Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6022_Библиотеки_им_академика_М_И_Перельмана
.pdf
versusvasculitis).
SpinalIntramedullaryAbscess
Intramedullaryabscess formation is also distinctly uncommon. Such abscesses
areusuallysolitarybutmayoccurmultiply.Mosthavebeendescribedatmid-to
low thoracic levels. Over half appear to have resulted from hematogenous
dissemination, and about 20% develop contiguously from an adjoiningsite of
infection,suchasvertebralosteomyelitis(51).Staphylococcusaureusisthemost
commonlyisolatedorganism.Thepresenceofacapsuleandthepredominating
inflammatory cell type (lymphoplasmacytic or neutrophilic) will depend on
whethertheinfectionischronicoracute.
SuppurativeSpinalLeptomeningitis
Spinalsubarachnoidsuppurationaccompaniesthatseenintracranially.Following
large-scale immunization against type b Hemophilus influenzae, bacterial
meningitisis now predominantly a disease of adults (52). In the post-neonatal
period, Streptococcus pneumoniae accounts for approximately one-half and
Neisseriameningitidisforone-quartertoone-thirdofcases(53,54).
Pathologically, the exudate tends to localize by gravity along the dorsal
surface of the lower thoracic spinal cord (Figure 3.19). It mainly consists of
neutrophils for the first few days, after which time lymphocytes and fibrin
appear.Afteraweek,microglialcellswithintheunderlyingparenchymabeginto
proliferate.If the exudatesextends into theunderlyingneural parenchyma,the
resultisameningomyelitis.Healingischaracterizedbyfibroblasticorganization
ofthe exudates. Local complications mayincludeocclusivevasculitis, abscess
formation,oradhesivearachnoidopathy.
OtherBacterialInfections
Tuberculosis of the spine may lead to vertebral body collapse, usually in the
thoracicor lumbarregion. Chronicepiduralabscess formationmayalso occur.
Tuberculousspinal meningitis is virtually always associated with concomitant
intracranialinfection.
Tabes dorsalis represents the classical spinal form of neurosyphilis and is
rarely seen today. The lumbosacral region is most frequently affected.
Pathologically, there is degeneration of the dorsal root ganglia, dorsal spinal
roots, and posterior columns (Figure3.20), without evidence of infiltration by
inflammatory cells or stainable microorganisms. The pathogenesis of this
conditionisnotunderstood.
ViralInfectionsoftheSpinalCord
Many viral agents are capable of producing myelitis. Only few have been
describedhere.
FIGURE3.19Acute suppurativeleptomeningitisduetoHemophilus
influenzaeina14-month-oldchild.Theexudateisconfinedwithinthe
subarachnoidcompartmentandisheavieralongthedorsalsurface.
FIGURE3.20Tabesdorsaliswithinthecervicalspinalcordshowing
darkening within the posterior columns due to loss of myelinated
axons.
Poliovirus is a single-stranded RNAenterovirus that, on the rareoccasion
when symptomatic CNS involvement occurs, tends to damage spinal anterior
horn cells and other motor neurons, presumably because they bear relatively
largenumbersofviralsurfacereceptors.Histologically,intheactivephaseofthe
disease, the affected areas show the presence of many pleomorphic microglia
with evidence of neuronophagia. At later stages, there is striking focal tissue
pallor(Figure3.21) withnerve cell loss and astrocytosis andshrinkage of the
ventralspinalroots.
West Nile virus, a culex mosquito-borne member of the flavivirus
phylogenetic group, is harbored in birds but is capable of infecting many
animals.SymptomaticCNSinvolvementisuncommonbut,whenitdevelops,is
seen in widespread distribution. Pathologically, it is characterized by the
presenceofneuronalnecrosisandneuronophagia,microglialnoduleformation,
andperivascularcuffingbymononuclearinflammatorycells.Asmallsubsetof
patients will develop a poliomyelitis-like syndrome characterized by flaccid
paralysis; in such cases, spinal anteriorhorn pathology is strikingly similar to
thatobservedwithpoliovirusinfection(55).
