelriillthei'IICIIIIIIiilllllltion1Dgivepltients
injly. trocal Mlation "' 81Ch of these trillsthe 'If' led tliele din to usess1hellellm lird.iding tlil NASCIS tri*I1D riMYtttlil evidse belind Malhodr,fgpulllion: Acrialllpllli5ll of the dB the NASCIS studies alonill'lilh a lflcl of MP on ICiill spilll injury. buill: Tlilllllhors r1il8 .-1 iau8l l'tilhmh of NASCS land incliding 1111 fltt
m ofthl
NASCIS I mil blnllill were only obserwd spinll ijlies. NASaS II was awlullad for lick of apilnllion 411 oplirun MP liming Ulng Mlllaikle ID "'llO'' mGtur claiiJIII post-tliellpl' on hotlllhe righl111d
11ft lid1 oftlil body. qgasting lhll ch-.gn in
tlllts1ldisticalanlysis wu
onlv
cr
tlilliillliingkbill&!itliii'IIUI!s. Odillior sUiies lliled Ill fel)rocb:e 1lie resuls NASC1S. IUdim is11i1 lactDrtllltlllldi Iince NASCIS lim II incUIId r.t' since it was tllrA9t 1D be LMiethiciiiD indMdulls111 aplacdlo111014). CliiCbiu: 1lia Dim conclidalhat basad on U.. mil OIW mlljarcriticilms al tlil NASCIS II mil Ill. nny lilllrougicll depltlmaiitl liM ttopped using MP as alllnillld rwlinl iiiiCIIIIi spinll cord inpy,liid also notetlilt its use is not Cllllllltt IICGIIII'IIndld bythl Food mil Drug Adirinistnltion il111e IXiW SIRs. They111ggest liltliarinvllltigltionis"'*''llllldto-rlhil
tJjeStionCOIIcUsNeiy.
NS34 Neuroaurgery
Neurotrauma
1'oroDio
2011
mlddle column: posterior half of vertebral body, dJsc and posterior longitudinal ligament posterior column: posterior arch, facet joints, pedicle, lamina and supraspinollll, interpinous and ligamentum ligaments
Types of Injury (Dennis Classification)
compression fracture (58%) produced by flexion posterior ligament complex (supraspinous and interspinous ligaments, ligamentum flavum and Intervertebral Joint capsules) remain Intact fractures are stable but lead to kyphotk deformity burst fracture (1796) stable: a.o:rerior and middle columns parted with bone retropulsed nelll'by hallmark is pedicle widening on AP X-ray spinal cord (seen on x-ray and CO: posterior colwnn is uninjured unstable: same as the stable but with posterior colwnn disruption (usually llgamentous) fl.exl.on diatraction injury (6%) byperfl.exion and distra.ctl.on of posterior elements middle and posterior columns fail in distraction classic: Chance = horizontal fracture through posterior arch, pedicle&, posterior vertebral body can be purely ligamentous, i.e. through PLL and disc fracture-dislocation (6%) anterior and aanial dislocation ofsuperior vertebral body -+ 3 colwnn fallure three types: flexion-rotation flexion-distraction shearthypermension (rare)
Figure 2&. Odcmtuid Fracture
Clasalllcatlo
vertl.cal compression forces the occtpltal condyles of the skull down on the Cl vertebra (atlas), pushing the lateral massea of the atlas outward and disrupting the ring of the atlas also am cause an occipital condylar fracture odontoid process fracture caW!e& Cl and odontoid of C2 to move independently ofC2 body
this occurs because normally Cl vertebra and odontoid ofC2 are a single functional unit
alar and transverse Ugaments on posterior aspect ofodontoid most commonly remain Intact following injury patients often report a feeling of instability and present holding their head with their hands C2 vertebral fracture (hangman fracture, traumatic spondylolisthesis of u:is):
bilateral fracture through the pars interarticularis ofC2 with subluxation ofC2 on C3 usu.ally neurologically intact
immobilimtion in cervical collar or halo vest until healing occurs. (usually 2-3 months) Type II and III odontoid fractures consider surgical :fintion for comminution, displacement or inability to maintam alignment with externallmmobili.zation onfirm stabillty after recovery with ftal.on-menslon x-rays
Neurotrauma
Neurosurgery NS35
------------------
