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MEKANISME NYERI

Nyeri merupakan suatu bentuk peringatan akan adanya bahaya kerusakan jaringan.
Pengalaman sensoris pada nyeri akut disebabkan oleh stimulus noksius yang diperantarai oleh
sistem sensorik nosiseptif. Sistem ini berjalan mulai dari perifer melalui medulla spinalis, batang
otak, thalamus dan korteks serebri. Apabila telah terjadi kerusakan jaringan, maka sistem
nosiseptif akan bergeser fungsinya dari fungsi protektif menjadi fungsi yang membantu
perbaikan jaringan yang rusak .

Nyeri inflamasi merupakan salah satu bentuk untuk mempercepat perbaikan kerusakan
jaringan. Sensitifitas akan meningkat, sehingga stimulus non noksius atau noksius ringan yang
mengenai bagian yang meradang akan menyebabkan nyeri. Nyeri inflamasi akan menurunkan
derajat kerusakan dan menghilangkan respon inflamasi.

Sensitisasi Perifer

Cidera atau inflamasi jaringan akan menyebabkan munculnya perubahan lingkungan


kimiawi pada akhir nosiseptor. Sel yang rusak akan melepaskan komponen intraselulernya
seperti adenosine trifosfat, ion K+, pH menurun, sel inflamasi akan menghasilkan sitokin,
chemokine dan growth factor. Beberapa komponen diatas akan langsung merangsang nosiseptor
(nociceptor activators) dan komponen lainnya akan menyebabkan nosiseptor menjadi lebih
hipersensitif terhadap rangsangan berikutnya (nociceptor sensitizers).

Komponen sensitisasi, misalnya prostaglandin E2 akan mereduksi ambang aktivasi


nosiseptor dan meningkatkan kepekaan ujung saraf dengan cara berikatan pada reseptor spesifik
di nosiseptor. Berbagai komponen yang menyebabkan sensitisasi akan muncul secara bersamaan,
penghambatan hanya pada salah satu substansi kimia tersebut tidak akan menghilangkan
sensitisasi perifer. Sensitisasi perifer akan menurunkan ambang rangsang dan berperan dalam
meningkatkan sensitifitas nyeri di tempat cedera atau inflamasi.
Sensitisasi Sentral

Sama halnya dengan sistem nosiseptor perifer, maka transmisi nosiseptor di sentral juga
dapat mengalami sensitisasi. Sensitisasi sentral dan perifer bertanggung jawab terhadap
munculnya hipersensitivitas nyeri setelah cidera. Sensitisasi sentral memfasilitasi dan
memperkuat transfer sipnatik dari nosiseptor ke neuron kornu dorsalis. Pada awalnya proses ini
dipacu oleh input nosiseptor ke medulla spinalis (activity dependent), kemudian terjadi
perubahan molekuler neuron (transcription dependent).

Sensitisasi sentral dan perifer merupakan contoh plastisitas sistem saraf, dimana terjadi
perubahan fungsi sebagai respon perubahan input (kerusakan jaringan). Dalam beberapa detik
setelah kerusakan jaringan yang hebat akan terjadi aliran sensoris yang masif kedalam medulla
spinalis, ini akan menyebabkan jaringan saraf didalam medulla spinalis menjadi hiperresponsif.
Reaksi ini akan menyebabkan munculnya rangsangan nyeri akibat stimulus non noksius dan pada
daerah yang jauh dari jaringan cedera juga akan menjadi lebih sensitif terhadap rangsangan
nyeri.

NOSISEPTOR (RESEPTOR NYERI)

Nosiseptor adalah reseptor ujung saraf bebas yang ada di kulit, otot, persendian, viseral
dan vaskular. Nosiseptor-nosiseptor ini bertanggung jawab terhadap kehadiran stimulus noksius
yang berasal dari kimia, suhu (panas, dingin), atau perubahan mekanikal. Pada jaringan normal,
nosiseptor tidak aktif sampai adanya stimulus yang memiliki energi yang cukup untuk
melampaui ambang batas stimulus (resting). Nosiseptor mencegah perambatan sinyal acak
(skrining fungsi) ke SSP untuk interpretasi nyeri.

