7Targeted Therapies for Localized Prostate Cancer: The Urologists PerspectiveJAMES JOHANNES, LEONARD G. GOMELLA, AND EDOUARD J. TRABULSIDepartment of Urology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, U.S.A.INTRODUCTION There have been great advances in both detection and treatment of prostate cancer over the past 20 years. Largely, because of the application of routine prostate-specific antigen (PSA) screening, cancer-specific mortality fromprostate cancer has decreased over this time period (1). With early detection and modern treatment modalities, prostate cancer five-year survival in the UnitedStated is now greater than 99% for all patients (2). In addition to these improvements, routine PSA screening has led to a marked stage migration with the majority of newly diagnosed patients presenting with localized disease. These epidemiological changes are prompting a reexamination of prostate cancer risk stratification and treatment algorithms. Patients with low-risk localized disease are eager to pursue minimally invasive, targeted therapies to avoid radical surgery orradiation therapy, because of the side effects and complications commonly seen with traditional treatment options. Treatment options for localized prostate cancer are expanding. Historically, patients decided among radical surgery, radiotherapy, or active surveillance (watchful waiting) (3). Treatment direction shouldbe made after a personalized discussion, ideally, in a multidisciplinary fashion(4). With the advent of laparoscopic and robotic radical prostatectomy, much ofthe perioperative morbidity of the procedure is minimized while offering thebenefits of a curative procedure with improved convalescence and cosmesis. Despite the technical advantages of laparoscopy, patients still face similar postoperative functional and quality of life side effects as with standard open radicalprostatectomy. In a recent review of roboticassisted laparoscopic prostatectomy(RALP), between 82% and 96% of patients required 0 to 1 pad daily for incontinence and only between 38% and 66% were able to perform sexual intercourse six months after surgery (5). Three-dimensional conformal external beam radiotherapy (3DCRT), intensity-modulated radiotherapy (IMRT), and prostate brachytherapy are targeted radiotherapeutic options for the treatment of localized prostate cancer.Technological improvements in modern radiotherapy have improved the accurate targeting of prostate cancer. These advances have decreased the dose administered to the adjacent tissues such as the bladder and rectum, significantly reducing toxicity, while concomitantly allowing a higher and potentially more efficacious dose administered to the target (prostate) tissue (6). However, there exists a significant number of patients who fail to get localized treatment from presumed understaging or radioresistant tumors (7). Finally, active surveillance in the correct patient population avoids the morbidity of treatment and may not affect their prostate cancerspecific mortality (8). However, many of these patients eventually opt for treatment or progress to advanced disease.7172Johannes et al.Today is an exciting time for prostate cancer specialists, both in the refinement of older technologies and development of new approaches for prostate cancer. Clinicians today have new minimally invasive treatment options including cryotherapy and high-intensity-focused ultrasound (HIFU) ablation. By implanting fiducial markers to improve radiation therapy, multimodality approaches to prostate cancer are expanding into treatment. Although these modalities are not yet widely available, tomorrows urologist will likely see these technologies become mainstream. CRYOTHERAPY History The first use of freezing for the treatment of cancer in

medical literature dates to 1850 (9). The first closed cryosurgical system was reported in 1938 when hollow bore instruments carried an ice mixture to treat metastatic tumors (10). Following the development of liquid nitrogen closed systemtechnology, cryosurgery of the human prostate was described as a treatment for benign prostatic hyperplasia (BPH) and cancer (11,12). Innovations in cryotherapyover the past several decades have marked milestones in the improvement of thistreatment modality (Table 1). First Generation Early cryosurgery of the prostate was used only on nonsurgical candidates. In the late 1960s and 1970s, a directtransurethral or transperineal approach using liquid nitrogen was used (13,14).In these early techniques, cystoscopic and digital rectal monitoring of the freeze sought to minimize injury or damage to periprostatic tissues. The morbidityfrom these procedures was extreme by modern standards. Despite the high risks ofincontinence, severe urethral sloughing, and stricture, first generation cryosurgery compared favorably to the radiation and radical surgery morbidity of the era (15). Second Generation Several technological advancements in the 1980s prompted reinvestigation in prostatic cryosurgery. TransrectalTable 1 Evolution of Cryotherapy Generation 1st (1960s) 2nd (1990s) 3rd (current) Cryogen Liquid nitrogen Liquid nitrogen Argon/helium Probe size 6.3 mm 3.4 mm17 gaugeultrasound proved to be an improved method of observing the extent of ice ball formation (16). Constant flow urethral warming catheters marked a major breakthrough in limiting cryotherapy morbidity. By keeping the urethral tissue from freezing, the rate of postsurgical urethral sloughing, stricture, and fistula improved greatly (17). The use of multiple cryoprobes improved the uniformity of freezeand improved efficacy by simultaneously freezing the entire gland (18). These technical advances were made in the setting of modern PSA testing. PSA screeningidentified prostate cancer earlier and provided a valuable method of monitoringtreatment response. It proved that cryotherapy was efficacious in properly selected patients with localized cancer (19). Third Generation Although cryotherapy is described in three generations, the modifications in technique and equipment were added as they became available, ultimately evolving into what is commonly described as the third generation of cryosurgery. A major limitation of liquid nitrogen is the requirement of relatively large bore needles. Utilizing the Joule-Thompson effect of gas compression, a new cryogen using argon and helium gasses made cryotherapy through small-bore needles possible. These thin needles now allow a direct percutaneous approach and multiple needle placements providing a moreexact freeze. Multiple small cryoprobes are inserted percutaneously in the perineum through holes in a brachytherapy-like template. Several coordinated systemsoptimize the treatment while seeking to minimize injury to nontarget tissues. The edge of the advancing ice ball is monitored not only by transrectal ultrasound but also by thermocouplers placed at the target margins. Urethral warmers prevent excessive urethral sloughing and its side effects. Finally, optimal treatment plans are calculated using computer modeling. Together with better patient selection, these advances culminating in todays cryosurgical technique have minimized the morbidity and optimized the efficacy of prostate cryosurgery. Tissue Destruction Physiology Refinements in cryoablative surgery have improved the abilityto efficiently kill cancer cells. Optimizing theUltrasound guidance No Yes YesUrethral warmer No Yes YesTemperature monitoring Manual Manual ThermocouplersTargeted Therapies for Localized Prostate Cancer73freeze temperature, duration of freeze, speed of cooling, and the number of cycl

es maximizes tumor death. The lethality of extreme cold to prostate tissue is due to both direct cell effects and secondary vascular causes. A rapid and prolonged freeze with a slow thaw maximizes lethality by a combination of intracellularice crystal formation and disruption of normal osmotic gradients (20). Furthermore, a double freeze-thaw cycle has been shown to have lower posttreatment positive biopsy rates and fewer PSA recurrences (21). In addition to intracellular effects, the freeze-thaw cycle destroys prostatic microvasculature that contributes to a delayed necrosis (22). Patient Selection Careful patient selection is crucial for all treatment modalities for prostate cancer and is particularly important for cryotherapy. As the indications for cryotherapy of prostate cancer continue to evolve, its applications are broadening. Most commonly, it is used as a primary treatment in patients who are nonsurgical candidates and are eligible forradiation therapy and decide against active surveillance or watchful waiting. Although use as a salvage therapy is controversial, secondary cryotherapy may have a promising future as a surgical option for local recurrence after initial radiotherapy treatment. Clinical risk stratification in patients with presumed organ-confined prostate cancer is a primary determinant of treatment options. With routine PSA screening, the majority of patients with localized cancer present with clinical stage T1c disease (23). Risk stratification is estimated by pretreatment PSA, Gleason score on TRUS biopsy, and clinical stage on digital rectal exam. Several nomograms are used routinely by urologists and radiation oncologists to estimate pathological stage and recurrence rates on the basis of these variables (2330). Primary cryotherapy for localized prostate cancer is an option, in general, for patients with clinical T1c to T3 disease. However, patients with periurethral disease are poor candidates as urethral warmers prevent an adequate killtemperature from reaching this tissue zone. Furthermore, high impotency rates associated with cryotherapy makes patients interested in preserving potency poorcandidates. Prostate size is an important consideration in offering cryotherapy.Patients with large pretreatment volumes (larger than 50 cm3) or those with a serum PSA level >10 ng/mL, may benefit from neoadjuvant hormone blockade (21,31).After hormonally induced size reduction, the entirety of the gland is more reliably treated. Additionally, shrinking the prostate can help separate it from therectum, preventing rectal wall damage (32).Despite these limitations, cryotherapy offers advantages over primary radiationtherapy or surgery. First, it is administered in a single day as compared to theseveral week course of treatment for radiation therapy. Due to the minimal blood loss, shorter operative time, and quick recovery, patients with a prohibitiveoperative risk can typically undergo cryotherapy safely, even under spinal anesthesia. In patients with high-risk disease, a pretreatment laparoscopic pelvic lymph node dissection can help determine the status of lymphatic metastasis (33).Patients with evidence of extraprostatic involvement should not be offered cryotherapy, but counseled on other treatment options. Finally, cryotherapy is safe to repeat, improving local control of locally recurrent disease. Follow-up AfterCryotherapy Patient follow-up after cryotherapy is based on PSA surveillance. Initially, PSA is checked every three months for the first year and every six months thereafter for the first few years. Due to cell necrosis, there is an initialbump in serum PSA that falls over time to a nadir (34). Unlike the postprostatectomy setting, in which the PSA should nadir to undetectable, and similar to radiation therapy, there is no consensus postcryotherapy nadir PSA indicative of biochemical failure. Biochemical failure has been variably defined in a range from0.3 up to 1.0 ng/mL (35,36). Others advocate the use of the accepted American Society for Therapeutic Radiology and Oncology (ASTRO) criteria of three consecutive PSA rises following nadir (37). There have been several studies describing five-year follow-up of patients treated with cryotherapy (Table 2). For low-riskpatients, the biochemical recurrencefree range from 60% to 80% (36,38,39). The largest single institution experience reported cryotherapy outcomes in 590 consecutive patients with seven-year follow-up (36). Although the first 350 patients were treated with a second generation machine, the results are consistent with other smaller more recent series (Table 2). Overall, 15.9%, 30.3%, and 53.7% were l

ow-, intermediate-, and highrisk patients, respectively. All patients were followed with both PSA measurements and routine biopsies at 6, 12, 24, and 60 monthspostoperatively. Using the ASTRO criteria, the seven-year actuarial biochemicaldiseasefree survival (DFS) was approximately 90% for all risk groups. Overall, 13% of patients had a positive posttreatment positive biopsy although the authorsdid not stratify these patients according to preoperative risk. Together, theseresults suggest there were some recurrences or treatment failures identified bybiopsies that were not identified by PSA recurrence. Although definitions of recurrence vary,74 Table 2 Outcomes in Modern Prostate Cryotherapy Series Series Han et al. (45)Donnelly et al. (39) Year 2003 2002 Number of patients 122 76 Generation 3rd 2nd Length of follow-up 12 mo 5 yr PSA recurrence criteria (ng/mL) !0.4 >1.0 >0.3>0.4 ASTROJohannes et al.PSA recurrence-free rate % (risk) 76 73 75 89 76 60 77 48 84 92 92 89 87 79 71 61 68 61 76 71 61 60 61 36 (low) (all) (low) (intermediate) (high) (low) (intermediate) (high) (low) (intermediate) (high) (low) (intermediate) (high) (low) (high) (high) (low) (intermediate) (high) (low) (intermediate) (high)Ellis (44) Bahn et al. (36)2002 200275 5903rd 2nd/3rd3 mo 7 yr>1.0 >0.3 Long et al. (38)a >1.0 >0.520019752nd/3rd5 yraPooled analysis of five series. Abbreviations: ASTRO, American Society for Therapeutic Radiology and Oncology; PSA, prostate-specific antigen. Source: From Ref.81.patients generally undergo biopsy once recurrence is suspected. A smaller seriesreporting results of 65 men with highrisk prostate cancer defined as a preoperative PSA >10 ng/mL or Gleason score !8 utilizing the ASTRO criteria for PSA recurrence shows that cryotherapy is a viable primary option for high-risk cancer (40). Eighty three percent of their patients were free of biochemical recurrence at a median of 35-month follow-up. Moreover, only one of the eight patients who underwent biopsy had histological evidence of cancer. This highlights the difficulty in using both the ASTRO criteria to screen for recurrence and reliability ofthe small sample prostate biopsy to confirm recurrence. Although these numbersare promising, ten-year follow-up data with modern cryotherapy is awaited to determine the long-term recurrence-free rates. Although cryotherapy is often a secondary option for many patients who cannot be offered radical surgery and choose