Definition irreversible and diffuse brain injury resulting in absence of clinical brain function cardiovascular activity may persist for up to two weeks Criteria of Diagnosis prerequisites: no CNS depressant drugs/neuromuscular blocking agents, no drug intoxication/ poisoning, temperature >32<>C, no electrolyte/add-base/endocrine disturbance absent brainstem reflexes: absent pupillary light reflex absent corneal reflexes absent oculocephalic response absent caloric responses (e.g. no deviation of eyes to irrigation of each ear with 50 cc of ice water- allow 1 min after injection, 5 min between sides) absent pharyngeal and tracheal reflexes absent rough with tracheal suctioning absent respiratory drive at PaC02 >60 mmHg or >20 mmHg above baseline (apnea test) 2 evaluations separated by time, usually performed by two specialists (e.g. anesthetist, neurologist, neurosurgeon) confirmatory testing: flat EEG, absent perfusion assessed with cerebral angiogram
Clleric Refllllll
cows
Cold Opposite Warm
:sam.
Coma
Definition an unrousable state in which patients show no meaningful response to environmental stimuli Pathophysiology lesions affecting the cerebral cortex bilaterally, the reticular activating system (RAS) or their connecting fibres focal supratentorial lesions do no alter consciousness except by herniation (compression on the brainstem or on the contralateral hemisphere) or by precipitating seizures
NS36 Nearomrgery
Clauificlll:ion structural. lesions (tumour. pus, blood, infarction, CSF): 1/3 af comas supratentoriallll88slesion -leads to herniation infratentoriallesion- compression af or direct damage to the RASor its projections metabolic disorders!clitfuse hemispheric damage: 2/3 of comas deficiency of essential substrates (e.g. oxygen. glucose. vitamin Bu) exogenous tm1ns (e.g. drugs, heavy metals, solvents) endogenous toxins/sywtemic metabolic diseases (e.g. uremia, hepatic encephalopathy, electrolyte imabalances, thyroid stmm) infections (meningitis, encephalitis) trauma (concussion, diffuse shear uonal damage) lnvestiglll:ions and Management
ABCs
l.ab3: electrolytes, TSH, I.Ffs, Cr, BUN, Ca, Mg, PO" toxin screen, glucose Cf/MRI, LP, BEG
Definition
Etiology/Prognosis most commonly caused by cardiac arrest or head Injury due to irreversible loss ofcerebral cortical function BUT intact brainstem function avenge life expectancy is 2-5 years
Pediatric Neurosurgery
Spinal Dysraphism
SPINA BIADA OCCULTA
---------------------------------
Definition congenital absence ofa spinous process and a variable amount aflamina no visible exposure ofmeninges or neural tissue Epidemiology 15-2096 ofthe general population; most common at LS or SI
Hair tuft
Etiology
failure of fusion of the pollterior neural arch
Clinical Felll:ures
no obvious clinical signs
presence aflumbosacral cutJLneous abnormalities (dimple, sinus, port-wine stain. or hair tuft) should increase suspiclon ofan underlying anomaly (lipoma. dermoid, diastomatomyella)
Investigations plain film - absence ofthe spinous proceas along with minor amounts of the neural arch U/S or MRI to exclude spinal anomalies Tralll:ment requires no treal::nlellt
MENINGOCELE (SPINA BIFIDA APERTA)
herniation of meningeal tissue and CSF through a defect in the spine, without associated herniation of neural tissue
Definition
Pecliatric Neurosurgery
Neurosurgery NS37
Etiology
primary fiillure of neural tube closure
Clinical Features most common in lumbosacral area usually no disability, low inddence ofassociated anomalies and hydrocephalus
Investigations plain film&, cr, MRI, UIS, echo, geniiDurinary (GU) investigations Treatment surgical adsl.on and tissue repair (excellent results)
MYELOMENINGOCELE
Definition herniation of meningeal and CNS tissue through a defect in the !pine
Etiology same as meningocele Clinical Features sensory and motor changes distal to anatomk level producing varying degrees of weakness urinary and fecal incontinence 65-8596 of patients with myel.omeniDgocele have hydrocephalus most have Type II Chiari malfonnatlon, see NS38
Investigations plain film&, cr, MRI, UIS, echo, GU investigations Treatment
i
Figu111 21. Myelaaningacela
."' ..