Saraf nosiseptor bersinap di dorsal horn dari spinal cord dengan lokal interneuron dan
saraf projeksi yang membawa informasi nosiseptif ke pusat yang lebih tinggi pada batang otak
dan thalamus. Berbeda dengan reseptor sensorik lainnya, reseptor nyeri tidak bisa beradaptasi.
Kegagalan reseptor nyeri beradaptasi adalah untuk proteksi karena hal tersebut bisa
menyebabkan individu untuk tetap awas pada kerusakan jaringan yang berkelanjutan. Setelah
kerusakan terjadi, nyeri biasanya minimal. Mula datang nyeri pada jaringan karena iskemi akut
berhubungan dengan kecepatan metabolisme. Sebagai contoh, nyeri terjadi pada saat beraktifitas
kerena iskemia otot skeletal pada 15 sampai 20 detik tapi pada iskemia kulit bisa terjadai pada 20
sampai 30 menit.

Tipe nosiseptor spesifik bereaksi pada tipe stimulus yang berbeda. Nosiseptor C tertentu
dan nosiseptor A-delta bereaksi hanya pada stimulus panas atau dingin, dimana yang lainnya
bereaksi pada stimulus yang banyak (kimia, panas, dingin). Beberapa reseptor A-beta
mempunyai aktivitas nociceptor-like. Serat serat sensorik mekanoreseptor bisa diikutkan untuk
transmisi sinyal yang akan menginterpretasi nyeri ketika daerah sekitar terjadi inflamasi dan
produk-produknya. Allodynia mekanikal (nyeri atau sensasi terbakar karena sentuhan ringan)
dihasilkan mekanoreseptor A-beta.

Nosiseptor viseral, tidak seperti nosiseptor kutaneus, tidak didesain hanya sebagai
reseptor nyeri karena organ dalam jarang terpapar pada keadaan yang potensial merusak. Banyak
stimulus yang sifatnya merusak (memotong, membakar, kepitan) tidak menghasilkan nyeri bila
dilakukan pada struktur viseralis. Selain itu inflamasi, iskemia, regangan mesenterik, dilatasi,
atau spasme viseralis bisa menyebabkan spasme berat. Stimulus ini biasanya dihubungkan
dengan proses patologis, dan nyeri yang dicetuskan untuk mempertahankan fungsi.

PERJALANAN NYERI (NOCICEPTIVE PATHWAY)

Perjalanan nyeri termasuk suatu rangkaian proses neurofisiologis kompleks yang disebut
sebagai nosiseptif (nociception) yang merefleksikan empat proses komponen yang nyata yaitu
transduksi, transmisi, modulasi dan persepsi, dimana terjadinya stimuli yang kuat diperifer
sampai dirasakannya nyeri di susunan saraf pusat (cortex cerebri).

Proses Transduksi

Proses dimana stimulus noksius diubah ke impuls elektrikal pada ujung saraf. Suatu
stimuli kuat (noxion stimuli) seperti tekanan fisik kimia, suhu dirubah menjadi suatu aktifitas
listrik yang akan diterima ujung-ujung saraf perifer (nerve ending) atau organ-organ tubuh
(reseptor meisneri, merkel, corpusculum paccini, golgi mazoni). Kerusakan jaringan karena
trauma baik trauma pembedahan atau trauma lainnya menyebabkan sintesa prostaglandin,
dimana prostaglandin inilah yang akan menyebabkan sensitisasi dari reseptor-reseptor nosiseptif
dan dikeluarkannya zat-zat mediator nyeri seperti histamin, serotonin yang akan menimbulkan
sensasi nyeri. Keadaan ini dikenal sebagai sensitisasi perifer.

Proses Transmisi

Proses penyaluran impuls melalui saraf sensori sebagai lanjutan proses transduksi melalui
serabut A-delta dan serabut C dari perifer ke medulla spinalis, dimana impuls tersebut
mengalami modulasi sebelum diteruskan ke thalamus oleh traktus spinothalamikus dan sebagian
ke traktus spinoretikularis. Traktus spinoretikularis terutama membawa rangsangan dari organ-
organ yang lebih dalam dan viseral serta berhubungan dengan nyeri yang lebih difus dan
melibatkan emosi. Selain itu juga serabut-serabut saraf disini mempunyai sinaps interneuron
dengan saraf-saraf berdiameter besar dan bermielin. Selanjutnya impuls disalurkan ke thalamus
dan somatosensoris di cortex cerebri dan dirasakan sebagai persepsi nyeri.