against radiotherapy, the cryotherapy cancer control rates are comparable to reported rates for radical prostatectomy and radiotherapy. A representative study of 743 patients receiving dose escalation conformationalradiation therapy were followed prospectively for PSA recurrence (41). These patients were stratified into favorable risk (stage T1 or T2, Gleason score 6 or less, PSA 10 or less), intermediate risk [one adverse feature or unfavorable (twoadverse features)]. The five-year PSA-free recurrences were 85%, 65%, and 35%, respectively. For patients treated with brachytherapy, similar results are seen.One study of brachytherapy with a long mean follow-up period of 82 months showedPSA-free recurrence rates according to ASTRO criteria in low-, intermediate-, and high-risk patients of 91%, 80%, and 66%, respectively (42). Unfortunately, arandomized trial comparing cryotherapy and radiotherapy options that could compare the oncological efficacy of these modalities has not been performed, and mostclinicians shy away from cryotherapy for higher-risk patients. Cryotherapy as an Option for Recurrent Disease Cryotherapy has an emerging role as salvage therapy for local recurrence or progression following primary radiotherapy modalities, based on PSA or biopsy data.Targeted Therapies for Localized Prostate Cancer75Radiation therapy has long been a salvage therapy for patients with biochemicalfailure and presumed local recurrence after prostatectomy. Similarly, cryotherapy is a potential salvage therapy for local recurrence after radiation failure. Once residual cancer is confirmed by biopsy and evidence of systemic disease is excluded, curative options for these patients are limited. Salvage cryotherapy offers an attractive alternative to salvage prostatectomy, which is technically difficult and carries significant risk and morbidity than primary radical prostatectomy. Salvage cryotherapy, in properly selected patients, may be an appropriatechoice for radiotherapy failures. In the largest cohort of patients failing primary radiotherapy, salvage cryotherapy showed a five-year 79% diseasespecific survival (DSS) and 40% DFS rate (43). Examining the relatively modest five-year DFS, it is clear that patient selection is paramount, since the majority of patients will fail despite additional local therapy, indicative of likely micrometastatic disease at the time of salvage treatment. Several factors predictive of a durable response to salvage cryotherapy were identified, including hormone-sensitive prostate cancer, PSA dermoid (5%) In temporl one: Grdenigos, Cholestetom ( T1 & T2, chronic otitis), glomustympnicum, mlignnt externl otitis (DM), jugulr ul Bells & Rmsy-Hunt enhnce. Posterior foss: Kids: Pilocytic strocytom > medullolstom (homogeneous enhncement) > ependymom (clcified, hemorhhgic, cystic, extend thru Luschk). Adult: Met, hemngiolstom, strocytom IAC: neuritis (Bells, Rmsy-Hunt)Oritl: cvernous hemngiom > melnom > retinolstom (kids) Optic n.: Meningiom, pseudotumor, gliom Anterior skull se: meningiom, met, mucocoele, osteom, polyposis, inverted ppillom, esthesioneurolstom, cocine grnulomtosis. Middle skull se: mets, juvenile nsophryngel ngiofirom (dolescent mles, origintes t sphenopltine formen), meningiom, chordomFlotte Outline of Neurosurgery28Nsophryngel: squmous cell CA, denoCA, denoid cystic CA, chondrosrcom, esthesioneurolstom. Durl (meningiom mimics): hemngiopericytom, durl cvernous mlformtion, srcoms, met, extrmedullry hemtopoesis (focl enhncing mss), melnocytom, srcoid, Temporl loe: glioms, HSV, limic encephlitis Pituitry Lesions Lymphocytic Hypophysitis: More common in femles, periprtum/pregnncy (20%), utoimmune disese (30%) Presenttion: hedche (75%), hypopituitrism (DI 30%; lethrgy, loss of liido), mss effect Imging: Enhncing sellr mss, 80% suprsellr extension, 30% thickened infundiulur stlk. Other types ofinflmmtory hypophysitis: grnulomtous, xnthogrnulomtous, xnthomtous, necrotizing o Infundiuloneurohypophysitis: Involves stlk only. Resolves with conservtive tretment. Tretment: o Steroids: Lws recommends tril of high-dose steroids with clinicl suspicion (pregnnt ptients with hypopituitrism) exceptwith progressive visul loss, ut response is inconsistent (60% response) nd hypophysitis my recur upon discontinuing steroids o TSRP: Hedche nd visul fields improve, hypopituitrism doesnt. o SRS. Grnulr Cell Tumor (Choristom): From posterior pituitry pituicytes. Cliniclly resemles nonsecretory denom. Noclcifiction (vs crnio). Strongly enhnces. Densely pcked, lrge PAS+ eosinophilic cells. Pituicytom (GFAP+) proly sme tumor. (per WHO).Skull lesions: Firous dysplsi: Thick, sclerotic, enhnces. Young. Lionlike fcies. 70% monostotic. Woven one: immture. No srcomtous degenertion. Visul loss/ CN deficits. Alrights syndrome: unilterl polyostotic firous dysplsi, precocious puerty, skin lesions, femles Eosinophilic Grnulom: No sclerotic rim, pinful, gint cells, excision or XRT. sclerotic phses. CN compression, osteosrcom trnsformtion. Men >40yo. Hyperostosisfrontlis intern, prietl formin: norml vrints (HFI elderly women) Idiopthic hypertrophic pchymeningitis: diffuse durl enhncement (lso occurs w/ srcoid, histiocytosis, intrcrnil hypotension)Flotte Outline of Neurosurgery29Epilepsy Intrctle: filed t lest 3 meds. Occurs in 30% Antiepileptics Non-enzyme inducing: Kepr (po only), Lmictl (po only), Depkote (cuses leeding?) Tegretol: cuses leucopeni, heptitis Hippocmpl Sclerosis AKA Ammons Horn Sclerosis (AHS) Correlted with Mesil Temporl Sclerosis (MTS) on MRI ( FLAIR/T2). Hypometolism on PET Correlted with ferile seizures Seen with Timm stin CA1 & CA3 loss Hypothlmic hmrtom Cuses gelstic seizures initilly, then complex-prtil or generlized. Responds well to rdiosurgery. o Gelstic seizures: lughing fits. Other cuses: hypothlmic gliom, 3rd ventricle tumor, temporl loe epile

psy, infntile spsms, etc. Tumors Seizure focus is usully in the surrounding rin, not in the tumor Single or controlled seizures do lesionectomy. Intrctle seizures lesionectomy plus intropertive ECOG nd resection of seizure focusCorticl Dysplsi With complete resection of epileptogenic focl corticl dysplsi, 87% hve good seizure outcomeGenerlPreopertive EvlutionPhse I: Imging MRI (FLAIR) If nonlesionl then proceed with: PET o Ictl PET shows hypermetolism in focus. Interictl PET shows hypometolism in focus in 70%. o Sensitvity in TLE 60-90% o Does not correlte with histopthologicl chnges (eg trophy) SPECT o Sutrction Ictl-Interictl SPECT shows hypermetolismin focus Cn coregister T1 MRI with PET, SPECT, grid xry for imge guidnce (JN3/04) Sclp EEG/Video-EEG Neuropsychologicl Testing Phse II: Invsive monitoring Sudurl Grids & Strips: Sclp EEG fils to loclize focus in 30%. Stndrd:2 plced perpendiculr to temporl loe (consider 1 medil & prllel) Electrocorticogrphy my ssist in grid plcement Low-mplitude high-frequency ctivityt onset correltes with good surgicl outcome. Electrodes recording higher-frequency spikes re closer to focus Depth Electrodes WADA test: Injection of sodiummoritl into ICA. Used to predict lnguge & memory locliztion. Speech: rrest not enough, must hve nming errors. Memory: Uses: o 1) Memory locliztion: less relile thn speech. (Note hippocmpl lood supply minly from PCA) o2) Focus locliztion: le to detect side of eplieptogenic focus in 40-80%, incorrect in 5.5cm posterior) o Anterior choroidl . cn loop into choroids plexus void cogulting choroid plexus Anterior temporl loectomy: o 70-94% Engle I-II. o Diplopi 19% (due to CN4 plsy, resolves). o Extent: 4-5cm in nondominntloe, 3.5-4cm dominnt loe. o Open choroidl fissure etween hippocmpus nd choroids plexus (vessels run etween choroids plexus & thlmus). Be wre of sl temporl lnguge re (N5/04) o Temporl lootomy: See N6/04 Amygdlohippocmpectomy: Trnssylvin pproch descried y Ysrgil. 74% Engle clss I-II in kids. Versus ATL: No difference in dults, worse control in peds. Corpus Cllosotomy: Indictions: Secondry generlized, tonic, infntile hemiplegi, Rsmussens,Lennox-gstut. Contrindicted in crossed dominnce (left-hndedness with left-sided speech) otin WADA in ll left-hnded ptients. Complictions: o Anterior: spontneous speech (SMA), nondominnt leg presis & grsping, urge incontinence (ll usully temporry). Permnent speech deficit with mixed cererl dominnce (speech & motor on opposite sides). o Posterior: interhemispheric disconnection syndrome ( tctile senstion & vision on nondominnt side, rdyphreni, incontinence o Complete: s ove + nondominnt hnd doesnt perform commnds (cn perform ntgonistic ctions) Hemispherectomy Indictions: Hemiplegi with intrctle seizures: Rsmussens disese, corticl dysplsi, hemispheric infrct. Antomic: Complete resection of hemisphere. Complictions: hydrocephlus, superficil siderosis. Functionl: Removl of centrl cortex nd temporl loe, sl gnglileft intct ut disconnected from cortex, disconnection of contrlterl hemisphere. 25% reopertion for recurrent seizures. Other techniques: Hemisphereotomy(JN:P2/04). Vgl Nerve Stimultor: Effective on left side only (reson unknown). Efficcy: All seizure types eqully reduced. 42% reduction in szs @ 18mo, very