FIGURE3.21Focaltissuepallorwithinthespinalanteriorhornsofa
patientwhohadsufferedparalysisafterhavingsufferedacuteanterior
poliomyelitis27yearsearlier.
FIGURE 3.22 AIDS-associated vacuolar myelopathy showing
nonsystematizedmicrocysticrarefaction within the dorsal and lateral
whitematter.Thepatternofdamagecloselyresemblesthatofvitamin
B12deficiencymyelopathy.
After varicella-zoster virus infection, the agent is typically stored within
spinal dorsal root ganglia. In subjects who have been immunosuppressed
(particularlythosewithAIDS),recrudescenceofinfectiontypicallyresultsinthe
appearanceofadermatomaleruption.Pathologically,thedorsalrootganglionat
that level shows the presence of a ganglioradiculitis, sometimes withCowdry
typeAintranuclearinclusionbodyformation.Onrareoccasionthismayleadto
the development of a granulomatous vasculitis or a focal necrotizing
myelopathy.
HIV-infectedindividualsmaydevelopasymptomaticmyelopathy(vacuolar
myelopathy of AIDS) that is clinically characterized by spastic paraparesis,
impairmentof proprioception, and posterior column ataxia, andpathologically
by nonsystematized vacuolar degeneration, particularly within the dorsal and
lateralfuniculi(Figure3.22)thatcloselyresemblesthatassociatedwithvitamin
B12deficiencymyelopathy(56).
Other viral agents that may be associated with myelitis, such as herpes
simplexvirustypes1and2,cytomegalovirus,andhumanT-cellleukemiavirus
typeI,typicallyproducenecrotizinglesions.
NEOPLASMSWITHINTHESPINALCANAL
Although virtually any neoplasm that occurs within the cranial cavity can be
seen within the spinal canal, the most common spinal neoplasms are nerve
sheath tumors and meningiomas (which are extramedullary and intradural),
ependymomas and astrocytomas, (which are intramedullary), and secondary
(metastatic) tumors (which are more commonly extramedullary but may be
intramedullary)(57–59).
Nerve sheath tumors are of two types: schwannomas and neurofibromas.
Schwannomas,whichaccountforroughly30%ofprimaryspinalneoplasms,are
benign and tend to occur at and below lumbar regions. When multiple, they
should raise the suspicion that type 2 neurofibromatosis (NF-2 or “central”
neurofibromatosis) may be present. These sharply circumscribed extra-axial
neoplasms,two-thirdsofwhichareextradural,areusuallysituatedwithindorsal
spinal nerve roots (Figure 3.23). They are composed of spindle-shaped cells
arranged in interlacing fascicles and typically show both compact (Antoni A)
andloose-meshed (Antoni B) areas with nuclear palisading and Verocay body
formation, nuclear atypia, vascular hyalinization, and immunoreactivity for S100protein.
FIGURE3.23Schwannomaaffectingaspinalnerveroot.
Neurofibromas, which are also of Schwann cell origin, account for about
25% of primary spinal neoplasms. These benign tumors are typically
encounteredwithintheintraduralportionsofdorsalspinalnerveroots.Theyare
usually solitary and, when seen multiply, should raise the suspicion that the
patientmay be sufferingfrom type 1 neurofibromatosis (NF-1 or “peripheral”
neurofibromatosis).Pathologically,thesefusiformlesionstendtoseparaterather
than displace nerve fibers. Typically, they are composed of spindle-shaped or
stellatecells in a loose connective tissuematrixand, like schwannomas, show
immunoreactivityforS-100protein.
Meningiomas, which account for approximately 25% of primary spinal
neoplasms, are benign intradural lesions that are most commonly observed at
thoracic levels (Figure 3.24). Roughly 80% of affected subjects are women.
When meningiomas occur multiply, the possibility of NF-2 should be
considered. Pathologically, these tumors, which are of arachnoidal cell origin,
are composed of uniform, process-bearing cells with abundant cytoplasm and
roundtoovalvesicularnuclei,withatendencytowardwhorlingandpsammoma
bodyformation.