Proses Modulasi
Proses perubahan transmisi nyeri yang terjadi disusunan saraf pusat (medulla spinalis dan
otak). Proses terjadinya interaksi antara sistem analgesik endogen yang dihasilkan oleh tubuh
kita dengan input nyeri yang masuk ke kornu posterior medulla spinalis merupakan proses
ascenden yang dikontrol oleh otak. Analgesik endogen (enkefalin, endorphin, serotonin,
noradrenalin) dapat menekan impuls nyeri pada kornu posterior medulla spinalis. Dimana kornu
posterior sebagai pintu dapat terbuka dan tertutup untuk menyalurkan impuls nyeri untuk
analgesik endogen tersebut. Inilah yang menyebabkan persepsi nyeri sangat subjektif pada setiap
orang.

Persepsi

Hasil akhir dari proses interaksi yang kompleks dari proses tranduksi, transmisi dan
modulasi yang pada akhirnya akan menghasilkan suatu proses subjektif yang dikenal sebagai
persepsi nyeri, yang diperkirakan terjadi pada thalamus dengan korteks sebagai diskriminasi dari
sensorik.

Menurut smeltzer, S.C bare B.G (1996) terdapat beberapa pengukuran skala nyeri yaitu sebagai
berikut:

1) Skala intensitas nyeri Bourbonais

Keterangan :

0 :Tidak nyeri

1-3 : Nyeri ringan : secara obyektif klien dapat berkomunikasi dengan baik.

4-6 : Nyeri sedang : Secara obyektif klien mendesis, menyeringai, dapat menunjukkan lokasi
nyeri, dapat mendeskripsikannya, dapat mengikuti perintah dengan baik.

7-9 : Nyeri berat : secara obyektif klien terkadang tidak dapat mengikuti perintah tapi masih
respon terhadap tindakan, dapat menunjukkan lokasi nyeri, tidak dapat mendeskripsikannya,
tidak dapat diatasi dengan alih posisi nafas panjang dan distraksi

10 : Nyeri sangat berat : Pasien sudah tidak mampu lagi berkomunikasi, memukul.
2) Skala intensitas nyeri numerik

3) Skala analog visual

4) Skala nyeri enam wajah dengan ekspresi yang berbeda, menampilkan wajah bahagia hingga
wajah sedih, juga di gunakan untuk mengekspresikan rasa nyeri.

Gambar 2.1 Skala wajah untuk nyeri


Karakteristik paling subjektif pada nyeri adalah tingkat keparahan atau intensitas nyeri tersebut.
Klien seringkali diminta untuk mendeskripsikan nyeri sebagai yang ringan, sedang atau berat.
Namun, makna istilah-istilah ini berbeda bagi perawat dan klien. Dari waktu ke waktu informasi
jenis ini juga sulit untuk dipastikan. Skala nyeri harus dirancang sehingga skala tersebut mudah
digunakan dan tidak menghabiskan banyak waktu saat klien melengkapinya. Apabila klien dapat
membaca dan memahami skala, maka deskripsi nyeri akan lebih akurat. Skala deskriptif
bermanfaat bukan saja dalam upaya mengkaji tingkat keparahan nyeri, tetapi juga mengevaluasi
perubahan kondisi klien. Perawat dapat menggunakannya setelah terapi atau saat gejala menjadi
lebih memburuk atau menilai apakah nyeri mengalami penurunan atau peningkatan (Potter &
Perry, 1997).
RCesoeamrchparison of numerical and verbal rating
scales
to measure pain exacerbations in patients with
chronic cancer pain
Cinzia Brunelli*1, Ernesto Zecca1, Cinzia Martini1, Tiziana Campa1, Elena Fagnoni1, Michela
Bagnasco2, Luigi Lanata2
and Augusto Caraceni1
Abstract
Background: Numerical rating scales (NRS), and verbal rating scales (VRS) showed to be reliable and
valid tools for
subjective cancer pain measurement, but no one of them consistently proved to be superior to the other.
Aim of the
present study is to compare NRS and VRS performance in assessing breakthrough or episodic pain (BP-
EP)
exacerbations.
Methods: In a cross sectional multicentre study carried out on a sample of 240 advanced cancer patients
with pain,
background pain and BP-EP intensity in the last 24 hours were measured using both a 6-point VRS and a
0-10 NRS. In
order to evaluate the reproducibility of the two scales, a subsample of 60 patients was randomly selected
and the
questionnaire was administered for a second time three to four hours later. The proportion of
"inconsistent"
(background pain intensity higher than or equal to peak pain intensity) evaluations was calculated to
compare the two
scales capability in discriminating between background and peak pain intensity and Cohen's K was
calculated to
compare their reproducibility.
Results: NRS revealed higher discriminatory capability than VRS in distinguishing between background
and peak pain
intensity with a lower proportion of patients giving inconsistent evaluations (14% vs. 25%). NRS also
showed higher
reproducibility when measuring pain exacerbations (Cohen's K of 0.86 for NRS vs. 0.53 for VRS) while
the reproducibility
of the two scales in evaluating background pain was similar (Cohen's K of 0.80 vs. 0.77).
Conclusions: Our results suggest that, in the measurement of cancer pain exacerbations, patients use
NRS more
appropriately than VRS and as such NRS should be preferred to VRS in this patient's population.