few seizure free. Equivlent to dding nother medicine. Complictions: Coughing, voice chnges, drooling, lughing, torticollis, urinry retention. (No crdic chnges reported.) Multiple Supil Trnsections Used to mke disconnections in eloquent cortex Used lone: 15% seizure-free, 35% improved, 50% unchnged. Comined with resection: 40% seizure-free, 40% improved, 20% unchnged. Used in Lndu-Kleffner Syndrome in which epileptic phsi develops in previously norml child Intropertive Electrocorticogrphy Done either with strips or the Hellriser Under generl nesthesi void enzodizepines nd itutes. Under locl useonly nrcotics (fentnyl) nd droperidol. Periopertive Tper nd discontinue AEDs 24hrs preop. Continue AEDs 1-2 yers.Rdiosurgery Dose limited y optic chism nd rinstem. Tkes >9mos to work; urs or seizures my increse efore decresing. My tke up to 3yrs efore considering retretment. One report using 20Gy (N6/04) showed 0/5 improvement with MTS nd possily worsened cognitive testing. Mrseilles group (Regis) report 82% seizure-free nd nother 12% significntly improved using 25Gy. T2 signl peks t 1yr. Multicenter tril (led y UCSF) currently ongoing.Deep rin stimultion: of nterior thlmic nucleus nd other res (centromedin nucleus, STN, hippocmpus) eing investigtedFlotte Outline of Neurosurgery31InfectiousCererl scess Most common orgnisms: neroic/ microerophilic Strep. Immunocompromised: Nocrdi, Toxo. Neontes: Proteus, Citrocter. Predisposing fctors: Sinus/dentl infection, pulmonry scess/empyem, cynotic crdic disese (Tetrlogy, kids), pulmonry AVF (Osler-Weer-Rendu, hereditry hemorrhgic telngectsi), endocrditis (rre), AIDS Symptoms: 50% hve low-grde fever. L: CXR, ESR/CRP, CBC (WBC >10K), BCx (10% positive), HIV, Toxo testing. LP contrindicted. Imging o Cereritis vs encpsulted scess: On delyed CT cpsule enhncement decys, cereritis doesnt. Cereritis usully thicker o MR-Spect: lctte,cette, pyruvte. My use to follow response to tretment. Also WBC-tgged scns. Tretment o Medicl: ntiiotics steroids o Indictions: Cereritis, 10yers. Tpeworm (intestinl) infection results from eting undercooked pork. Cystercercosis results from eting tpeworm eggs (ie through fecl contmintion of food or utoinocultion). My e meningel, prenchyml, ventriculr. Usully ring-enhncing lesions with miniml edem. My hve sucutneous nodules. CSF my show eosinophili. Serum nd CSF ntiody titers cn e checked. Tretment: Prziquntel nd steroids. Rrer prsities: echinococcus (hydtid cysts) dogtpeworm. (my grow to e lrge, e creful not to rupture cyst); meisis Grdenigos Syndrome: osteomyelitis of petrous pex. CN6 plsy & retrooritl pin, from otitisFlotte Outline of Neurosurgery32Whipple disese: Cused y cteri Tropherym whippelii. Symptoms: gstrointestinl symptoms nd migrtory rthrlgis. Pth: perivsculr mcrophges with distse-resistnt PAS (+) grnules. Involves CNS in 25%: dementi, multifocl grey-mtter lesions, especilly temporl cortex, thlmus, etc.Flotte Outline of Neurosurgery33Peripherl Nerve Neuroprxi > Axonotmesis (perineurium nd epineurium intct) > Neurotmesis. Sunderlnd clssifiction I-V. Spontnteous recovery: 40% C5/6, 18% C5-7, 5% C5-T1(flil rm) Motor recovery occurs within 18mos (no limit on sensory) Tretment Lcertion: Repir within 72hrs if shrp. 2-4 weeks if lunt (to llow delinetion of injury) Penetrting: explore when 1 wound heled. GSW: 2-5 mos for GSW withcomplete or severe lesions-in-continuity with intropertive o Erly explortionis dvocted y some Trction/Blunt : 3-6mos. Seril EMG/NCVs (& SSEP?) q3mos,repir if no improvement on EMG or cliniclly. Repir possile for upper elements only. Also for pin, pseudoneurysm. Most effective if ptient is 3wks), norml SNAP (lost in postgnglionic lesions. More sensitive thnn sent SSEP), MRI/CT shows meningocoele. Root vulsion No spontneous recovery. Grfting not yet fesile (experimentl). Most tretment is y nerve trnsfer. Intropertively some dissect the nerve root into the formin to prove vulsion Brchil Plexus Explortion Trunks t lterl order of nterior sclene. Cords t level of 1st ri. Suprclviculr exposure: Supine, shoulder roll, hed turned wy. Incision posterior order SCM, long clvicle. Pltysm divided. EJ

divided. Trnsverse cervicl . & v. ligted only if suclvin . ptent. Clviculr hed SCM detched. CN11 under SCM preserved. Omohyoid divided. Phrenic n.identified on nterior side of nterior sclene & moilized medilly. Brchil plexus runs etween nterior & middle sclenes. 1-2cm of nterior sclene resected. Thyrocervicl trunk preserved if possile. Infrclviculr: Incision long clvicle to deltopectorl groove. Cephlic v. exposed. Clviculr hed of pectorlis m. divided. Pectorlis minor detched from corcoid process. Suclvius m. detched from clvicle. Lterl cord identified. Avoid sectioning clvicle hels poorly. Axillry: Extend infrclviculr incision long pectorlis to humerl insertion (my e detched). Musculocutneous n. elow pectorlis. Posterior pproch: useful fter nterior pproch filure or TOS. Ptient prone, rm ducted &flex, hed turned contrlterl. Incision etween medil order of scpul & spine. Trpezius, levtor scpule & rhomoids divided. 2nd ri divided medilly,1st ri & T1 trnsverse process resected. Sclenus posterior & medius trnsected. Trunks visile Neurotiztion (Nerve Trnsfer) Spinl ccessory n. (CN11) worksest for suprscpulr nerve, less for xillry or musculotneous nn. (where interposed grfts re necessry) Intercostl-musculotneous n. restores iceps in70%Flotte Outline of Neurosurgery 35Medil pectorl-musculocutneous n. works if these rnches re sustntil Oerlin procedure: fscicle of ulnr n. copted to distl musculocutneous n. o Preferred y some to restore iceps in ptients presenting over 8mos fter injury C7: ipsilterl or contrlterl (requires lengthy grft). Crries smll risk of wekness. Cervicl plexus or C3-4 provide some wek motor function Phrenic n.: Kline voids using it. Hypoglossl n. not effective per Kline Exmples (see JN 9/04) C5-T1 vulsions: Accessory-suprscpulr, intercostls-musculocutneous/xillry/medin (or medil pectorl, or phrenic). Thorcic Outlet Syndrome/Cervicl ri From C7 my e incomplete ri or firous nd. Elevtes nd stretches thelower rchil plexus, suclvin . & v. Affects lower trunk: wekness in llhnd muscles (ulnr nd medin), ulnr numness No neck pin. My hve mild ching pin of ulnr forerm/hnd. Hnd wekness/clumsiness is prominent. Atrophy (guttering) of the lterl thenr eminence (APB) is chrcteristic. Bilterl in 50%, ut less ffected side is usully suclinicl, dignosed y EMG Chest or (olique) c-spine Xrys or CT usully show cervicl ri NCV shows low APB mplitudes(1st dorsl interosseous ulnr is norml or slightly low), low ulnr sensory potentils with norml medin sensory potentils Adsons test: turn hed ck & to ffected side & lose rdil pulse Other Brchil Plexopthies Acute Brchil Neuritis (Prsonge-Turner Syndrome): Sudden onset of very severe pin (ptient presents to ER) in shoulder girdle. Pin persists for hours or weeks then ecomes dull che. As pin susides rpid proximl rm wekness ecomes prominent (deltoid, supr/infrspintus, iceps). Wekness usully recovers (90% t 3 yers), utdegree nd durtion of recovery re vrile. Sensory chnges re mild. 33% ilterl. Occurs t ny ge, ut peks in 20s nd 60s. Mles fvored 4:1. 25% follow virl illnesses or vccintions. My occur postop, even with distnt surgery. No fever. WBC nd ESR re norml. No tretment. Steroids ineffective.Ulnr nerve Entrpment o Signs: Interosseous wsting. Wrtenergs sign (weknessduction 5th digit); Froments sign (grips pper /t thum & fingers w/tip only dductor policis wekness) o Cuitl tunnel: Medil elow etween 2 heds of FCU. Surgicl options include simple decompression, medil epicondylectomy, or trnsposition (sucutneous, sumusculr or intrmusculr) controversil. o Guyonscnl: Wrist sensory to dorsum of hnd spred,Flotte Outline of Neurosurgery

36o Arcde of Struthers: 8cm proximl to elow, rre Exposure t elow: Incision t medil epicondyle. Follow distlly thru cuitl tunnel & FCU. Trnsposition: moving ulnr n. out of ulnr foss (/t medil epicondyle & olecrnon process) Exposure t wrist: Incision over ulnr rtery etween pisiform & hmte, followedproximlly.Medin entrpment 1) Crpl tunnel Sxs: wkens @ night, numness/ tingling, myhve pin in 5th digit & up rm (reson uncler), thenr trophy, Phlens (61%sens, 83% spec) /Tinels (74% sens, 91% spec). Doule-crush: CTS + cervicl rdiculopthy DDx: DeQuervins syndrome: tendonitis of APL, tenderness t se of thum, ssoc. with pregnncy. Dx: NCV/EMG: medin sensory (> motor) ltency (normlin 20-30%). Tretment: Wrist splint, steroid (no nesthetic) injection (ulnr to plmris longus). Crpl Tunnel Relese: Plmr cutneous rnch is superficil to flexor retinculum on rdil side. Recurrent motor rch usully exits distl to ligment ut my pierce it. 2) Prontor teres syndrome More prominent plmr pin (medin plmr cutneous rnch rises proximl to TCL). Aching forermfter use, wek hnd. No night sxs. Dx: Pin on resisted prontion. NCV not useful (episodic) Cuse: repet prontion. Tretment: rest forerm. 3) Anterior interosseous syndrome No sensory loss. Loss of Prontor, FPL, index FDP. NCV not helpful. Usully resolves. Rdil nerve Supintor tunnel syndrome: At elow. Mimicsrefrctory tennis elow. Posterior interosseous syndrome: finger drop without wrist drop (ECR spred). No sensory loss (?). Trpped t rcde of Frohse. Tretment: conservtive Mergli Presthetic: Lterl femorl cutneous n. Sensory only, lterl thigh. Dx: Locl lock just medil to ASIS. Electrodignostic studies only helpful to rule out other cuses. Tretment: Neurectomy more effective thn decompression. Incision medil to ASIS (longitudinl or trnsverse), Sectionfsci lt over nterior order of srtorius. Section inguinl ligment. LowerExtremity Oturtor n.: Adductor wekness Femorl n.: JN 6/04. Injured in thighfter herni or hip opertions. From lumr plexus (L1-L4). Supplies iliopsos,qudriceps Scitic n.: L4-S2. Hmstrings nd ll mm elow the knees Common Peronel n.: Deep n.: dorsiflexion (nterior tiilis), toe extension. Superficil n.: foot evertors. Lesion cuses foot drop. Gnglion cysts: resection recommended. Surgicl exposure: prone. S-shped incision. See N6/04. Tiil n.: plntr flexion, toe flexion, inversion, senstion to sole of foot. Gstrocnemius, soleus mm. Trsl tunnel syndrome: tiil n. t medil mlleolus. presthesis sole of foot no motor loss. Tinels. NCV. 90% improved. (only 50% in reops) (N11/03)Flotte Outline of Neurosurgery37FunctionlPrkinsons DiseseEtiology unknown. Decresed neurons in SNpc, DMN vgus & locus ceruleus. Pth: Lewy odies (eosinophilic intrcytoplsmic inclusions with hlo). Symptoms: resting (pill-rolling) tremor, rdykinesi, cogwheel rigidity. Also: microgrphi, decresed link, msked fcies, festinting gin, pin in 50%, GI prolems, dysutonomi, weight loss. Symptoms usully symmetric. 20% hve dementi. Dignosisis clinicl. Prkinsons Plus syndromes: DBS is ineffective, even when responsiveto levodop. o Prkinsonism: 80% due to Prkinsons disese, 10% Prkinsons-Plus(MSA, PSP, CBGD, diffuse lewy ody dz), 10% secondry. (drugs: neuroleptics, reserpine, C-chnnel lockers, lithium) o Multisystem trophy (MSA): Younger. Pth: -synuclein positive glil cytoplsmic inclusions, no Lewy odies. Poor responseto dopmine. Includes: Stritonigrl degenertion: syncope, stridor. Putmen trophy Olivopontocereellr trophy: AD, Chr 6, 15yo, LE txi, trophy middle cererl peduncle Shy-Drger: utonomic pros, impotence, no lewy odies(?); lossin putmen, SN, & interomediolterl horn cells o Progressive Suprnucler Pls