Q
operative mortality close to 0%, 95% 2-year survival 80% have IQ >80 (but most are 80-95), 40-85% ambulatory, 3-10% have normal urinary
continence
early mortality usually due to Chiari malformation complieuions (respinltory arrest and aspiration), whereas late mortality is due to shunt malfunction
Hydrocephalus in Pediatrics
Etiology congenital aqueductal anomalies, primary aqueductal stenosis in infancy secondary gliosis due to intrauterine viral infections (mumps. varicella, TORCH) Dandy-Walker malformation (2-4%) Chiari malfimnation, especially Type II myel.omen1Dgocele
acquired
post meningitis post hemorrhage {SAH, IVH) masses (vascular malformation, neoplastic) Clinical Features symptoms and &igns of hydrocephalus are age related in pediatrics increased head circumference (HC), bulging anterior fontanelle. widened cranial sutures lrrltabillty,lethargy. poor feeding and vomiting "cracked pot" sound on cranial percussion scalp vein dilation (increased collateral venous drainage) sunset sign - forced downward deviation of eyes episodic bradycardia and apnea
NS38 Neuro1urgery
Investigations skull x-ray, U/S, CT, MRI, ICP monitoring Treatment similar to adults (see Hydrocephtdus. NS7)
1'oroDio
2011
Dandy-Walker Malformation
Definition
atresia offoramina ofMagendle and Luschka, resulting in complete or Incomplete agenesis of the cerebellar vermia with widely separated. bypoplaat!c cerebellar hemispheres posterior fossa cyBt. enlarged posterior fossa
dilatation of 4th ventricle (also 3rd and lateral venbicles) associated anomalies hydrocephalus (9096) agenesis ofcarpus callosum (17%) ocdpital encephalocele (7%)
Epidemiology
20% are asymptomatic, seizures occur in 15% symptoms and signs of hydrocephalus combined with a prominent occiput in infancy ataxia, spasticity, poor fine motor conttol common in childhood
Investigations ultresound.CT,MRI Treatment
asymptomatic patients require no t:reatment associated hydrocephalus :requires surgl.cal treatment supratentorial lateral ventricular or cystoperitoneal shunt
Progosis 75-10096 survival, 5096 have normal IQ
Chiari Malformations
Definition maltbrmations at the medullary-spinal junction
Etiology Wldear, llkel.y maldevelopment/dysgenesis during fetal life Categories Type I (cerebellar ectopia)
definition: cerebellar tonsils lie below the level of the foramen magnum epidemiology: average SF at presentation 15 years
clinical features: many are asymptomatic
i u
..