J Pain Symptom Manage. 2011 Jun;41(6):1073-93. doi: 10.1016/j.jpainsymman.2010.08.016.

Studies comparing Numerical Rating Scales, Verbal Rating


Scales, and Visual Analogue Scales for assessment of pain
intensity in adults: a systematic literature review.
Hjermstad MJ, Fayers PM, Haugen DF, Caraceni A, Hanks GW, Loge JH, Fainsinger R, Aass
N, Kaasa S; European Palliative Care Research Collaborative (EPCRC).
Collaborators (23)

Source
Regional Center for Excellence in Palliative Care, Department of Oncology, Oslo University Hospital-
Ullevl, Oslo, Norway. m.j.hjermstad@medisin.uio.no
Abstract
CONTEXT:
The use of unidimensional pain scales such as the Numerical Rating Scale (NRS), Verbal Rating Scale
(VRS), or Visual Analogue Scale (VAS) is recommended for assessment of pain intensity (PI). A literature
review of studies specifically comparing the NRS, VRS, and/or VAS for unidimensional self-report of PI
was performed as part of the work of the European Palliative Care Research Collaborative on pain
assessment.
OBJECTIVES:
To investigate the use and performance of unidimensional pain scales, with specific emphasis on the
NRSs.
METHODS:
A systematic search was performed, including citations through April 2010. All abstracts were evaluated
by two persons according to specified criteria.
RESULTS:
Fifty-four of 239 papers were included. Postoperative PI was most frequently studied; six studies were in
cancer. Eight versions of the NRS (NRS-6 to NRS-101) were used in 37 studies; a total of 41 NRSs were
tested. Twenty-four different descriptors (15 for the NRSs) were used to anchor the extremes. When
compared with the VAS and VRS, NRSs had better compliance in 15 of 19 studies reporting this, and
were the recommended tool in 11 studies on the basis of higher compliance rates, better responsiveness
and ease of use, and good applicability relative to VAS/VRS. Twenty-nine studies gave no preference.
Many studies showed wide distributions of NRS scores within each category of the VRSs. Overall, NRS
and VAS scores corresponded, with a few exceptions of systematically higher VAS scores.
CONCLUSION:
NRSs are applicable for unidimensional assessment of PI in most settings. Whether the variability in
anchors and response options directly influences the numerical scores needs to be empirically tested.
This will aid in the work toward a consensus-based, standardized measure.
Copyright 2011 U.S. Cancer Pain Relief Committee. Published by Elsevier Inc. All rights reserved.

Generated at: Sun, 03 Mar 2013 08:59:28 -0600 (00001a73) http://www.ispub.com:80/journal/the-


internet-journal-of-anesthesiology/volume-8-number-1/a-comparison-of-the-verbal-rating-scale-and-
the-visual-analog-scale-for-pain-assessment.html

Abstract
This survey was performed to determine if the simple Verbal Rating Scale (VRS) could be
substituted for the Visual Analog Scale (VAS) to measure pain intensity in chronic pain patients.
Eighty-five (85) chronic pain patients were surveyed using both VAS and VRS. Pearson
correlation coefficient(r = 0.906) and p value (< 0.0001) showed excellent correlation between
the two, although VRS showed a tendency to be higher than VAS (p=0.068). We propose that
the VRS provides a useful alternative to the VAS scores in assessment of chronic pain.

Discussion
Pain is a subjective sensation and therefore difficult to measure. It is, however, important to
quantify it for several reasons; one of the most compelling reasons is that assigning a
measurement of pain gives patients some sense of control over their condition and has positive
effects on their coping abilities. Pain measurements also provide a means of assessing the
efficacy of response to treatment and prognosis.