y (PSP): downgze plsy, pseudoulr, git plsy, eyelid freezing, no tremor, symmetric. MR: trophy of midrin & tectum. 70yos. No tretment. o CorticlslDegenertion (CBD): Prkinsonism, corticl signs (prxi, myoclonus) nd lienlim. No tretment. Tretment: Medicl: enztropin (Cogentin)/ Artne: nticholinergics. Amntdine: Releses dopmine. Loses effect with time. Sinemet: Dopmine + cridop ( dop decroxylse inhiitor). 2nd tier. SE: N/V, orthosttis,rrythmis, on-off periods, dyskinesis (Tx B6). Contrindicted with MonmineOxidse Inhiitors (MAOIs). Bromocriptine/ pergolide: Stimultes D2 receptors. SE: vsoconstriction, firosis (romocriptine is used for prolctinom, pergolideisnt). Selegiline/ Eldypryl: MAOI. Slows progression. deprenyl: MAOBI. Surgery Modlities Lesioning: GPi, VIM thlmus, STN Deep Brin Stimultion (DBS): of STN, (lso GPi, thlmus.). Up to 35% of ptients develop tolernce (for tremor) Rdiosurgery: only Vim Thlmus. 130Gy mrgin dose. One 4mm collimtor. Success: 82% good response. Onset 2mos. SE: Dysrthri. Experimentl surgeries: Fetl mesencephlic trnsplnttion into SN cused dyskinesis, some improvement 85yo, 2 prkinsonism. Withold meds dy of surgery. Avoid IC,optic trct. Trget: midpoint of AC-PC line: 2mm nt, 21mm lterl, 5mm inferior. Cn lst >5yrs. 2. Thlmotomy: VL: tremor/rigidity. VIM/VOP: tremor. Complictions: confusion, speech normlity ( w/ ilterl). 3. STN stimultion: My edone ilterlly. Effective for rdykinesi, tremor, rigidity. Mediction reduced or eliminted (rrely with pllidotomy overll results etter, however more expensive $36K vs $12K). Improved git usully requires ilterl stimultion. FDA pproved Jn. 2003. Appers to e 10% more effective thn GPi stimultion. STNcn e seen on T2 low ndwidth. Position vrile enough tht microelectrode recording is needed. (JN3/04) SE: cognitive decline, depression, hypophoni. Effect declines with time. Mechnism unknown. Also effective in essentil tremor. Essentil Tremor Occurs in elderly. Fmilil: Autosoml dominnt with vrile penetrnce, 60% of cses. Spordic in 40%. Bilterl ction (not rest) tremor of hnd/rms or hed. No other neurologic signs. Tretment: Propnolol, primdone, STN stimultion (or thlmotomy). (Neurologist 9/04) Torticollis Flotte Outline of Neurosurgery38Tretment: CN11 neurectomy & upper cervicl ventrl rhizotomies (97% success), thlmotomy (66% success), MVD (70% success), DCS, BotoxHemifcil spsm Intermittent, pinless. Begins oculr, goes cudlly. Persistsduring sleep. Femles. MRI (no ngio). o Atypicl spsm egins in uccl muscles, usully dorsl-rostrl surfce, hrder to tret or preserve hering. Tretment: o Botox injections q3-4mos for life (Tegretol, Bclofen). o MVD: 34% AICA, 31%PICA, 31% oth, 4% silr. Vessel usully contcts ventrocudl surfce of CNVII. Dissect DREZ only, not distl. Introp BAERS (Pek V ltency dely: 0.6ms =wrning, 1.0ms = criticl). SE: defness (3-10%) > fcil wekness (1%). My persist >3d postop. Success 94%, 10% recurrence, 86% t 1mo. Some use ppverine introp. Idiopthic Intrcrnil Hypertension (IIH, Pseudotumor Cereri): Dndy criteri: symptomtic, no loclizing findings (except CN6,7 plsy), lert, normlCT/MRI, ICP >25. Oese women, 20-45yo. Usully self-limited, trnsient during pregnncy. Sxs: Hedches in nerly ll worse in m, with Vlslv. Also trnsient visul chnges. Ppilledem in lmost ll (rrely sent not necessry for dignosis). Ventricles my e norml or slit. Empty sell nd enlrged optic n. sheth in 50%. LP: Some symptomtic oese women my hve ICP > 25. CSF norml. Ass

ocited with vitmin A & retinoids, ntiiotics (tetrcycline), hormones, steroid withdrwl, lithium. Stop meds if possile (stopping OCPs not necessry). Alsossocited with lupus, uremi, etc. Blindness most significnt sequele occursin 25%. Cn e rpid. Follow visul fields. Tretment: Weight loss. Dimox (SR 500mg BID, tertogenic) Decdron (for cute lindness). Progressive visul loss despite medicl tretment: 1. Seril LPs: cumersome 2. Sutemporl decompression: historicl 3. Optic nerve fenestrtion: 90% successful. Unilterl fenestrtion ppers to lower ICP, improves vision ilterlly nd CN deficits, help HAs (deted). 2% risk of lindness. 4. LP shunt: Use horizontl (high pressure) verticl (medium) vlve. Complictions: filure 55% in 1 yer, overdringe 15%, lumr rdiculopthy 5%, infection 1%, cquired Chiri nd syringomyeli. 5. VP shunt: for repeted LP filure. o Deted wether ONSF or LP shunt is est. Hve equivlent efficcy. Empty Sell syndrome 1 (incompetent diphrgm) or 2 (surgery, stroke, etc). Sxs: HA, CSF rhinorrhe, visul loss, menorrhe-glctorrhe. Surgery only for CSF rhinorrhe trnsphenoidl repir lumr drin. Shunt my cuse pneumocephlus Sheehns syndrome: ischemic necrosis 2 to intrprtum shock Intrcrnil hypotension: Cuses durl enhncement on MRI/CT. Cuses include shunts, CSF leks. Spontneous crnil CSF lek: Due to genesis of the nterior foss, empty sell, sinus infection, tumor. Spontneous spinl CSF leks My e due to osteophytes, durl ters, sent nerve root sheths. Connective tissue disorders my predispose. Cuses posturl hedches. MRI: durl enhncement, downwrd displcement of cererum. Dx: Myelogrm. (Low opening pressure on LP). Tretment: Most resolve spontneously. Bedrest, lood ptch, surgicl repir. (JN11/03) NormlPressure Hydrocephlus (NPH): Term coined y Hkim 1964. Idiopthic cses my e cused y unrecognized SAH, meningitis, etc. Symptoms: trid of dementi, gitinstility, nd incontinence. Usully occurs in the elderly. Dignosis: o High-volume LP: remove 30cc nd look for clinicl improvement. Consider multory lumr drin tril. o CT: Communicting hydrocephlus. o Cisterogrphy: positivend negtive predictive vlue only 50% - not recommended y most. Activity persisting >48hrs implies good response to shunting. Tretment: Shunt: Medium-pressure vlve. 66% improve. Incontinence improves first. Endoscopic third ventriculostomy hs een used (N7/04) o Better outcome seen with miniml chnge in ventriculr size thn in ptients with mrked decreseFlotte Outline of NeurosurgerySpsticity: Tretment: o Botox locl only; lsts 3mo. o Bclofen pump. Overdose:stop pump, IV physostigmine, remove 30ml from side-port or y LP39Dystoni Sustined muscle contrctions cusing twisting, repetitive movements. Cn e locl or generlized, primry (idiopthic) or secondry to rin insult. Primry: 30% hve utosoml dominnt DYT1 muttion Tretment: o Medicl, IT clofen: often ineffective. o Pllidotomy or GPi DBS eqully effective in primry nd cervicl dystoni. Neither effective in secondry dystoni or ptients with ny MRI sl gngli normlity. Selective Dorsl Rhizotomy: intropertive EMGto preserve useful spsticity. Preserves multion. Fcil Plsy: cn nstmoseCN12, 11, or 9 to CN7 OCD (Osessive-Compulsive disorder): Tretment: Bilterlnterior cingulotomy. Only 6-30% permnently respond (MGH reports 50% success).Mny relpse within 1yr my need repet procedure. Also used for mjor depression. Trget: 2.5cm posterior to tip of frontl horn. Bilterl nterior cpsulotomy (nterior lim of internl cpsule) Limic leucotomy. Aove my e done stereotcticlly or with SRS.PinDeep Brin Stimultion for Pin: Pericqueductl grey (PAG). SE: diplopi, nxiety. Periventriculr grey (PVG): Sfest. VPL/VPM Cingulotomy: must e ilterl;recurs 3mo; SE: 10-30% flt ffect Medil Thlmotomy: hed/neck pin. SE: 20-70% cognitive pros, phsi Mesencephlotomy: hed/neck pin Cordotomy Unilterlpin elow nipple, terminl pt, ching, defferentition pin Open: C1/2 lmino

tomies; Cut contrlterl spinothlmic tr., strt nterior to dentte, 5mm deep; Check PFTs, diphrgm fxn preop Percutneous: Awke, use stimultion Success:94% initil; 60% 1yr; 40% 2yr. SE: presis, incontinence Commisurl Myelotomy: ilterl pin, thorcic & elow, lminectomy 3 levels ove; 60% success SpinlCord Stimultor AKA dorsl column stimultor Plced epidurlly. Works when plced ventrlly lso (for unknown resons). Led tips C3-C6 for UE, T8-T12 for LE. Done wke w/propofol & locl nesthesi. My e done percutneously of vi lminectomy, with RF-controlled receiver or IPG. Results: Few RCTs. Metnlysis (n=3679), success rtes: SCI, filed-ck, phntom lim = 60%, peripherl neuropthy= 70%, ischemic lim pin, postherpetic neurlgi, CPRS = 80%. Poor for SCI, root vulsion (norml Centrl Conduction Time (CCT) on SSEPs, hypesthesi), or mlignncy. In RSD response my e predicted y sympthetic lockde. Used commonly for ngin in Europe (off-lel in US) MRI with DCS hs een reported (Sh RV04)Flotte Outline of NeurosurgeryDREZ rhizotomy: good for nerve root/ rchil plexus vulsion Intrthecl pumps:For nociceptive cncer pin ove C5. Suggest IT tril 1st40Complex Regionl Pin Syndrome (CPRS) Type I = Reflex Sympthetic Dystrophy (RSD), no nerve injury. Type II = Cuslgi, due to incomplete mjor nerve injury (ie GSW). Both types cn e symptheticlly mintined pin (SMP) or symptheticlly independent pin (SIP). Sxs: Hyperesthesi (not hypesthesi) Trid: urning pin, utonomic dysfxn ( or sweting & hir, vsoconstriction or diltion), trophic chnges. Sudeks trophy (skin, one, etc not nerve). Etiology unknown (epiphtic trnsmission discredited). Most hve onset 90%. Complictions: Thorcic: rdycrdi (usully symptomtic). Lumr: retrogrde ejcultion. Otlgi My come fromCN 5,7,9, or 10. Give tril of TGN meds. Intrctle: explore CNs MVD vs sectioning (nervus intermedius, 9, upper 2 roots of 10)Trigeminl neurlgiUnilterl, no deficits, sensory trigger. Due to epiphtic trnsmission. More common on right. V2&V3> V2> V3> V1&2> V1. R>L. Bilterl or V1 think MS. 50yo. Dignosis: MRI if typicl or considering surgery. DDx: zoster (continuous pin). Tretment Medicl: Tegretol > dilntin > clofen. Microvsculr Decompression (MVD): o 80% SCA (lso PPTA, AICA,). In 5% of cses compression is primrily venous (trnsverse pontine & trigeminl veins (N8/04) o Indictions: >5yr survivl, 50% improvement, 55% no pin with meds, 40% no pin. (55% t 3yrs). 58% for secondryTN, 0% for typicl. 13% relpse (t vg 15mos). Not s good s initil MVD, uts good for second procedure. o For repet SRS: 50-60Gy, nterior to 1st trget. o 25% new numness, 12% other complictions. Tkes 3 months to work. All improvement occurs y 1 yer, most y 6 mos. o 80 (70-90) Gy, one 4mm collimtor. Brinstem surfce t 30% isodose line, center t DREZ. Also: peripherl neurectomy(suproritl, infroritl, inf. dentl nerves only; nonopertive cndidtes); Intrdurl neurectomy (filed PTR w/ preexisting CN5 nesthesi. V1 superior, V3inferior. Cut lower ) Flotte Outline of Neurosurgery 41Reders syndrome: V1 & V2 pin with oculosympthetic prlysis ptosis nd miosis(no nhydrosis-pseudoHorners); due to ICA disese Tic convulsive: TGN w/hemifcil spsmGlossophryngel neurlgi Pin in er, tongue, tonsil, nd ngle of jw. 10% hve vgl rdycrdi/ systole. Dx: cocniztion of tonsillr foss relieves thepin. Tretment: MVD (PICA) or rhizotomy (9 & top 2 roots of 10). 11% risk of horseness/dysphgih (lso fcil presis). Crdic instility my occur introp, give tropine efore mnipulting nerve. Monitoring CN9-10 not helpful. (N4/04) MVD Used for trigeminl neurlgi, hemifcil spsm, glossophryngel neurlgi. Also reported for torticollis, Refrctory essentil hypertension: decompression of the left rostrl nteromedil medull. Jnett reported 75% success. Neurogenic hypertension: Bsilr rtery on left rostrl ventrolterl medull (RVLM), responds to MVD; my lso e due to silr impression & responsive to odontoidectomy. Geniculte neurlgi: otlgi, prosoplgi (deep fcil structures). Tretment: symptomtic Postherpetic neurlgi: Persists >3mos fter zoster. Lidocine ptch (lso IT lidocine, Zostrix, Elvil.) No surgery. Occipitl neurlgi:Block, TENS. Surgery poor. Neuropthic pin: Neurontin, TCAs, other AEDS, lidocine gel/ ptch, cpscinFlotte Outline of Neurosurgery42SpineLines McRe: formen mngum dimeter, >35mm, ny protrusion of odontoid ove isnorml; Chmerlin: plte to formen mgnum, odontoid not >1/3 or 6mm ove; Wckenheim: clivus, tip ehind; McGregor: plte to occiput, tip not >4.5mm ove; Fishgolds digstric: tip not ove; Pltysi: >145. Bsion-Dens intervl:3mm dults, >4mm kids. >4mm = trnsverse ligment disruption possile, >6mm likely. Preverterl shdow: 15ls overweek; Reducile: fusion C1 lminectomy; Nonreducile: odontoidectiomy.Degenertive DiseseNeck pin Differentil dignosis of neck/shoulder pin with no neurologic signs:rottor cuff ter, sucromil ursitis, dhesive cpsulitis (frozen shoulder),glenohumerl impingement, lterl epicondylitis (tennis elow) Differentil dignosis with neurologic signs: rdiculopthy, neuropthy, plexopthy (ie Prsonge-Turner syndrome), Thorcic outlet syndrome Cervicl Rdiculopthy/Hernited Disc Symptoms nd signs: o Rdiculr pin: rdites in distriution of nerve o Dermtoml numeness/prsthesis o Myotoml wekness: usully mild. (trophy/fsicultions re rre) o Decresed reflexes in root distriutionFlotte Outline of Neurosurgeryo43 Almost ll pts hve decresed neck motion nd neck pin initlly. Chroniclly pin ecomes dull, ching, tingling. Scpulr pin my develop. o Spurlings sign: rdiculr pin reproduced on tilting hed towrd ipsilterl side. Hyperextensionwith or without vertex compression lso reproduces pin. o C7: 15% suscpulror rest/chest pin. C6: intrscpulr pin. EMG: Firilltions, xonl loss. Prspinl muscle involvement confirms root involvement. NCV not useful Imging:MRI, CT-myelogrm (if MRI is equivocl) Tretment o 95% recover with conservtive tretment (lumr 85%). Conservtive tretment includes: NSAIDS, cervicl trction, physicl therpy o Surgicl options: Anterior cervicl discectomy & fusion(ACDF) Anterior forminotomy (Jhos procedure) Posterior forminotomyCervicl stenosis Cross-sectionl re of cord my e more ccurte predictor ofrisk of myelopthy thn cnl dimeter. DDx: ALS: (+) jwjerk, tongue fsicultions, dysrthri, no sensory s. Radiology: T2 signal controversial: reversile (edema) or not (cystic necrosis). Snake-Eye Appearance: poor recovery. Treatment: ACDF; laminectomies lateral stailization, laminoplasty. If needs anterior & posterior decompression do ACDF efore laminectomy. Canal 60% canal compromise. If no myelopathy at presentationthen patient has 30% risk of developing myelopathy. If myelopathic than chance of ecoming wheelchair dependent/ edound is 10% with surgery, 90% with conservative treatment. Surgery ineffective if already wheelchair dependent. Surgery: Anterior if it involves 2 levels, otherwise posterior. Ossification of Ligamentum