scoUosis brain compression central cord syndrome (6596) syr.i.ngomyell.a (50%) foramen magnum compression syndrome (2296) cerebellar syndrome (1196) hydrocephalUII (1096)
Typell
definition: part of cerebellar vermis, medulla and 4th ventricle extend through the foramen magnum often to midcervical region epidemiology: present in infancy cllnical features: findings due to brainstem and lower cranial nerve dysfunction syringomyelia, hydrocephalus in >80%
Neurosurgery NS39
Investigations
MRI or CT myelography
Treatment
indications for surgical decompression 'I)rpe 1: symptomatic patients (early surgery recommended; <2 years post symptom onset) -+ suboccipital craniectomy, duraplasty 'I)rpe II: neurogenic dysphagia, stridor, apneic spells -+ cervical laminectomy, duraplasty
Craniosynostosis
Definition
premature closure of the cranial suture(s)
Classification
sagittal (most common): long narrow head with ridging sagittal suture (scaphocephaly) coronal: expansion in superior and lateral direction (brachiocephaly) metopic (trigonocephaly) lambdoid: least common
Epidemiology
0.6/1,000 live births, most cases are sporadic; familial incidence is 2% of sagittal and 8% of coronal synostosis
Clinical Features
skull deformity, raised ICP, hydrocephalus ophthalmologic problems due to increased ICP or bony abnormalities of the orbit
Investigations
plain radiographs,
cr scan
Treatment
parental counseling about nature of deformity, associated neurological symptoms sutures involved) surgery for cosmetic purposes, except in cases of elevated ICP
Pwl:ent ('r.l
40 (23) (17)
20
8 8
Ependymoma
Mllignant glioma Craniopharyngioma
6 6
PNET
Pineal, oemn call tumour Other
4
3
Clinical Features
vomiting, seizure, rn.acrocrania, hydrocephalus developmental delay, poor feeding, failure to thrive often initially escape diagnosis due to expansile cranium and neural plasticity in children
Rlpi1t8d !tom Petflttie ri North Alrllrm. Vol44{4L KIN! LE. hill'illxlfn: r:1r1111tngu IDidillcfirw,pp. penrission !tom BIIIVilr.
cn:s
NS40 Neurosurgery
Functional Neurosurgery
Functional Neurosurgery
Movement Disorders
see
Disease, Tremor, Dystonia, and Multiple Sclerosis sections in Neurology, N27, N26, N28, N49, respectively
Tabla 14. Surgical Targets for Monmant Disordars
Morbidity
Simultaneous, biateral surgery/ stimulation is most comon Preferred target: anterodorsal subthalamic nucleus (SlNJ Other targsts: atellllllactic ablation (pallidotamyVstimulation of posteroventral pallidus interna (GI'i) Caudalmna incerta Parkinsonian tremor: sl!reotactic ablation (thalamotomyVstimulation of venlnll intermediate (Vim) nucleus of thalamus Prefumld targat (primary dystonia): sterea1actic ablation (pallidDIDmy/ stimulation of posteruvenlnll Gl'i Secondary dystonia: stimLJation of
39-48% improvament in Unified Parkinson's Disease Rating Scale (UPDRSJ scores Reduced dosage rJ medications (STNJ More effectiwlhan medical management in advanced PD Early intavention may reduce severity, course, and pi'OIJ'85Sion rJ disease Of little benefit for patients with atypical
Intracerebral hemanhage, infection. seizure ( 1%-4%) Paresthesias Involuntary movements Cognitive functioning: decreased laxicel fluency, impaired executive function (STN > GPi) Psydliatric: depression, mlllia, anxiety, apathy (SlN > Gl'i)
presentations
Dystonia
Canirlllallnl primary (generalized) dystcnias; cervical and brdive dyttonias (GI'i) Cantrlllataral secondary dyskinasia (i.e. drug-ilduced: L-dopa, neuroleptics; STNJ Canirlllall!ral appendicular ET (first disorder to be treated by DBS; DBS i& viable alternative to Rx) htention (cerebellar) tremor (IT] resuking from demyalination of cerebellar outflow lnlclll (i.e. in multiple sclerosis) Brainstem tremor (Homes tnrnor)
anterodorsal S1N
Stimulation of vanlnll poaterior lateral thalamic nucleus (VPL) Preferred target: stereotactic ablation (1halamotomyYstiTIJiation of Vim nucleus of 1halamus Other targets: stimulation of caudal mna incerta Parkinsonian tremor: slirnulalion of
Primary dy5tonia: 51% reduction in Burb-Ftim-Marsden Dystonia Scale (BFMDS) score Secondary dystonia: 628!1'1. improvement in dystonias Delayad efleclll: weala! months
