Correspondence / Journal of Clinical Neuroscience 15 (2008) 1071–1072 1071

Reply to ‘‘Is there sentinel demyelination before developmentof primary CNS lymphoma?”

Dear Professor Kaye,

We thank Dr Habek and his colleagues for their interestin our case report.1 They discuss the possibilities that theproposed sentinel demyelination in our patient is coinci-dental or an undiagnosed primary central nervous systemlymphoma (PCNSL).

First, we agree that demyelinating lesions of the cen-tral nervous system (CNS) can be caused by many dis-eases other than multiple sclerosis (MS) and we wouldlike to emphasise that our patient does not have MS.We have labelled the initial presentation as ‘‘pseudo-tumoural demyelination” because the MRI appearanceof the lesion resembled a tumour and the biopsy showedprominent inflammatory demyelination. We did not per-form a CSF examination at the initial presentation as weelected to perform a brain biopsy instead. Serum mark-ers for vasculitis (ANA, dsDNA, SS-A and SS-B, anti-cardiolipin antibody) were all negative. The patient hadneither viral prodrome to suggest a viral aetiology norclinical features of Lyme disease. Furthermore, Lymedisease is very rare in Australia. Visual evoked potentialsand spinal cord MRI were performed within threemonths of the initial presentation and were normal.Although acute disseminated encephalomyelitis can causesimilar histopathologic changes, the presenting lesionwas solitary with no evidence of dissemination in theCNS.

Dr Habek and his colleagues discuss the importantpossibility that the proposed sentinel demyelination ofour case represents an undiagnosed PCNSL, with a fouryear remission induced by a single course of methylprednis-olone. They also commented on the possibilities that thesteroid treatment masked the histopathology findings andthe biopsy specimen was not truly representative of thelesion due to sampling error.

The site of the lesion is unhelpful in this respect.Although it is not common, there have been case reportsof basal ganglia demyelination mimicking brain tumours.2

PCNSL can certainly occur in the basal ganglia,3 but this isby no means a ‘‘typical” location as stated by Dr. Habekand colleagues.

As mentioned in the case report, the original biopsyshowed inflammatory demyelination. The dominant lym-phoid population, both perivascular and diffusely infiltrat-ing the parenchyma consisted of small T lymphocytes, ofboth CD4 and CD8 immunophenotypes. A minor popula-tion of small B lymphocytes was identified. These cells didnot morphologically resemble the neoplastic large B cellsseen in the subsequent biopsy. There was no necrotic cell

population to support lysis of a treated lymphoma. Ofcourse any such biopsy consists of only a small amountof the lesional tissue. However, small samples were takenat different sites, maximising the likelihood of representa-tive tissue having been visualized.

Finally, Dr Habek and his colleagues mentioned severalcase reports resembling our case.4,5 These cases hadPCNSL diagnosed up to several years after an initial senti-nel lesion that regressed without treatment. However, noneof these cases had histological confirmation and thereforediagnosing the initial lesion retrospectively as lymphomawas speculative.

While we have acknowledged the possibility of the initiallesion being an undiagnosed PCNSL, there is no evidenceto support such a conclusion in our case. Indeed, thebiopsy findings argue strongly against it. Although it isnot possible to prove the relationship between the demye-lination and the subsequent lymphoma, our case demon-strates an interesting association that has been observedby several groups previously.6–8

References

1. Ng S, Butzkueven H, Kalnins R, et al. Prolonged interval betweensentinel pseudotumoral demyelination and development of primaryCNS lymphoma. J Clin Neurosci 2007 Sep 21; [doi:10.1016/j.jocn.2006.05.003].

2. Hayashi T, Kumabe T, Jokura H, et al. Inflammatory demyelinatingdisease mimicking malignant glioma. J Nucl Med 2003;44:565–9.

3. Hochberg FH, Baehring JM, Hochberg EP. Primary CNS lymphoma.Nat Clin Pract Neurol 2007;3:24–35.

4. Kon T, Kakita A, Koide A, et al. A primary CNS lymphoma inspontaneous remission for 3.5 years after initial detection of thelesions by MRI. Brain Tumor Pathol 2003;20:27–31.

5. Al-Yamany M, Lozano A, Nag S, et al. Spontaneous remission ofprimary central nervous system lymphoma: report of 3 cases anddiscussion of pathophysiology. J Neurooncol 1999;42:151–9.

6. Heckmann JG, Druschky A, Kern PM, et al. [‘‘Ghost and mimicry-tumor–primary CNS lymphoma”]. Nervenarzt 2000;71:305–10.