Flavum: very rare, occurs in Japan Rheumatoid Arthritis AA suluxation, BasilarInvagination common. Flex/extend all patients efore intuation. Fuse if symptomatic or >8mm sulux.Thoracic SpineThoracic Herniated Disc Back pain most common symptom. Treatment: 1) laminectomy: highest risk of injury 2) transpedicular, 3) costotransversectomy (risk: Adamkiewicz A. T9-12 on Left); 4) transthoracic / thoracoscopic 5) lateral extracavitaryLumar SpineLow-Back Pain Pain may e axial (low-ack) or radicular. May also e referred touttock, hip, or thigh Pain generators include nerve, disc, facet joint, and paraspinal muscles Pain may e mechanical (exacerated y movement) or neuropathic(constant, usually radicular) Differential Diagnosis o SacroilitisFlotte Outline of Neurosurgery Workup o Xrays: L-spine series, flexion/extension o CT scan for previous surgical instrumentation o MRI L-spine o Injections/locks: nerve root, facet, triggerpoint in paraspinal muscles Treatment o Injections/locks: may e done as a series of 2-3 locks, repeated every 6mos as indicated44Lumar Herniated DiscSymptoms o Straight Leg Raise (SLR): tests L4 to S1. Postive if it produces sciatic pain, NOT ack pain. Reverse SLR positive for L3. o L1-3 and facet pain referred to uttocks/thigh thru superior cluneal nn (not elow the knee). o HNP without sciatica: 0.1% o Great toe weakness: L5/S1 60%, L4/5 30% o L2-4: weakness walking up stairs Differential Diagnosis: Hip pathology perform Patricks test (hiprotation) Treatment Conservative treatment o Intradiscal steroid injection failed in RCT Lumar Discectomy o Pain etter @ 1 year, no difference @ 4yrs. o L3/4: 94% improvement for leg pain, 87% for ack pain. L2/3 and aove: only 50% improve. o Arthroplasty: Artifical disc. Far Lateral Disc: males >50yo, DM, upper lumar levels (N4/04) Lumar stenosis Neurogenic claudication (vs vascular): variale distance, slow relief, requires sitting persists while standing. Canal Diameter: Avg. 22mm, Lower limit normal 15mm, severe stenosis 75%. Instaility: >4mm movement. Types: 1) Isthmic: due to spondylolysis. If sclerosis do nothing, if not then Boston race. 2)degenerative, 3) dysplastic (congenital), 4) traumatic, 5) pathologic. Treatment: o Decompression: for foraminal or spinal stenosis without instaility. o Posterolateral fusion: with or without reduction & decompression o PLIF: with posterolateral fusion. Distracts disc space, strengthens posterior construct. o Reduction necessary in Grades III & IV, controversial in I & II. Easier if younger, L45(harder if L5S1). o No clinical difference in outcome etween PLIF & posterolateral fusion, ut PLIF mechanically stronger (less translation, disc space decrease. (JN:S9/03) o Benzel feels Disc space distraction may e unnecessary after decompression, and compression may make posterolateral fusion stronger. Failed Back Syndrome Causes: Arachnoiditis (Surgery only improves 10-20%), epidural firosis. Diagnosis: o L-spine xrays, flexion/extension, oliques (look for postlaminectomy fractures of the pars interarticularis) o MRI with contrast: Firosis enhances, recurrent disc doesnt. o Consider CT scan myelography Treatment: medical, spinal cord stimulator (poor for axial or ilateral leg pain), intrathecal morphine pumps (palliative) See Neurologist 9/04 Coccydynia Treated with NSAIDS and local steroid injections Ankylosing Spondylitis 90% HLA-B27, onset 2mm diameter. Occurs in kids or adults. Adults: pain more common (perineal). Kids: foot deformities, scoliosis, cutaneous stigmata (80-100% vs adults meningioma(thoracic, one erosion rare). Extradural: metastases. (Rare: spinal angiolipoma: Acom (30%)> MCA (20%) > asilar tip (5%). Risk factors: age, smoking (3-10x), heavy alcohol use, HTN (3x), ?hormones Rupture risk: Large size (no critical size), high dome/neck ratio, high aspect (aneurysm depth:neck width). Smaller aneurysms produc

e more extensive SAH (JN8/03). Slow flow increases rupture risk. If two or morefamily memers have aneurysms, others should e screened y MRA or CTA (9% positive). Frequency is deated (every 6mos to 5yrs) (N8/03) Predisposing factors: Aortic coarctation, AD polycystic kidney disease, firomuscular dysplasia, Marfans, Ehlers-Danlos, homocystinuria, NF1, AVMs Complications: o Rerupture: 20% 2wks,50% 6mos, then 3%/yr. Unruptured 1-2% (95% for aneurysms >7mm. Look for neck calcification or plaques. Especially eneficial for emergent ICH evacuation. With SAH: If aneurysm seen it is reliale. Perform angio to confirm (-) CTA. No SAH: If (+) consider angio to confirm small aneurysms. If (-) then proaly reliale. o Angiogram-negative (or Occult) SAH 10% of SAH. Most common cause is non-visualized aneurysm due to aneurysm thromosis or inadequate study. Other causes: Perimesencephalic Benign SAH, spinal AVM, Spontaneous thromosis ofaneurysms may occur (10% of autopsy series); however they may reappear and rupture years later. Acom is most common location. Hemorrhage rate is 0.5%/year (lower than angiogram (+) SAH). Other SAH complications occur (vasospasm may e lesslikely). Consider repeat angiogram at 10-14 days. Overall 2-25% positive yieldon repeat angiogram, ut up to 70% with interhemispheric SAH. Do not repeat forperimesencephalic SAH. Surgical exploration has een advocated y some, especially if releeding occurs or if the SAH is in a typical aneurysm location (interhemispheric, Sylvian fissure) Benign Perimesencephalic SAH: aka PerimesenchephalicNonaneurysmal SAH. May e due to rupture of small perimesenchephalic vessels. May have similar presentation to SAH (headache, meningismus), ut Hunt-Hess is 12. All are angiogram-negative. CT/MRI shows SAH only in interpeduncular/amient/prepotine cisterms. 3% of asilar tip aneurysms mimic BPS, so angiogram is mandatory. Repeat angiography is controversial. Releeding and vasospasm in true BPShave not een reported. Nimodipine not recommended. Treatment o Unruptured: ISUIA (International Study of Unruptured Intracranial Aneurysms, NEJM, 1998): 200 cm/, ratio >6. o HHH: IVF + colloid, HCT 30-35 prophylactically. For deficit raie SBP >200. (unclipped CVP & PCWP 6-10, SBP 50% t onetime if multiple feeders, use locl/propofol, pedicles tested with moritl.o Risks: ICH 1-4%. AVM my recnlize fter successful emoliztion. Rdiosurgery: o Bleeding risk unchnged for 2-3yr ltency (controversil some studies report lower or higher rtes). o Mrgin doses: Smll AVMs 23Gy (no enefit from higher doses). Lrge, risky loction: 16-18Gy. (4cm3 = 40-60%, 15cm3 consider stged SRS t 6mo intervls. o Hemtom my compress vessels, my trgeting difficult. Perform SRS 2-3mos fter hemorrhge. o Complictions: cyst formtion, edem (10% symptomtic, 4% need surgery), necrosis 3-6%. oRepet ngio not performed until 3yrs, then consider retretment, repet SRS. If erly drining vein ut no nidus, consider it treted. o Follow-up MRI hs 100% positive nd 85% negtive predictive vlues some get only MRI only for followup. o Brinstem AVMs: 66% success, 10% permnent deficits. Risk higher in tectum. (JN2/04,3/04)Durl AVFs Acquired, due to venous sinus thromosis, fed from ECA. Corticl/ leptomeningel venous dringe is #1 SAH risk 10% mortlity. Trnsverse/ sigmoid: most common. Symptoms: Pulstile tinnitus (lso cused y errnt ICA, glomus tympnicum.), occipitl ruit. Less SAH risk (higher with oritl/nterior flx, tentoril) Cvernous sinus (CCF) Tretment: If only retrogrde or corticl dringe requires urgent tretment. If hs nterogrde dringe cn tret symptomticlly. o Emoliztion: trnsrteril (higher recurrence) or trnsvenous (riskier)o SRS o Surgery (excision nd pcking of sinus). Single leptomeningel driningvein cn e treted with vein ligtion. Crotid-cvernous fistul: Types: o 1) Posttrumtic. o 2) Spontneous ) Durl AVF: women, 50% thromose. ) Cvernousneurysm rupture. Symptoms: Proptosis, chemosis, oritl ruit. My cuse epistxis, visul loss (emergency), intrcererl ICH (through temporl veins). Tretment: Blloon occlusion (trnsrteril or trnsvenous thru ophthlmic veins), CCAligtion intrcrnil trpping Cvernous mlformtion Hemorrhge rte 0.5%/yr.50% multiple (80% in fmilil cses). Fmilil: Hispnics. 3 loci identified (CCM1= Krit1) MRI: popcorn ppernce. (Look for dditionl lesions w/ grdient echo). Angio norml. Tretment: o Surgery: Most recommend resection only for recurrent hemorrhge (except in rinstem higher hemorrhge rte) or intrctle seizures. o Rdiosurgery controversil. Some mintin its ineffective. Venous ngiom: Meduss hed on MRI, ngio. Hemorrhge rre. 33% hve ssocited cvernous mlformtion. Vein of Glen Mlformtion: Type I: true AVF from posterior choroidl, presents in neontes s CHF, infnts s hydrocephlus or seizures. Type II: Midrin or thlmic AVM tht drins into VOG. Presents in dults s SAH, ICH, dementi. Tretment: Trnsrteril or trnsvenous (trnstorculr) emoliztion.Flotte Outline of NeurosurgeryCrotid ligtion Used for cvernous or ophthlmic neurysms, or intrcrnil crotid dissection. Asolute CI: Vsospsm on grm. Reltive CI: ilterl neurys

