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Mexiletine on segmentalhyperhidrosisIshibashi et al1 reported the excellent efficacyof mexiletine for the treatment of segmentalhyperhidrosis in two patients (who had syrin-gomyelia and cavernous haemangioma of thespinal cord, respectively). They presented thedecrement in the patients sweat rate by oraladministration of mexiletine.1

Previously we performed a clinical studyfocusing on sweating and identified 10 pa-tients with segmental hyperhidrosis among30 patients with syringomyelia. We followedup the patients with hyperhidrosis for 110(mean 5.0) years. The amount of sweating didnot change in any of them during the followup period,2 although we did not perform aquantitative analysis. Consequently, wespeculated that hyperhidrosis persists for at

least a year. It is possible that the course ofsigns in the cases reported by Ishibashi et alwere modified by the growth or activity ofspinal cord lesions. We consider it imperativethat these authors describe any spinal cordlesions and how they may have shifted. How-ever, although they did not mention the dura-tion and time courses of the improvement intheir patients,we suppose that the duration ofthe follow up for each patient would not haveexceeded several months, judging from howthe authors described their experience. Inaddition, even though they did not test theeffects of mexiletine on control subjects or onother parts of the body in the same patients,we can be assured that the improvement inhyperhidrosis was due to the oral administra-tion of mexiletine, on the assumption that thespinal cord tumour could not have changed insuch a short time. We consider that it wouldbe informative for clinicians if Ishibashi et alwere to disclose the drug dosage and the timecourse of its effects and to describe thefeatures of the spinal cord lesions.

K Sudo, Y Miyazaki, Y Tajima, A

MatsumotoDepartment of Neurology, Sapporo City General

Hospital, Kita 11, Nishi 13, Chuo-Ku, Sapporo,060-8604 Japan

K Tashiro, F MoriwakaDepartment of Neurology, Hokkaido University

School of Medicine, Sapporo, 0608648, Japan

Correspondence to: Dr K Sudo;[email protected]

References1 Ishibashi S, Yokota T, Inaba A, et al.

Mexiletine is effective on segmentalhyperhidrosis: report of two cases. J NeurolNeurosurg Psychiatry2002;72:122.

2 Sudo K, Fujiki N, Tsuji S, et al. Focal(segmental) dyshidrosis in syringomyelia. JNeurol Neurosurg Psychiatry1999;67:1068.

Authors reply

We are grateful Sudo et al, as they allow us toclarify a point of our study that was notdiscussed in the paper recently published inthis Journal.1 They asked about the possibilityof natural remission and the non-specificeffect of mexiletine on sweating.

We administered 200 mg/day mexiletine or400 mg/day carbamazepine to our patients.Both patients noticed their hyperhidrosis wasrelieved within two days after administration.Although we did not perform a quantitative

analysis several months after treatment, theclinical improvement of hyperhidrosis per-sisted. In addition, the magnetic resonanceimages of spinal cord lesions (syringomyeliaand cavernous haemangioma) in both pa-tients were followed up for two years. Duringthe follow up period, the spinal cord lesionsdid not change their size, position, and inten-sity on magnetic resonance imaging. There-fore, the natural course of the spinal cordlesions could not explain the improvement ofhyperhidrosis during the treatment and quan-titative analysis in our patients.

The sweat rate of the area of observedhyperhidrosis was decreased without achange of the absolute sweat rate on thehealthy side after oral administration ofmexiletine. We calculated the ratio of thesweat rate on the affected side to that on thehealthy sidethe ratio was 2.13 before treat-ment and decreased to 0.97 on day 7 after thetreatment. We therefore consider that themexiletine had an excellent effect only on thearea with hyperhidrosis. Although we did nottest the effects of mexiletine on controlsubjects, we think that the result on a healthyarea of each patient was an appropriate inter-nal controls for the evaluation of the drugseffect on hyperhidrosis.

S Ishibashi, T YokotaDepartment of Neurology and Neurological

Science, Graduate School of Medicine, TokyoMedical and Dental University, 1-5-45, Yushima,

Bunkyo-ku, Tokyo 113-8519, Japan

Correspondence to: Dr T Yokota;[email protected]

Reference1 Ishibashi S, Yokota T, Shiojiri T, et al.

Mexiletine is effective on segmentalhyperhidrosis: report of two cases. J NeurolNeurosurg Psychiatry2002;72:122.