The VAS (1, 2, 3) is a well-studied method for measuring both acute and chronic pain, and its
usefulness has been validated by several investigators. However, the VAS is comparatively time-
consuming and requires ability to understand the abstract concept of the VAS line and then relate
it to distance from a zero mark. It also requires the use of a paper and pen. As line length in VAS
is the response continuum, many patients find it difficult to judge distance accurately. Therefore
the VAS has some practical limitations in a clinic setting.

The VRS as described above is easily assessed, takes less time than the VAS, and can be
performed without the need of paper and pen. It is relatively simple to understand (e.g., 6 is a
higher value number than 4 and so on), and thus provides a correlation which is more definitive
than a distance mark. Comparisons between VRS and VAS have been performed by some
investigators (4, 5, 6, 7, 8). These comparisons have defined VRS in different ways. Some
physicians are employing the method that we have described above; however no study has been
published which compares VRS with the VAS. Our analysis takes a measurement engineering
approach by looking at the reliability and validity of VRS, using VAS as the standard. Reliability
is assessed with an analysis of correlation, while validity is assessed with Student's t-test for
paired data. The VRS is a simple instrument that can save time and compares favorably to the
VAS.
The pain is often paroxysmal at first, severe, moderate
in intensity, throbbing but obviously all these adjectives are
strictly linked to the specific time of the tumours evolution.
Headache usually could worsen on awakening; moreover
it may wake up the subject at night, but these aspects
are not diagnostic. The attacks may last without any rule
and as the mass increases pain becomes more frequent and
finally is continuous, due to disturbance of CSF dynamics.
The pain is characteristically worsened by changes in posture,
or bending down, and is improved by rest. It is accentuated
by exertion, coughing, sneezing or vomiting. The
headache is often generalised but if unilateral it is likely to
be on the side of the lesion.
Posterior fossa tumour can give rise to orbital pain due
to innervation of the tentorium by the first division of the
trigeminal nerve, but more commonly gives rise to occipital
and neck pain.
The most
common type of brain tumour-headache is tension type
seen in 77% of patients, and described as severe, worse in
the morning and accompanied by nausea and vomiting in
only 17% of cases [1].

Generally the headaches localisation does not match


with tumours location. The patients in 70% of cases complain
of pain on the frontal area and usually the ache occurs
bilaterally. A peculiarity is the fact that headache is not
manageable with pain-relieving drugs. It is a common myth
that the headache starts in the early morning; it occurs over
night or at any time, not necessarily following any effort. It
could occur during rest. In addition, its progressive course
is a myth too. Worsening is assessed in 15% of cases; more
frequently its trend in 60% of cases is discontinuous [2]. A
headache hiding a brain tumour is rather similar to a tension
headache in 77% of cases and its beginning could be
deaf, deep heavy and the pain is wide-ranging the whole
brain. In 510% of cases it could mimic a classic migraine;
otherwise it is present as a mixed form with tension and
classic migraine combination [1].

Table 1 The main factors causing headache


a. Distortion of the dura mater and pain-sensitive intracranial
vessels traction or dilatation and displacement of blood
vessels occurring in intracranial hypertension
b. Inflammation involving pain-sensitive structures
c. Meningeal irritation or its involvement in spreading tumours
d. Finally headache can emerge due to psychological
and biochemical causes

Table 2 Brain tumour patients treated at National Neurological


Institute C. Besta between 2001 and 2003
Malignant glioma (Grade IIIIV) 524
Medulloblastomas 44
Astrocytoma and meningiomas 570
Metastases 115

Table 3 Headache characteristics in brain tumours (including low grade) according to Forsyth and Posner
Description Tension type dull ache pressure like and sinus like in 77%
Migraine in 9%26% of cases
Worsens with cough, Valsalva manoeuvre and bending in 23% of cases
Interferes with sleep in 32% of cases
Timing Intermittent, develops and resolves in several hours
Duration Less than 1 month 29%
For 16 months in 26%
More than 6 months in 45% of cases
Intensity May be mild, moderate or severe. Mean intensity in 8.5/10 or in 6.5/10 of cases if associated or not with intracranial
hypertension respectively
Associated Nausea and vomiting 38%
symptoms Visual disturbance 40%
Seizures 50%

References
1. Forsyth PA, Posner JB (1993) Headaches in patients with brain
tumors: a study of 111 patients. Neurology 43:16781683
2. Vazquez-Barquero A, Ibanes FJ, Herrera S, Izquerdo
Berciano J, Pasqual J (1994) Isolated headache as the present
clinical manifestation of intracranial tumors: a prospective
study. Cephalalgia 14:270272

Headache Classification Committee of the International


Headache Society. (1988) Classification and diagnostic criteria
in headache disorders, cranial neuralgia and facial pain.
Cephalalgia 8:196

Wang HZ, Simonson TM, Greco WR, Yuh WT (2001) Brain


MR imaging in the evaluation of chronic headache in
patients without other neurologic symptoms. Acad Radiol
8:405408
Intracranial germ cell tumors: a single-institution experience.