Intracerebral hemonhage, infection. seizure (1%--4%) Minor effects on cognitive functioning (esp. decreased lexical fluency; SlN > GPi)
TIWIDr
Durable reductions in essential tremor rating scale (ETRSJ scores Reduced dosage of medications Conflictilg data on VOCBl/IBcial tremor
anterodorsal S1N
Intracerebral hemonhage, infection. seizure (1%--4%) ParesthasiiW'pain Dysarthria Ataxia Minor effects on cognitive functioning (esp. decreased lexical fluency) Tolerance may develop over time
Neuropsychiatric Disorders
see
Disanlar Obleaiva Compulsive Disanlar (OCD) Taunrtte" Syndro1111
Syndrome, Obsessive Compulsive Disorder and Depression sections in Neurology, N29 and PSJFchiatry. PSIS, PS7
Pro-.ras
Anterior capsulotamy/stimulatian of the anterior limb of the internal capsule (IC)
Table 15. Surgical Targets for Neuropsychiatric Disorders Indications Severe syrl'1l!onns refraclllly to medical management Outcom Currently under investigation Reportelly 2575% response rate Morbidity lnlnlcerebral hemorrhages (1 %-2%) Mild effects on cognitive functioning Anxiety panic disorder (case report) lnlnlcerebral hemorrhages (1 %-2%) Mild sexual dysfunction
Stimullltion of midline inlnllaminar Currently under investigation nuclei Ill the thalamus Reportelly >70% reduction in vocal Stimulation of motor and limbic or mDIDr tics + urge portions rJ GPi Stimullltion of the antarior limb of the IC Stimullltion of the subgenual cingulate cortex Currently under investigation Reportelly 60% response rate; 35% remission rate
Neurosurgery NS41
Chronic Pain
Tabla 16. Surgical Targats for Chronic Pain
Dilonl
Neuropllhic Pain
lndicatio
Pracedur.
Oub:ama1
Severe, intractable, Preferred 1Brget: stimLJation organic neuropathic of 1he contralateral ventral pain (i.e. post-stroke posterior lateral (VPL) and pain. phaniDm lilt pain. medial (VPM) thalamic trigemillll neuralgia. nuclei periventriruler/ chronic low-Mck pain. grey matter complex: regional pain (PVGIPAG) syndrome) Other blrgm: &timulirtion of the contralatenJIIC Stimulirtion of the contralalenll motor cortex Severe, intractable, organic nociceptive pain Bilateral (most common) stimulirtitll of tha PVG,IPAG
47'l. in pen:eptit11 of pain intEnsity Less favourable results in cenlnll pain syndromes and poorly localized pain
Noc:iceptiva Pain
Intracerebral hemonhages
(1%-2%)
Indications medically refractory seizures, usually defined as seizures resistant to two first line anti-seizure medications used in succession identification of a distinct epileptogenic region through clinical history, EEG, MRI, and neuropsychological testing. Other localizing investigations include magnetoencephalography, SPEer and PET if a distinct epileptogenic region cannot be identified. the patient may be a candidate for a palliative procedure such as corpus callosotomy Procedure most commonly adults: resection of the hippocampus and parahippocampal gyrus for mesial temporal lobe epilepsy arising from mesial temporal sclerosis children: resection of an epileptogenic space-occupying lesion hemispherectomy and corpus callosotomy are less common Outcomes and Goals freedom from seizures 41 79% of adult patients are seizure free for 5 years after temporal lobe resection 58 78% of children are seizure free after surgery surgery is associated with improvements in preexisting psychiatric conditions such as depression and anxiety, a well as improvement in quality of life measures Morbidity 0.4-4% of surgical patients will have partial hemianopsia, aphasia, motor deficit, sensory deficit, or cranial nerve palsy following anterior mesial temporal lobectomies most patients will have some decline in verbal memory following dominant temporal lobectomy and in visuospatial memory in non-dominant temporal resection the degree of memory decline stabilizes after 1-2 years Predlcton positive predictive factors for seizure freedom following anteromedial temporal lobe resection hippocampal sclerosis (unilateral) focal localization of interictal epileptiform discharges absence of preoperative generalized seizures twnoural cause complete resection of the lesion
........