Patent foramen ovale,cerebrovascular risk, andcomplement

Nedeltchev et al1 report that the presence of apatent foramen ovale (PFO) is a significantrisk factor for recurrent cerebrovascularevents, the risk being higher in patients withmore than one previous embolic event. Theyhighlight the absence of a current provenmedical treatment or prevention regimen.

Cardiac right to left shunting is present in aquarter of the population. It is thus worthdrawing attention to a particular subgroup ofpatients with PFO that may be at an evenmore increased risk than the authors reportsport divers, most of whom fall within the agerange of the above study.

Neurological sequelae constitute 80% ofdecompression sickness. Not only has neuro-imaging shown an increased frequency ofbrain ischaemic lesions in divers, but alsomultiple such ischaemic lesions have beenfound specifically in sport divers with PFO.2

While PFO patency of haemodynamic signifi-cance is a risk factor that necessitates habitmodification, often the radiological lesions do

not correspond well to the neurologicaldeficits of experienced divers.

This point, coupled with the increased riskof arterialisation of venous bubbles and theparadoxical nature of bubble genesis, suggest

that a PFO is a risk factor in this subgroup forthe development of neurovascular disease.3

Unknown is the added risk with age thatremains to former divers.A poorly understoodmechanism of bubble induced complementinvolvement in the pathogenesis of theneurological sequelae in decompression sick-ness has been suggested.4 Similarity of suchsymptoms to the postcoronary bypass syn-drome lends support (and hope?) to comple-ment based neuroprotective strategy optionsfor the future.5

A K DemetriadesThe National Hospital for Neurology and

Neurosurgery, Queen Square, LondonWC1N 3BG, UK

Correspondence to: Dr A K Demetriades;[email protected]

References1 Nedeltchev K, Arnold M, Wahl A, et al.

Outcome of patients with cryptogenic strokeand patent foramen ovale. J NeurolNeurosurg Psychiatry 2002;72:34750.

2 Knauth M, Ries S, Pohimann S, et al. Cohortstudy of multiple brain lesions in sport divers:role of a patent foramen ovale. BMJ1997;314:7015.

3 Schwerzmann M, Seiler C, Lipp E, et al.Relation between directly detected patentforamen ovale and ischemic brain lesions insport divers. Ann Intern Med 2001;134:214.

4 Ward CA, McCullough D, Fraser WD.Relation between complement activation andsusceptibility to decompression sickness. JAppl Physiol1987;62:11606.

5 DAmbrosio AL, Pinsky DJ, Connolly ES. Therole of the complement cascade inischemia/reperfusion injury: implications for

neuroprotection. Mol Med2001;7:36782.

Authors reply

We thank Dr Demetriades for his commentsonour study. While the average person with apatent foramen ovale (PFO) may not be atincreased r isk for neurological events, thereseem to be subgroups of patients at increasedrisk. PFOs with large diameters, right to leftshunting at rest, or high membrane mobilityand PFOs associated with atrial septal aneu-rysms have been identified as dangerousPFOs by several investigators.13 In addition,coagulation abnormalities may promote para-doxical emboli in patients with PFO.4 To thislist, Dr Demetriades adds special occupationsorsports thatmay be dangerousin people with

PFOs, specifically divers. Playing wind instru-ments has also been mentioned previously.5

However, many problems related to PFOremain unresolved. Even in groups that arebelieved to be at high risk for neurologicalevents, deciding whether and how to treat aPFO cannot be derived from evidence basedmedicine. Deciding how to proceed dependson the opinion of the attending physician andis not based on data from randomised studies.

The PICSS (PFO in cryptogenic strokestudy) showed that secondary prevention ofcryptogenic stroke in patients with PFO byusing warfarin or aspirin does not result inany difference.6 The PC-trial is an ongoingrandomised trial we initiated to compare

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endovascular PFO closure versus medicaltreatment alone. We hope that it will provideuseful information on secondary stroke pre-vention in patients with presumed paradoxi-cal embolism. It is also conceivable that diverswho have ever had the bends would benefitfrom PFO closure.

Recently reported data suggest links be-tween decompression illness, migraine withaura, and right to left shunts.8 These observa-tions not only extend the clinical manifesta-tions of PFO but also bring into discussionnew pathophysiological aspects of migraine.If the association between complicated mi-graine and PFO can be corroborated, arandomised trial on PFO in such patients maybe worth while.