Authors:

Khafaga Y ; El Weshi A ; Nazmy M ; Hassounah M ; Alshail E ; Moussa E ; Allam A ; Alkofide A


; Jamshed A ; Elhusseiny G ; Ezzat I ; Jenkin D

Affiliation:

Professor Yasser Khafaga, MBC 34, Consultant Radiation Oncology, King Faisal Specialist
Hospital and Research Center, PO Box 3354, Riyadh 11211, Saudi Arabia T:+ 966502957642
F:+96614424566 ykhafaga@hotmail.com

Source:

Annals of Saudi Medicine (ANN SAUDI MED), 2012 Jul; 32 (4): 359-65.

Publication Type:

journal article - research

Language:

English

Major Subjects:

Brain Neoplasms -- Therapy


Neoplasms, Germ Cell and Embryonal -- Therapy
Tumor Markers, Biological -- Metabolism

Minor Subjects:

Adolescence ; Adult ; Age Factors ; Antineoplastic Agents -- Administration and Dosage


; Antineoplastic Agents -- Therapeutic Use ; Brain Neoplasms -- Diagnosis ; Brain Neoplasms --
Pathology ; Child ; Child, Preschool ; Combined Modality Therapy ; Prognosis ; Female
; Prospective Studies ; Human ; Male ; Neoplasm Recurrence, Local ; Neoplasms, Germ Cell and
Embryonal -- Diagnosis ; Neoplasms, Germ Cell and Embryonal -- Pathology ; Radiation Dosage
; Retrospective Design ; Saudi Arabia ; Survival ; Time Factors ; Treatment Outcomes ; Young
Adult

Abstract:

BACKGROUND AND OBJECTIVES: Intracranial germ cell tumors (GCTs) are not a common
disease. We reviewed the experience of a single institution to determine the variables that
affect treatment outcome. DESIGN AND SETTING: A retrospective review of patients with the
diagnosis of intracranial germ cell tumors treated in a single institution (KFSHRC) during the
period from March 1985 to December 2007. PATIENTS AND METHODS: Fifty-seven patients
with the diagnosis of intracranial GCT were recorded in the KFSHRC Tumor Registry during the
period from 1985 to 2007. Seven patients with a pineal region tumor treated as germinomas in
the earlier years without a tissue diagnosis were excluded. This retrospective study was
restricted to the remaining 50 patients with a tissue or marker diagnosis: 31 germinomas and
19 non-germinomatous germ cell tumors (NGGCTs). RESULTS: The 10-year overall survival
(OS), event-free survival (EFS) and relapse-free survival (RFS) were 87%, 88% and 96% for
patients with germinoma, with a median follow-up of 4.5 (range 2-17) years, compared with
26%, 29% and 46% for patients with NGGCT with a median follow-up of 3 (range 1.5-13)
years. For NGGCT, variables favorably influencing OS were younger age (< 16 y vs >=16 y,
P=.01), higher tumor dose (>50 Gy vs <=50 Gy; P=.03) and later year of diagnosis (>1990 vs
<1990 P=.002). CONCLUSIONS: Tissue diagnosis of GCTs is mandatory prior to treatment
except for patients with elevated markers. In germinoma, localized radiotherapy (RT) for M0
patients may be adequate. Long-term follow-up is needed to define the benefit of adding
chemotherapy. For NGGCT, the use of combined modality treatment and RT dose ;gt;50 Gy are
important factors that influence the outcome. Second-look surgery and resection of residual/
refractory tumors is always recommended.

Journal Subset:

Biomedical; Middle East; Peer Reviewed

ISSN:

0256-4947

MEDLINE Info:

PMID: 22705605 NLM UID: 8507355

Entry Date:

20121123

Revision Date:

20121123

Accession Number:

2011586804

Database:

CINAHL Plus with Full Text