ms, extrcrnil therosclerosis.55Crotid stenosisAsymptomtic ruit: CVA risk 2%/yer Angio: mesure ICA distl to plque for norml; U/S & MRA overestimte. U/S: mesure norml distlly. Higher velocity = red. Systolic velocity is est velocity prmeter. Medicl Tretment: detle. ASA (325 qD) Ticlid (more expensive, neutropeni, use only of ASA intolernt). Only lowers risk in symptomtic pts. o Intrcrnil: ASA, if fil EC-IC ypss. Endovsculr ngioplsty & stenting: 5-7% M&M. Higher restenosis thn CEA ut equivlent stroke prevention (CAVATAS rndomized tril, Lncet 2001). 2 single centertrils for symptomtic & symptomtic ptients showed equivlent efficcy. Restenosis occurs w/in 1 yer due to myointiml hyperplsi, ut my remodel & reopen w/in 3yrs. SAPPHIRE (high-risk) tril: Stroke, deth & MI: ngioplsty + stent6% vs CEA 12%. Stroke & Deth: 4% vs 7% (NS). CREST (low-risk) tril in progress. Crotid endrterectomy (CEA) Indictions: 1. Symptomtic >70%. NASCET: lowersrisk of CVA 26 to 9% t 2yrs (NEJM 91) 2. Asymptomtic >50%. ACAS: lowers CVA risk 11% to 5% (JAMA 95) 3. Ulcerted plque; 4. Symptomtic refrctory to medicl tretment 5. Crescendo TIAs (urgent); 6. 2hrs for cute deficit. Resolving deficit operte ASAP Recommend: wit 4-6wks fter CVA? CI: (Sundt) CompletedCVA w/in 1 wk, MI w/in 6mos, ngin, HTN (>180/110), contrlterl ICA occlusion, siphon stenosis, plque >3cm in ICA Preop: crdic workup; Preop CT; ASA x 25d (continue DOS) If ilterl operte on symptomtic side 1st Angio: look t level of ifurction vs mndile, extent of ICA plque, contrlterl disese (forshunt) Introp: 0.1%-0.3% lidocine to crotid ul to prevent rdycrdi & hypotension; vgus my e nterior; rteriotomy 5000U heprin (reversl not needed), SBP 110-150 (Stump pressure < 40-50 > shunt). Postop: check prontor, speech,pupil, tongue, horseness, lip depressor (mndiulr r. of fcil n.) Complictions: TIAs: emergent CT, then ngio CVA: in PACU: reexplore, others s ove; check ckflow from ICA if none use #4 Fogrty; fluids, pressors for SBP 180, O2,heprin? Hyperperfusion Syndrome: (Norml Perfusion Pressure Brekthrough): 1-3%. Focl edem or ICH. Unilterl hedche, fce/eye pin, seizures, focl deficit. Occurs d3-8. Risks: severe or ilterl stenosis, previous CVA, periopertive hypertension. TCDs felt to e unrelile. Tretment: BP control. Hemtom: reexplore immeditely if stridorous, intute, use Dekey Verteroslir Stenosis/Insufficency Usully occurs t verterl origin. Emoli less common thn in crotid stenosis. 11%/yr stroke rte (30% 5yr fter TIA). Requires 2 of: ilterlmotor/sensory, diplopi, dysrthri, homonymous heminopi. Suggested y positionl syncope. Dx: ngio. Tretment: o Intrcrnil: nticogultion (ASA unprovenut consider if mild). EC-IC ypss for filure. Endovsculr lloon ngioplsty stenting. Proximl occlusion. o Extrcrnil: Verterl . trnsposition (vert to CCA) or endrterectomy. Endovsculr lloon ngioplsty stenting (43% restenosis, ut most remined cliniclly improved, low complictions). Vsculr Dissection: Between intim & medi (dissecting neurysm = medi & dventiti. Pseudoneurysm = encpsulted hemtom). Flotte Outline of Neurosurgery Extrcrnil: suintiml, rupture rre. Intrcrnil: lcks externl elstic memrne, rupture more common.56Extrcrnil Dissection: Crotid: Cn occur spontneously (OCPs, FMD, collgen dz, migrines, HTN), during delivery, phryngel infections. Usully 2cm ove ifurction. Sxs: Fcil/eye pin, pseudo-Horners (no nhydrosis), crtotidyni, cervicl ruit, cn ffect CN10,11,12. HA preceeds deficit y dys/weeks. If SAH

gretest risk of rerupture 1st 24hrs, unlikely fter 1mo. Verterl: Between skull se & C2. Occipitl HA. Dx: ngio/MRA: string sign, perl nd string sign (higher releed rte?), doule lumen, fusiform diltion. Tretment: Anticogultion 6-12 wks or until >50% recnlized on MRA/ngio then ntipltelets. If persistent emoli: vein grft, EC-IC ypss, ligtion. Fusiform (Dissecting) Aneurysms: SAH: 30% releed rte, highest in first 24hrs. Commonly verterosilr. Tretment: Becuse of high releed rte erly tretment is wrrnted Options: 1) Proximl (Hunterin) ligtion or trppping: Fvored tretment. Done with GDC coils orclips. Blloon test occlusion (BTO) necessry first (20 minutes). Bsed on loction: VA Involving PICA tkeoff: clip/coil proximl only VA Proximl to PICA: trp (clip proximl nd distl) VA Distl to PICA: clip/coil distl to PICA (ut proximl to neurysm). Bsilr: stged ilterl verterl occlusion if pcoms dequte. (N8/03) If ptient does not tolerte BTO comine with PICA ypss, VA-PCAnstmosis (with rdil rtery grft), or oth. Others feel tht clipping proximlly only does not gurntee ginst re-leeding nd ll VA neurysms must etrpped with PICA revsculriztion if ptient doesnt tolerte BTO or neurysm involves PICA (JN 12/03) Risk of permnent deficits: 14% silr, higher with hypoplstic pcoms. Note if vert is dominnt, or contrlterl vsospsm exists. Mynot cuse resolution, occsionl releed. 2) Wrpping: Unproven efficcy. 3) Clipping/Reconstruction 4) Endovsculr lloon occlusion coils stenting. MCA fusiform neurysms: Occur in children, young pts ( HTN (#1 modifile) > DM > crdic disese (ll types) > smoking. OCP in smokers >35yo risk (due to estrogen content), PostmenopuslHRT no effect Smll vessel therosclerosis = lipohylinosis TIA: 20-30% risk ofCVA in 5 yrs. Higher risk of MI needs crdic workup. ImgingFlotte Outline of Neurosurgery57o CT: 1-3d: wedge, hyperdense vessel, loss of insulr rion. 4-7d: gyrl enhncement. o MRI: 2h: intrvsculr enhncement. 12h: gyrl/ meningel enhncement,edem. o Diffusion-weighted MRI most sensitive for erly ischemi. Tretment: ot-PA: give within 3hrs from symptom onset if stroke hs non-crdic origin. 30%increse in excellent outcome. 6% incidence of ICH. Hold ASA/ heprin x 24hrs, keep BP thlmus> pons> cereellum. Lterl to internl cpsule: etter prognosis, surgery fvored. Hypertensive encephlopthy/ Eclmpsi: occipitl hemorrhges Oculr findings: Thlmic: persistent downgze. Putminl: devition towrd. Cereellr: devition wy & oculr oing. Pontine: pinpoint.Fluid-fluid levels common w/ cogulopthy. 40% enlrge >33% y 24hrs. Angio yield: lor, >45yo = 10%. IVH = 65%. Volume = (AxBxC)/2 Anticogultion: with mechnicl hert vlves wit 1-2wks efore restrting nticogultion Medicl: o Recominnt Fctor VII: Phse II tril, (GCS >6, within 3hrs of onset). Thromoemolic complictions twice s common. Mortlity reduced ut not sttisticlly significnt. (N9/04) Surgery: o Crniotomy 20-60cc est (>85cc: 0% survivl regrdless of tretment). Lor, cereellr, externl cpsule. Young. L5. My e symptomticove L5. No studies needed if t L5/S1 nd no cutneous normlities. Tethered cord Occurs in kids or dults. Conus elow L2 (L2 t term, L1/2 t 6mos). Mye due to lipomtous filum, firous nd from conus to dur (dorsl or ventrl),epidurl scrring. Lipomtous (Ftty) filum: >2mm dimeter Found in 5% of popultion. Ptients my hve symptoms with norml conus level, nd ptients with thick filum my remin symptomtic. Adults: pin more common (LBP/ perinel). Trum cn produce cute deficits. Kids: foot deformities, scoliosis, cutneous stigmt (80-100% vs dults 3mm distsis to occur. Cephlohemtom: superiostel, does not cross sutures, Cput succedneum in sucutneous ft, crosses sutures; Suglel hemtom; ll my cuse significnt lood loss, check Hct. Archnoid Cyst Cn occur nywhere. Most common in middle foss (seizures), suprsellr (visul loss, precocious puerty, ole-heded doll).Flotte Outline of Neurosurgery