Ependymomas are low-grade glial neoplasms that are observed most
frequently within the cauda equina and the lumbosacral region. The most
commonsiteoforiginisthefilumterminale(Figure3.25),presumablybecause
of the presence of residual nests of cells left by the embryonic ventriculus
terminalis.Ependymomasarewellcircumscribedlesionscomposedofprocessbearing cells with uniform vesicular nuclei, a tendency toward perivascular
pseudorosetteformation,and,occasionally,thepresenceofependymalrosettes.
Mostoftheneoplasmsarisinginthecaudaequinaareofmyxopapillarytypeand
arecharacterizedbythepresenceoftumorcellsarrangedaroundbloodvessels
thatareseparatedbyamucopolysaccharide-richstroma.
FIGURE 3.24 “Dumbbell” spinal meningioma with both extradural
andintraduralcomponents.
FIGURE3.25Filumterminaleependymoma.
FIGURE 3.26 Spinal intramedullary metastasis of small cell
carcinomaofthelung.
Some80% to 85% of spinal astrocytomasarise in the cervical or thoracic
regions. These infiltrative neoplasms are typically associated with fusiform
enlargementofthe spinalcord andare composedof stellateor spindle-shaped,
process-bearing cells with rounded or oval vesicular nuclei that show
immunoreactivity for glial fibrillary acidic protein. Higher-grade neoplasms
show a greater degree of nuclear pleomorphism with a higher proliferation
index,evidenceofvascularhyperplasiaandtumornecrosis.
Metastasesproduce symptomaticspinal corddysfunction usuallyfollowing
involvementof the vertebral column, especially in the thoracicregion.Rarely,
metastasis may develop within the spinal leptomeninges or within the spinal
cordparenchyma(Figure3.26).Lungisthemostcommonprimarysiteinboth
menandwomen,andbreastisacommonsiteinwomen.
In most cases of spinal cord “compression” due to metastatic extradural
disease,thespinalcord,whenexaminedpathologically,typicallydoesnotshow
deformityofthetypethatmightbeexpectedonthebasisofdirectcompression.
Rather,therearewedge-shapedfociofperivenousmicrocysticrarefaction,often
with hemorrhagic extravasation (Figure 3.27). This finding, coupled with
experimental evidence, suggests that spinal cord damage associated with
vertebral/epidural metastatic disease is attributable largely to epidural venous
obstruction(60).
FIGURE3.27 Ischemic perivenous microcystic rarefaction at spinal
T7, particularly dorsally and laterally, owing to epidural venous
obstructionbymetastaticprostaticadenocarcinoma.
REFERENCES
1. LazorthesG.Pathology,classificationandclinicalaspectsofvasculardiseasesofthespinalcord.In:
VinkenPJ,BruynGW,eds.HandbookofClinicalNeurology.Vol.12.Amsterdam,NL:NorthHolland
PublishingCompany;1972:492–506.
2. Charles YP, BarbeB,BeaujeuxR,et al. Relevance of theanatomicallocationoftheAdamkiewicz
arteryinspinesurgery.SurgRadiolAnat.2011;33:3–9.doi:10.1007/s00276-010-0654-0
3. KimRC.Pathologyofnon-neoplastic,regionaldisordersofthe spinalcord.InNelsonJS,MenaH,
Parisi JE, Schochet SS, eds. Principles and Practice of Neuropathology. 2nd ed. New York, NY:
OxfordUniversityPress;2003:459–496.
4. KimSW,KimRC,ChoiBH,GordonSK.Non-traumaticischaemicmyelopathy:areviewof25cases.
Paraplegia.1988;26:262–272.doi:10.1038/sc.1988.40
5. HughesJT,MacIntyreAG.Spinalcordinfarctionoccurringduringthoracolumbarsympathectomy.J
NeurolNeurosurgPsychiatry.1963;26:418–421.doi:10.1136/jnnp.26.5.418
6. Tosi L, Rigoli G, Beltramello A. Fibrocartilaginous embolism of the spinal cord: a clinical and
pathogenetic reconsideration. J Neurol Neurosurg Psychiatry. 1996;60:55–60.
doi:10.1136/jnnp.60.1.55
7. AbdelRazekMA,MowlaA,FarooqS,etal.Fibrocartilaginousembolism:acomprehensivereviewof
anunder-studiedcauseofspinalcordinfarctionandproposeddiagnosticcriteria.JSpinalCordMed.