flom.m.1bal..-r- ollrllland
NS42 Neurosurgery
Common Medications
Neurosurgery NS43
Common Medications
The folowing are ONLY; follow clinical judgment and to adults unless otherwise specified prescription reconmendlllions i1 practice; dosages refer
Tabla
n. Common Medications
Doling Schadule 4 mg IV over 2minutes, q1 0-15 milutes (do not axcaad 8 m!V'I2hr) Trigeminal neuralgia (tic douloureux): 100 bid, increase by 200 day up to a maximum of 1,200 mQI'day 200 mgtid Seizures: 200 mg PO bid. increase by 200 mg (inpatient: q3 days; outpatient q clays) 7 until tharapeutic lewl achievad (usual opti'lllm dosege: 800-1,200 mQI'day; range: 60()..2,000 mQI'day] lndic:lltians Status apilepticus Side Effacts Cammon lniBI'II:ticm Canlrlinllcatians Cammllllll Drowsin111s. sedation OtharCNS depressants, digoxin (increaSIII digoxin levels) Worsening of seizures, heart failure, anhytllnias, AV block. aplastic anemia. agranulocytosis, tlrorDiocytopenia, hepatitis, erythema multifurme, StuwnsJohnson syndrome Lithium (increases lithium toxicity), MAOI Other meds may increase carbammpine II!Vllb ortlave decreased ella Hypersensitivity to TCAs. previous bone marrow suppression, MAOI in past 14 days
{TegnltuPJ
cublmmpina
hematological toxicity)
phytain (Dilanti..)
Seizures: Loading dose: Seizures 18 mg./kg &low IV or 300-600 mg Status apilepticus PO/day divided bid/lid Maintenance: 201J..500 mg W/day (max. rate: <41J..50 mQI'min or 300 mg PO average mainlllnance ose: 300 mQI'day PO Status epilepticus: 200 mg W over 30 miootes (-20 miVlcu; not taking 11111ularly), or 500 mg Wover 10m1nutes (if alraedy on phenytoin) Cerebral edema (e.g. secondlry to 1urnour, head injury, pseudotumour cerebri) Preoperative preparation for patients with increased ICP secondlry to brain neoplasms
Other meds may incree&e phenytoil levels and toxicity or have decreesad effects
dllliiii1IIIIIISIIII Loading dose: 10-20 mg IV; Maintenance: 4-6 mg W/day divided qid (may be PO)
Psaudotumour cerebri, seizures, heart failure, anhytllnias, tlromboembolism, pancreatitis, acute adfl!lllll insufficiency; avoid abrupt withdrawal
Aminogkrtethimide, antidiabetics,I>SA, NSAIDs, balbituata&, phenytoin, rifampin, cardiac glycosides, cyclosporine, ephedrine, oral potassiumdrugs. selicytates, skin-tasting antigens, toxoicls, vaccines
man1itol
1-1.5 wkg Wrapid i'lusion (350 ml of 20% solution] followed by 0.25 glkg q6h
Raised ICP
Anuria, severe pulmonary congestion, fnd edema. severe eart failure, severe dehydration, metabolic edema, progressive renal di&asse or dysfunction, active intracranial bleeding except during craniotomy Nona known
Effect occurs in 1-5 mins, maximal Ill Often altemllled with furosemide 1()..20 mg Wq6h Indwelling urnry catheter to measure ins and outs Causes vasodilation Only calcium channel blocker (CCB]1hat crosses BBB (blood brain berrier] Use half the nonnal dose for liver failure; monitor BP always
nimclllpila
Vasospasm in SAH
Decraased blood Antihypertansives pressure, tachycardia, (may increase dyspnea hypotansive elfacts], CCB (may ilcreese ellec:b), cimetidine (increases nimodipine bioavailability]
NS44 Neurosurgery
References
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