61Symptoms: seizures, deficits, hedche, visul deficits, developmentl dely, endocrinopthies. Cn rupture, cuse hyperostosis or hydrocephlus. Associted with intrcystic nd sudurl hemorrhge. Nturl history is vrile: my enlrge,regress, or remin sttic Tretment .Most recommend treting only if symptomtic (intrctle hedches, seizures, focl deficits) or incresing size o Needle/urrhole most recur o Crniotomy & fenestrtion: most effective if fenestrted into silr cisterns (2cm Microcrniotomy: N11/03). Improves seizure control ndfocl deficits; visul disturnces, developmentl dely, nd endocrinopthiespersist. o Cystoperitonel shunt: usully if fenestrtion fils. Shunt dependency my develop. o All cses presenting with hydrocephlus required VP shunting regrdless wether fenestrtion ws performed. o Endoscopic fenestrtion o Suprsellr: trnscllosl, ventriculocystostomy. HCP my increse fter tretment. Concomitnt hydrocephlus usully requires VP shunt. Outcome: Improvement (keyhole crni) hemipresis & CN6 plsy 100%, hedches 66%, seizures 50%. Chiri I 3-5mmtonsillr hernition. Controversil whether degree of hernition correltes withsymptoms or postop improvement. Hedches: clssiclly occipitl, worsen w/Vlslv. Also crnil nerve, rinstem & spinl cord syndromes. Downet nystgmus. 60% hve syrinx (my e thorcic or lumr); 25% hydrocephlus; 25% crniocervicl junction normilities; 20% scoliosis; 5% Klippel-Fiel, 5% GH deficency. Not ssocited with other developmentl rin normlities; No recommendtion forprticipting in thletics. Dignosis: MRI. Otin preop flexion/extension c-spine xrys. Cine-MRI not of mjor dignostic vlue Tretment o Asymptomtic: Decompress only for syrinx; if no improvement then shunt. (But - Nishizw (N01) 8/9 w/ syrinx remined symptomtic.) o Symptomtic: If HCP: shunt. No HCP: decompression, if fils then syringosurchnoid shunt. o Anterior compression (VBSC): trnsorl odontoidectomy BEFORE decompression. o Scoliosis: improves with decompression; perform spinl fusion only for Co ngle >50. (JN8/03) o Chiri Decompression: 3x3cm suoccipitl crniectomy, C1 (or lower) lminectomy, durplsty, shrinking tonsils. If extensive scrring cn use ultrsound to find 4th ventricle.Stenting worsens outcome. Postop: wtch for sleep pne. 50-85% success. If hsoccipitlcervicl instility, cn do concomitnt OC stiliztion (N6/04). Bestif done within 2yrs of onset. SE: cereellr sg: requires crnioplsty. Chiri II 100% ssocited with myelomeningocoele. 90% hve hydrocephlus. Decompress forpne, stridor, dysphgi, progressive spsticity or txi, opisthotonus, recurrent spirtion pneumoni. Check shunt function first. Dndy-Wlker Syndrome Associted with crdic normlities, polydctyly, genesis of the corpus cllosum, 80% hydrocephlus. Tretment: 4th ventriculr shunt (low pressure vlve) withor without lterl ventricle shunt (medium pressure). 3rd & lterl ventriclescommunicte with the cyst in 50% - requires iohexol CT to identify. Dndy-WlkerVrint: vermin hypoplsi, norml posterior foss, no HCP Meg cistern mgn: norml vermis, cereellum IVH Source: Neonte = germinl mtrix; full-term = choroid plexus. Tretment: seril LPs 7-15cc/d. If unle to remove enough CSF tonormlize ICP then ventriculostomy or Ommy. Shunt: >1500g, protein sutemporl crniectomies. Ptients with shunts should not e restricted from plying sports (N5/04)Isolted 4th Ventricle Occurs due to shunting for communicting hydrocephlus (IVH, meningitis) Cuses hedches, txi, qudripresis, pne, rdycrdi. Tretment: 4th ventriculr shunt, endoscopic queductoplsty stent, endoscopic interventriculostomy Benign sudurl collection of infncy: Usully resolves y 9moSuglel/superiostel hemtom: void spirting, follow HctFlotte Outline of Neurosurgery63TrumHed TrumIntrcrnil pressure (ICP)Cererl Perfusion Pressure (CPP) = ICP MAP (Men Arteril Pressure) ICP monitoring: o ICP Wveform: P1 = percussion wve, systolic contrction, decresed with ICP, complince; P2 = tidl wve; P3 = ortic vlve closure. o Lunderg Wves: A(Plteu) = > 50mmHg rise for > 20min. B = >20mmHg, lsts 1-2min. C = 4-8Hz. o Monitors: Intrventriculr Ctheter Intrprenchyml Monitor Surchnoid Bolt: less ccurte Sudurl & Epidurl monitors: less ccurte Signs of incresed ICP:o Pupilry diltion/ CN3 plsy: 90% ipsilterl mss. Hemipresis (cererl peduncle compression): 70% contrlterl mss. Jugulr Venous Monitoring o Necessry during riturte com. Norml SjO2 >50%. ICP Tretment mesures HOB 20-30 Sedtion/Prlysis Ventriculr dringe Mnnitol o Contrindictions: hypotension,renl filure. o Common dose: 1mg/kg initilly, then 0.25-0.5 mg/kg q6hrs. CheckSerum N & Osm efore giving. Hold if N > 150-160, or Osm > 320 (limits cn vry depending on the sitution). o High-dose (1.4g/kg) given wide open in ptients GCS3 & fixed pupils hd 33% more fvorle outcome. (JN3/04) o Alterntives ordjuncts include Lsix, hypertonic sline (ie 9%). Hyperventiltion: Keep CO2 30-35. Use cutely (CO2 to 25 y mnul gging) only for cute plteus. Decompressive crniectomy o 14cm dimeter ppers optiml. o Reconstruction: Timing controversil Britute Com o To urst-suppresion on EEG. Serum levels re used,ut hve poor correltion to clinicl enefit. o Pentoritl: Loding: 10 mg/kg over 60min, then 5mg/kg/hr x3hrs, then 1mg/kg/hr (Thiopentl my e sustituted). o Side-effects: hypotension Hypothermi: to 95 is ccepted. 8) Nutrition:prlyzed 100% BME, non-prlyzed 140% BME Steroids re not indicted in TBI. Peditric TBI Br com, CSF dringe more effective thn in dults. Hyperventiltion, mnnitol my lower ICP without lowering CBF. Incresed risk of seizures. Flotte Outline of Neurosurgery Diffuse Cererl Swelling: Due to venous congestion nd hyperemi (not cytotoxic/ vsogenic edem). 50% mortlity. Denny-Brown syndrome: Brdycrdi, gittion,HA due to vgl syncope, mimics EDH64Child use (Shken By) Common findings: Interhemispheric SDH, skull frctures, multiple long-one frctures of different ges. Diffuse Axonl Injury (DAI): Pth: Axonl retrction lls. Loctions: White mtter, corpus cllosum, dorsl rinstem Trumtic Crnil Nerve injury Indirect optic nerve injury: No prospective tril showing decompression etter thn steroids except for delyed onset lindness. Surgery: Done within 1-3weeks, trnsethmoidl route Trnsient corticllindness: Children my develop lsting 1-2d fter hed injury. CN7 injury: follow ENOG, decompress if no improvement on steroids. Posttrumtic Seizures Antiepileptics prevent erly (with 7 dys), not lte (fter 7 dys) seizures Begin AEDs for: GCS 1cm or thickness of the skull, neurologic deficit, CSF lek, open frcture. o Elevtion my improve deficits, not seizures o Frctures over mjor venous sinuses: controversil criteri. Hve Fogrty ctheter redy. Prep out sphenous vein. Bsilr skull frcture: o Give Pneumovx & Tdt. o Get CT with thin cuts. o In the sence of n open frcture, pneumocephlus is dignostic of silr skull frcture. o Require tretment:trumtic neurysm, C-C Fistul, persistent CSF rhinorrhe, meningitis/scess(my occur yers lter) o Prophylctic ntiiotics controversil. Most tret with rod-spectrum ntiiotics (Cipro) 7-10 dys. Temporl frcture: o Trnsverse:Perpendiculr to IAC. Higher risk of CN 7,8 trnsection. o Longitudinl: Prllel to IAC. Delyed fcil plsy is usully due to edem, resolves. o Fcil plsy: Tret with steroids. Immedite onset: if no improvement on steroids, considerexportion (timing controversil). Delyed onset: Follow with ENOG (fcil EMG). Consider explortion for continuous deteriortion on steroids nd 2wks. Frontl: Intrdurl explortion preferred over extrdurl. Epidurl Hemtom (EDH) / SudurlHemtom (SDH) Delyed enlrgement in 10-30%.Flotte Outline of NeurosurgeryChronic SDH Get intermedite CT windows. Blck nd on internl memrne on T2-MRI

my predispose to enlrgement Penetrtiong Brin Injury (PBI)/ Gunshot Wound (GSW) to the Hed Tdt, ntiiotics (not proven). Consider ngio for: delyed hemorrhge, trjectory involving vessels, lrge hemorrhge in slvgele pt (on d2-3). Only remove frgments which come out with gentle irrigtion.65Spine TrumSpinl Cord Injury Level: motor 3/5 AND pin/temperture senstion intct. Senstion or scrl spring (nl motor/sensory) = incomplete. Complete: 3% hve recovery w/in 24hrs. After 24hrs no recovery Conversion disorder (hystericl prlysis): preservtion of norml reflex pttern, norml rectl senstion, nd norml ldder nd owel functions. Flex ptients knees nd relese conversion disorder will mintin knees in flexed position. Some uthors recommend motor or somtosensory evoked potentils. Tretment: Solumedrol (methylprednisolone) 30mg/kg x1hr then 5.4mg/kg/hr x 23 hr only if nl contrction, lowest ville reflex). SCIWORA (Spinl Cord Injury Without Rdiogrphic Anormlity) MRI, CT, Xrys (including flexion/extension) negtive with neurologic deficit. Most common 1-16yo. Tretment: Bedrest, C-Collr until norml Flex/ext. Guilford rce for 3mos or hlo for 1-3wks recommended y some. Discontinue if flexion/extensionxrys norml t 3mo. No sport prticiption for 3mos. Whiplsh: Grde I = pin/stiffness, Grde II = limited ROM, point tenderness. Both: ROM exercises, II = c-collr < 72hrs (hrd only) Centrl cord: no evidence erly surgery enefits orhurts. With myelopthy pts fre etter w/fusion

Spine frctures Cervicl Spine Xrys: A/P, lterl, odontoid. Must see to C7/T1 disc. If no ftures on Xrys ut hs neck pin or tenderness, then get flexion/extension xrys. If cervicl muscle spsm is present then keep in c-collr nd repet flexion/extension films in 1 week. Otin CT for non-visulized res on Xry, level of neurologic deficit D/C collr fter norml flexion/extextension xrys (under flouro if otunded) OR norml MRI (within 48hrs) Bone scn to delinite old versus new frctures (remin hot for 24-48hrs up to yer). White-Punji guidelines forinstility: 4mm suluxtion, 11o ngultion (inferior endpltes). Dont get flexion/extension xrys. If 1cm. Use Vlium/Demerol. o Do not use trction with AO disloction or type IIA, III hngmnsfrctures. Externl stiliztion o Cervicl collr (C-collr). Soft: for comfort only, no stility. Hrd. o Cervicl-thorcic orthoses (CTO): Guilford, SOMIrces o Hlo vest AO disloction: immeditely pply hlo, no trction. (surgeryvs hlo) AA disloction: MRI to look t trnsverse ligment. If intct, hlo. If disrupted, surgery. Flotte Outline of Neurosurgery66

Jeffersons Frcture: Anterior nd posterior ring frctures of C1 Rule of Spence:>7mm overhng needs hlo, 2mm displcement = hlo, 6mm suluxtion (or instility in hlo) needs surgery. Others 1012 wks in hlo. Type III: hlo. C2 frcture: Lmin: collr. Fcets, ody, lterl mss: CTO or hlo. Cly shovelers: Collr prn pin. Anterior wedge: CTO if mild, hlo if severe Terdrop: True Trerdrop ssocited with: sgittl ody frcture, retrolisthesis, nterior wedge, fcet disruption, preverterl swelling, loss of disc height inferiorly, neurologic deficit. Requires stiliztion. Simple terdrop: If none of the ove re present then otin flexion/extension xrys. Ifnorml then keep in c-collr nd repet in 4-7d. Qudrngulr frcture: Oliquefrcture through ody (nterior-superior to inferior), retrolisthesis, nteriorwedge, disruption of disc & ligments. Tretment: Anterior & Posterior stiliztion. C3-C7 frctures: Follow White-Punji guidelines. Anterior stiliztion(ACDF) my need to e supplemented y posterior stiliztion if posterior tension nd is disrupted. Locked fcets: Mnul reduction in trction: Unilterl: torque towrds locked side. Bilterl: xil distrction nd flexion Once reducedleve in 5-10ls for stiliztion. Hlo x 3mos my e tried if fcet frcturefrgments re present. Otin Flexion/Extension Xrys in hlo efore dischrge.If no fcet frcture surgery. Posterior pproch preferred. Mechnisms: Flexion:ilterl locked fcets (neck flexed w/ flexing force), wedge, cly-shoveler, terdrop (neck flexed w/ compression). Flexion-Rottion: unilterl locked fcet Extension-Rottion: pillr frcture (neck flexed, compressing force) Axil compression: Jeffersons, urst (oth neck neutrl) Extension: hngmns (distrcting force, neck extended), posterior frcture-disloction, lminr frcture PeditricFrctures C23 pseudosuluxtion: C2 posterior spinl line should e less thn 2mm posterior to line etween C1 & C3 posterior spinl lines Odontoid synchondrosis (fuses @ 7yrs) ADI intervl wider thn dults 40, progressive kyphosis, or 3+ frctures in row. Burst frcture:Flotte Outline of Neurosurgeryo67 If deficit, ngultion >20, nterior height 50% cnl compromise: surgery. If not void erly multion, TLSO, seril xrys to look for progression. o Surgicl Options: o Posterior: Pedicle screws 1 level ove& elow w/distrction trnspediculr decompression (push frgments out of cnlw/ngled curette), NOT lminectomy. Some report 20-50% screw filure, worseningkyphosis. Some recommend 2 levels ove & elow. Consider djunctive verteroplsty o Anterior corpectomy. L4 nd ove only. o Comined nterior/posterior. oL5 (rre): 2wks edrest, TLSO w/thigh cuff x 4-6mos, seril xrys Set-elt/Chn