2016;39:146–154.doi:10.1080/10790268.2015.1116726
8. WilmshurstPT,ByrneJC,Webb-PeploeMM.Relationbetweeninteratrialshuntsanddecompression
sicknessindivers.Lancet.1989;2:1302–1306.doi:10.1016/s0140-6736(89)91911-9
9. HallenbeckJM,BoveAA,ElliottDH.Mechanismsunderlyingspinalcorddamageindecompression
sickness.Neurology.1975;25(4):308–316.doi:10.1212/wnl.25.4.308
10. KimRC,SmithHR,HenbestML,et al.Non-hemorrhagicvenousinfarctionofthespinal cord.Ann
Neurol.1984;15(4):379–385.doi:10.1002/ana.410150413
11. Thompson TP, Pearce J, Chang G, et al. Surfer’s myelopathy. Spine. 2004;29:E353–E356.
doi:10.1097/01.brs.0000134689.84162.e7
12. Freedman BA, Malone DG, Rasmussen PA,et al. Surfer’s myelopathy: a rare form of spinal cord
infarction in novice surfers: a systematic review. Neurosurgery. 2016;78:602–611.
doi:10.1227/NEU.0000000000001089
13. NakamotoBK,SiuAM,HashibaKA,etal.Surfer’smyelopathy:aradiologicstudyof23cases.AJNR
AmJNeuroradiol.2013;34:2293–2398.doi:10.3174/ajnr.A3599
14. ReisnerA,ChernJJ,Grattan-SmithJD,etal.Letter:surfer’smyelopathy:arareformofspinalcord
infarction in novice surfers: a systematic review. Neurosurgery. 2017;80:E213.
doi:10.1093/neuros/nyw104
15. BarnettHJM,JousseAT,BallMJ.Pathologyandpathogenesisofprogressivecysticmyelopathyasa
late sequel to spinal cord injury. In: Barnett HJM, Foster JB, Hudgson P, eds. Syringomyelia.
Philadelphia,PA:WBSaunders;1973:179–219.
16. Quencer RM, Bunge RP, Egnor M, et al. Acute traumatic central cord syndrome: MRI-pathological
correlations.Neuroradiology.1992;34:85–94.doi:10.1007/bf00588148
17. Kim RC, Collins GH. The neuropathology of rheumatoid disease. Hum Pathol. 1981;12:5–15.
doi:10.1016/S0046-8177(81)80236-5
18. Koeppen AH. The hereditary ataxias. J Neuropathol Exp Neurol. 1998;57:531–543.
doi:10.1097/00005072-199806000-00001
19. LamarcheJB,LemieuxB,LieuHB.Theneuropathologyof“typical”Friedreich’sataxiainQuebec.
CanJNeurolSci.1984;11:592–600.doi:10.1017/s0317167100035113
20. KoeppenAH,BeckerAB,QianJ,etal.Friedreichataxia:hypoplasiaofspinal cordanddorsalroot
ganglia.JNeuropatholExpNeurol.2017;76:101–108.doi:10.1093/jnen/nlw111
21. Fink JK. Hereditary spastic paraplegia: clinico-pathologic features and emerging molecular
mechanisms.ActaNeuropathol.2013;126:307–328.doi:10.1007/s00401-013-1115-8
22. DeLucaGC,EbersGC,EsiriMM.Theextentofaxonallossinthelongtractsin hereditary spastic
paraplegia.NeuropatholApplNeurobiol.2004;30:576–584.doi:10.1111/j.1365-2990.2004.00587.x
23. Kato S, Shaw P, Wood-Allum C, et al. Amyotrophic lateral sclerosis. In: Dickson D, ed.
Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders. Basel,
Соседние файлы в папке Библиотека им академика М.И. Перельмана