7. Alarcia R, Ara JR, Marta E, et al. [Demyelinating pseudotumorallesion prior to a primary cerebral lymphoma]. Rev Neurol 2000;31:955–8.

8. Alderson L, Fetell MR, Sisti M, et al. Sentinel lesions of primary CNSlymphoma. J Neurol Neurosurg Psychiatry 1996;60:102–5.

Steven NgChristopher Rowe

Department of Nuclear Medicine and Centre for PET,

Austin Health, 145 Studley Road,Heidelberg, Victoria 3084,

Australia

Tel.: +61 3 9496 5534; fax: +61 3 9458 5023

E-mail address: ng128@hotmail.com (S. Ng)

doi:10.1016/j

Dear Prof

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doi:10.1016/j

1072 l Neuroscience 15 (2008) 1072

Helmut ButzkuevenDepartment of Neurology,

Royal Melbourne Hospital,

Parkville, Victoria,

Australia

Correspondence / Journal of Clinica

.jocn.2007.12.006

Venous oxygen embolism with use of hydduring craniotomy in the supine

essor Kaye,

en peroxide wound irrigation has been employede haemostasis and clean the surgical field. How-en embolism has been reported following its

luding following posterior fossa tumour excisionne position4 and craniotomy for craniopharyngi-cently, we encountered oxygen embolism in ad male undergoing left frontal craniotomy for anvexity meningioma in the supine position. Hisistory was unremarkable and the preoperativeons were normal. Intraoperative monitoring in-ygen saturation, electrocardiography, inspired

ed gas concentrations, intra-arterial blood pres-central venous pressure monitoring (via a right

central venous catheter). The anaesthetic andurse was otherwise uneventful. During anaesthe-gs were ventilated with isoflurane in a mixture ofd nitrous oxide (1:2). At the end of the surgery,haemostasis was achieved at the surgical site.d was then gently irrigated with 20 ml hydrogen% (diluted with normal saline 1:1). Immediately

ation, a sudden decrease in the end-tidal carbonTCO2) was noted (34 mmHg to 25 mmHg).

ously, the systolic arterial blood pressure de-om 110 mmHg to 75 mmHg, and the heart ratefrom 96 beats per minute to 58 beats per minute.on was immediately informed, the hydrogen per-tion aspirated and the surgical field was irrigatedal saline. At the same time, nearly 50 ml of gasted from the central venous catheter. The lungslated with 100% oxygen, and the patient becamemically stable. The ETCO2 increased to 30o further use of hydrogen peroxide was allowed.from anaesthesia was uneventful, and postopera-

tively, the patient rwithout any neurol

Oxygen embolismcan develop whenspaces. We suggesting intracranial suHydrogen peroxidecountries, but cliniwhen using this see

References

1. Haller G, Faltin-Trhydrogen peroxide2002;88: 597–9.

2. Morikawa H, Mimhydrogen peroxideAnaesth 1995;42:231

3. Despond O, Fiset Pperoxide during lum

4. Dubey PK, Singh Aperoxide irrigationAnesthesiol 2000;12:

5. Prabhakar H, Bithhydrogen peroxidegioma. J Clin Neuro

Tel.: +91 11

E-mail addres

.jocn.2006.10.011

Renate KalninsDepartment of Anatomical Pathology,

Austin Health,

Heidelberg, Victoria,

Australia

rogen peroxideposition

emained haemodynamically stable andogic sequelae.

is a potentially fatal complication thathydrogen peroxide is used near venousthat the use of hydrogen peroxide dur-rgery is dangerous and unwarranted.

is still commonly used in developingcians should be aware of the dangersmingly innocuous solution.

aub E, Faltin D, et al. Oxygen embolism afterirrigation of a vulvar abscess. Br J Anaesth

a H, Fujita H, et al. Oxygen embolism due toirrigation during cervical spinal surgery. Can J

–3.. Oxygen venous embolism after use of hydrogenbar discectomy. Can J Anaesth 1997;44:410–3.K. Venous oxygen embolism due to hydrogenduring posterior fossa surgery. J Neurosurg

54–6.al PK, Pandia MP, et al. Bradycardia due toirrigation during craniotomy for craniopharyn-sci 2007; in press. doi:10.1016/j.jocn.2006.01.029.

Hemanshu PrabhakarGirija P. Rath

Department of Neuroanesthesiology,

Neurosciences Centre,

All India Institute of Medical Sciences,

Ansari Nagar, New Delhi 110029,

India

26588700 4347; fax: +91 11 26862663

s: prabhakarhemanshu@rediffmail.com(H. Prabhakar).