K Nedeltchev, M Arnold, H MattleDepartment of Neurology, Inselspital, University of

Bern, 3010 Bern, Switzerland

S Windecker, A WahlDepartment of Cardiology

Correspondence to: Prof Dr H P Mattle, Departmentof Neurology, Inselspital, CH-3010 Bern,

Switzerland; [email protected]

Reference1 Schuchlenz HW, Weihs W, Horner S, et al.

The association between the diameter of apatent foramen ovale and the risk of emboliccerebrovascular events. Am J Med2000;109:45662.

2 De Castro S, Cartoni D, Fiorelli M, et al.Morphological and functional characteristicsof patent foramen ovale and their embolicimplications. Stroke2000;31:240713.

3 Mas JL, Arquizan C, Lamy C, et al. PatentForamen Ovale and Atrial Septal AneurysmStudy Group. Recurrent cerebrovascularevents associated with patent foramen ovale,atrial septal aneurysm, or both. N Engl J Med2001;345:17406.

4 Chaturvedi S. Coagulation abnormalities inadults with cryptogenic stroke and patentforamen ovale. J Neurol Sci1998;160:15860.

5 Evers S, Henningsen H, Ringelstein EB.Transient ischemic attacks caused by trumpetplaying. Neurology1998;51:170910.

6 Homma S, Sacco RL, Di Tullio MR, et al. PFO

in Cryptogenic Stroke Study (PICSS)Investigators. Effect of medical treatment instroke patients with patent foramen ovale:patent foramen ovale in cryptogenic strokestudy. Circulation 2002;105:262531.

7 AGA Medical Corporation. PC-trial: patentforamen ovale and cryptogenic stroke. 18

January 2002. http://www.amplatzer.com/physicians/pfo/pctrial/.

8 Wilmshurst P, Nightingale S. Relationshipbetween migraine and cardiac andpulmonary right-to-left shunts. Clin Sci (Lond)2001;100:21520.

Demyelination in the brain as aparaneoplastic disorder:candidates include some casesof seminoma and central

nervous system lymphomaWe read with interest the report of Ayuso-Peralta et al,1 which describes a 58 year oldwoman who presented with several neuro-logical symptoms. Brain imaging was consist-ent withleukoencephalopathy, and analysisofblood and cerebral spinal fluid was unreveal-ing. A few months later the patient experi-enced further neurological deterioration andan open brain biopsy showed central nervoussystem (CNS) lymphoma, together with dif-fuse demyelination.

The authors observed that the presentationof cerebral lymphoma as a diffuse leukoen-cephalopathy is not frequent and they discuss

possible aetiologies of the predominant demye-lination in their case.They do not mention thepossibility of a paraneoplastic aetiology.

The authors reference a similar case2 previ-ously reported in the Journal. That report alsodoes not acknowledge a possible paraneoplas-tic aetiology for prominent diffuse brain demy-elination preceding the discovery of CNSlymphoma. Two other recent reports in theJournal34 described focal tumour-like lesions ofbrain demyelination that preceded the discov-ery of CNS lymphoma. Only one of thesereports4 mentioned laboratory data that sug-gested consideration of a paraneoplastic aeti-ology, the presence of serum antibodies directedagainst myelin oligodendrocyte glycoprotein.

One report elsewhere5 has described a patientwho had a non-neurological malignancy andseminoma and who subsequently developed aparaneoplastic syndrome simulating encephali-tis associated at autopsy with multiple foci ofdemyelination confined to cerebral white mat-ter. Two other reports elsewhere67 have de-scribed biopsy confirmation of large focaldemyelinating lesions in the brain associated

with seminoma. The authors of these threereports all strongly considered the possibility ofa paraneoplastic aetiology for the brain demy-elination associated with seminoma, probablybecause the temporal association was close and

the spatial association was distant.The associations between brain demyelina-

tion and CNS lymphoma have been close,both temporally and spatially, making consid-erations of aetiology more complex. Takentogether, the seminoma reports and the CNSlymphoma reports have many similarities intheir patterns of associated brain demyelina-tion, raising the possibility of similar mecha-nisms of demyelination. Many questions con-cerning aetiology remain unanswered. Giventhe information available, we suspect aparaneoplastic aetiology in all of these cases.We feel that future reports of brain demyeli-nation associated with CNS lymphomashould consider this possibility in their datacollection and in their discussion of results.