ce frcture: o Frcture through nterior nd posterior ony or ligmentous elements with no suluxtion nd no deficit. o Tretment: TLSO or surgery (Pedicle screws 1 level ove & elow with compression) Frcture-disloction: Surgery (Pedicle screws 2 levels ove & elow) Osteroporotic: Bedrest x 7-10d then PT, TLSOGSW Spine Surgery for: deteriortion, cud equin injury w/compression, nerve compression, CSF lek, instility, deridement, vsculr injuries, migrtion, plumism.Flotte Outline of Neurosurgery68MiscellneousCriticl CreAnesthesi Sedtives: Versed, Thiopentl Nrcotics Nitrous oxide: void with pneumocephlus Prlytics o Succinylcholine: 1mg/kg 3.5 to 5cc, lsts 5-10min. do not use with spinl cord injury, hyperklemi o Pvulon reversl: Neostigmine (2.5-5mg IV) + tropine (0.5mg/mg neostigmine) or Roinul (0.2mg/mg neo). Tkes 20min Mlignnt hyperthermi: Dntrolene (2.5mg/kg, up to 10mg/kg), 100% O2, D/C nesthesi & chnge tuing. Occurs w/ inhltionl + Sux. ETCO2. 50% previous norml nesthesi. Air Emolism Occurs when venous pressure is lower thn tmospheric pressure nd the venous system is open to the tmosphere. Most likely to occur in the sitting position Detection: precordil doppler (most sensitive), EtCO2(erliest), FEN2, CO, PAP, pulmonry vsculr resistnce, ventiltion-perfusionmismtch. Tretment: Lower the hed-of-ed, cover wound with wet lps, spirteir through centrl line. Ventiltion Intution/Extution: 100mg lidocine IVP, 100% O2 x 5min. Tue: 20-22cm t gum line, tip 5cm ove crin PCWP 24hrs. 0.3-10g/kg/min. Avoid in pregnncy Nitroglycerin: 10-20 g/min, 0.4mg SL q5m x 3 Both rise ICP. Hydrlzine: onset 3-5min, durtion 2-4hrs. OK in pregnncy. SE: tchycrdi. IM 10mg, IV 20-40mg prn. Letlol: onset 5m, durtion 3-3hrs; 20-40-60-80mg IV, 200mg po id Esmolol. Vsotec:1.25-5mg q6hrs prn Shock Dopmine: 2-20 g/kg/min, >. Doutmine: 2.5-10g/kg/min, y (inotrope, BP unchnged). Use for crdic filure if normotensive. Plple pulses: rdil 80, femorl 70, crotid 60 Steroids Cuse pncretitis Addisonin crisis: hydrocortisone (Solucortef) 100mg IVP then 50mg q6h (not Solumedrol) Anphylxis Tretment: Epinephrine 1:1000 5ml SQ, Bendryl 50mg IM, Decdron 10mg IV Urticri: Bendryl 50mg PO/IM + Cimetdine 300mg PO/IV Vsovgl rection: hypotension, rdycrdi. Tx: Atropine 0.75mg IV, q 15min to 3mg DVT Incidence in neurosurgicl ptients: 15-20% My e incresed in crniotomies due to relese ofrin thromoplstin Clf vein thromosis hs intution (fieroptic lryngoscope or tue chnger) > generl nesthesi o Inhltionl (isoflune, nitrous oxide) nd remifentnyl fter verifying muscle relxnts re worn off y trin offour. o Berger feels propofol my dversely ffect corticl depolriztion. Some use hed-pins, others use doughnut. Slow-growing lesions my shift eloquent res, even contrlterl Stopping resection 1-2cm from eloquent cortex gretly reduces postop deficits Corticl stimul

tion Done with Ojemnn ipolr stimultor (60Hz, 1msec, single-phse, 2-6mA wke, 4-16mA generl nesthesi). Increse current y 2mA until response is otined. Hold tips on cortex for 2-3 secs. Ptient temperture >36. EMG recording my improve sensitivity. My e done sleep or wke. Alwys hve cold irrigtion redy to irrigte cortex in the event of stimultion-induced seizure Some vry current t different sites (while monitoring fterdischrges), others dont (JN9/04) Afterdischrges monitored y electrocorticogrphy i.e. 5-grid strip lid next to stimulted re. This prevents seizures nd ensures tht stimultion effects re locl only (ie specific) Seizures stopped y cold irrigtion of cortex, ezodizpines, nd Dilntin Negtive results my not ensure sfe resection, positive result (ie speech rrest) is necessry to e sure of the loction of essentil lnguge sites My e done t edside with implnted electrode grids. LngugeMpping Hemispheric dominnce: Left hemisphere for 99% of right-hnders. Overll: 85% left, 9% ilterl, 6% right. In left-hnders use WADA test to determinelnguge dominnce. Otin seline lnguge function. Test the ptient preopertively nd eliminte ojects the ptient cnt identify. Nming errors must e less thn 25%. If ptient is unle to prticipte preopertively tril of higher-dose steroids cn e ttempted to see if enough improvement occurs thn lnguge testing cn e used. Awke crniotomy with corticl stimultion Oject nmingis the most relile test. Reding my lso e tested (posterior temporl) Echsite is tested 3 times, never twice in succession Essentil lnguge sites existprimrily on the surfce of the gyri nd not in the depths. Primry lnguge sites re verticlly orgnized with respect to sucorticl fiers, nd surfce stimultion cn e used to predict the results sucorticl resection. But sucorticl mpping cn e used to identify lnguge fiers ner the insul Motor Mpping Resection my e continued into the nterior nk of the precentrl gyrus without cusing n dverse event Resection my e performed in oth the dominnt ndnondominnt supplementry motor res without cusing permnent sequele, s long s the primry motor cortex is not violted Primry somtosensory cortex resection will produce temporry hypesthesi nd proprioceptive deficit. When theyffect the dominnt hnd, such deficits re prolemtic to the ptient nd the ptient should e counseled preopertively regrding this Corticl stimultion: Motor re identified in 94%. o My e done under generl nesthesi or wke. Motor stimultion is elicited in 50% under generl nesthesi nd 100% of conscious sedtion cses in smll series, with electrogrphic seizures in 30% nd 10%respectively (NF7/03) Generl nesthesi: inhltion gents comined with Versednd fentnyl without prlytics. o Children under ge 5 often cnnot e mppedwith stimultion ecuse of corticl inexcitility use SSEPs insted o After resection, motor pthwys should e stimulted gin to ensure their function. Ifmotor pthwys respond to stimultion fter resection, ny motor deficit oserved fter the opertion will e temporry Sucorticl stimultion: Identifies sucorticl motor trcts in 50%. If motor cortex is identified then trcts re mpped from there. If not, then white mtter is stimulted t 10-16mA. Stimultion ofcorpus cllosum does not elicit clinicl response. 8% of ptients hve sucorticl pthwys within gross tumor Reversl of SSEP wveCorticl MppingEvoked PotentilsFlotte Outline of Neurosurgery 73 Avoid inhltion gents, BZDs, rs; use nitrous or nrcotics, short-cting muscle relxnts (not for MEPs) Amplitude 50% or ltency 10% is significnt Motor Evoked Potentils (MEPs) o Used for intrmedullry spinl cord tumors, spinl AVM

s, mpping motor cortex, neurysm clipping. o Stiumltion my e done trnscrnilly or y corticl grids. o Twitch rtifct of erector spine muscles my limit. Leg MEPs my require too strong stimultion. (Suprtentoril MEPs N5/04) o MEPs superior to SSEPs in detecing motor impirment during neurysm clipping. Somtosensory Evoked Potentils (SSEPs) o Stimulte medin n. (unless operting on ACA use posterior tiil n.) o Squre wve, 300sec, 25-30mA mx, 5.3Hz. Brinstem uditory evoked responses (BAERS): o I cochler n. > II cochler nuc > III Superiorolive > IV lterl lemniscus > V Inf. Colliculus > VI MGB > VII Cortex o Intropertive: microphone plced in er, electrodes on sclpSurgicl AntomyExternl Lndmrks Rolndic sulcus: 30 line from oritl rim midpoint etween EACnd sgittl suture Formen of Monroe Coronl suture Cererl cortex Supplementry Motor Are Syndrome: Contrlterl kinesi with mutism (when on dominnt side very rrely on nondominnt side) fter dmge to SMA. SMA: re 8 - mesil posterior frontl loe, role in initting speech nd motor function. Recovery of speech occurs in 4-12 dys nd motor y 2-6mos. My not e evident during wke crni (my pper postop). Stimultion reuires high voltge to elicit responses (speech nd motor rrest, complex posturl movements, sensory & utonomic phenomenon.) Corpus Cllosum: o Anterior: Slow idetion o Middle: SMA syndrome o Posterior: Sensorimotor deficits. o Hemispheric Disconnection Syndrome Middle foss tringles: Glsscocks: Formen spinosum to rcute eminence to GSPN. Exposes petrous ICA. Posterior Foss Rhotons rule of 3: 1) Meckles cve, CN5, SCA, tentoril surfce. 2) IAC, CN7/8, AICA, petrosl surfce. 3) Jugulr formen, CN9/10/11, PICA, suocciptl surfce. Lndmrks: Trnsverse-Sigmoid junction t sterion. Mstoid emissry vein/formen t posterior edge of sigmoid sinus. Posterior end of incisur mstoide is t level of IAC. Veins Le: enters t trnsverse-sigmoid junction.ProceduresGenerl Durl grfts: pericrnium, fsci lt, cdveric fsci, ovine pericrdium (Dur-Gurd) Lser: NdYAG (not CO2) in loody tumors; focused em for gross removl, defocused for mrginsCrnioplsty Mterils: o Autologous one (crnium, ri, ilium): lower infectionrisk thn rtificil mteril, my resor o Methylmethcrylte one cement: hightensile strength, infection 23%, frctures occur o Hydroxyptite or clcium phosphte (Bonesource): iocomptile nd osteoconductive, indequte setting, settling, rittle, less stisfctory for lrge defects o Premde lloplstic implnts (polyethylene - Porex) o Titnium mesh Bone flp implnted in ptients domenor stored in freezer. Autoclving not recommended due to one protein denturtion. 50% one resporption in children when replced; no correltion with time toreimplnttion (JN:P2/04)LoctionsFlotte Outline of Neurosurgery743rd Ventricle No hydocephlus trnscllosl Inferior pterionl, sufrontl, sutemporl, trnsphenoidl, COZ Bsilr rtery ccess: Oritozygomtic: Top 2/5, SCA, CN3/4, midrin Trnscochler: Middle 1/5, AICA, pons, CN5-8 Fr lterl: Lower 2/5, PICA, CN9-12 (Henn, Spetzler, Clin NSurg 49) Perimesencephlic Cisterns Trnssylvin pretemporl, sutemporl, occipitl trnstentoril, suprcereellrinfrtentoril, trnstemporl trnschoroidl. See N6/04 Cvernous Sinus Some recommend resecting tumors (meningioms) from lterl comprtment only, treting the residul with SRS. If tumor touches ut doesnt encse ICA (C4) it cn e totlly resected. Excision of medil cvernous sinus lesion crries very high rte

of crnil nerve moridity. (N6/04)Positions Sitting o Risks: Air emolism, tension pneumocephlus, remote ICH, spinl cord injury/infction. o Avoid with ptent formen ovle, crdiovsculr disese, severe hypertension, cervicl stenosis. Consider preop cspine MRI to rule out cervicl stenosis (cnl should e >12mm)Anterior ApprochesTrnsorl Clivus, crniocervicl junction (Dorsum selle to C2-3). Extrdurl lesions primrily (Intrdurl used for silr neurysms.) Supine, hed extended.Retrctor hs groove for ET tue. Posterior phryngel wll incised, soft plte(lterl to uvul), hrd plte. Use Dingmnn mouth gg. (N1/04) Trn