J H JasterDelta Medical Center, 1905 Harbert Avenue,

Memphis, Tennessee 38104, USA

F C Dohan JrDivision of Neuropathology, Department of

Pathology, University of Tennessee, Memphis,Memphis, Tennessee 38163, USA

T F OBrienDepartment of Pathology, Methodist University

Hospital, 1265 Union Avenue, Memphis,Tennessee 38104, USA

Correspondence to: Dr J H Jaster, Department ofMedicine, University of Tennessee, 1905 Harbert

Avenue, Memphis, Tennessee 38104, USA;[email protected]

References

1 Ayuso-Peralta L, Orti-Pareja M,Zurdo-Hernandes M, et al. Cerebrallymphoma presenting as aleukoencephalopathy. J Neurol NeurosurgPsychiatry2001;71:2436.

2 Brecher K, Hochberg FH, Louis DN, et al.Case report of unusual leukoencephalopathypreceding primary CNS lymphoma. J NeurolNeurosurg Psychiatry1998;65:91720.

3 Alderson L, Fetell MR, Sisti M, et al. Sentinellesions of primary CNS lymphoma. J NeurolNeurosurg Psychiatry1996;60:1025.

4 Kuhlmann T, Schroter A, Dechent P, et al.Diagnosis of a multifocal B cell lymphomawith preceding demyelinating central nervoussystem lesions by single voxel proton MRspectroscopy. J Neurol Neurosurg Psychiatry2001;70:25962.

5 Kaluza J, Slowinski J, Bujny T, et al.Paraneoplastic syndrome simulatingencephalitis in the course of testicularseminoma. Folia Neuropathol1997;35:248.

6 Wong K, Poon P, Berry K, et al.Paraneoplastic demyelinating disorder in thebrain of a patient with seminoma. J ComputAssist Tomogr1998;22:1368.

7 Jaster JH, Bertorini TE, Dohan FC, et al.Solitary focal demyelination in the brain as aparaneoplastic disorder. Med Pediatr Oncol1996;26:1115.

Genotype predisposition toleukoaraiosisLeukoaraiosis, which can cause symptomsranging from a mild cognitive impairment tosevere subcortical dementia,1 is a significantpublic health problem. One quarter of subjectsaged 65 years or over are affected by somedegree of white matter changes.2 Ischaemicdemyelination and small vessel disease seemto be important features of the underlyingpathological process of this entity.1 2 Age,hypertension, anda previousstroke event havebeen proved to be the main clinical riskfactors.1 2 A number of genetic susceptibilityfactors for leukoaraiosis have been put for-ward, with the assumption of polygenic aetio-logical factors. We were pleased to read thearticle by Hassan et al in this journal.3 The

authors stated that the angiotensin convertingenzyme insertion/deletion (ACE I/D) polymor-phism D/D genotype was a significant inde-pendent predictor for leukoaraiosis in patientspresenting with classic lacunar syndomes.3 Weearlier conducted large prospective studies inwhich we also examined the importance of theACE D allele and other common mutations inthe development of small vessel infarction andleukoaraiosis.4 5 Our results were consistentwith the findings of Hassan et al and supporttheir results from several other aspects. (1)Our stoke study confirmed the genetic hetero-geneity of ischaemic stroke in that the ACED/D genotype proved a significant susceptibil-ity genotype for small vessel brain infarction,as did the Leiden V mutation for large braininfarction.4 (2) In our leukoaraiosis study, theACE D/D genotype was found to be a

significant risk factor for leukoaraiosis incombination with brain infarction.5 (3) Wealso reported that clustering of the homo-zygousMTHFR 677TT and ACE D/D mutationsin one person can mean a moderate (aboutfivefold risk), but highly significant(p


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2 van Gijn J. Leukoaraiosis and vasculardementia. Neurology1998;51:38.

3 Hassan A, Lansbury A, Catto AJ, et al.Angiotensin converting enzymeinsertion/deletion genotype is associated withleukoaraiosis in lacunar syndromes. J NeurolNeurosurg Psychiatry2002;72:3436.

4 Szolnoki Z, Somogyvri F, Kondacs A, et al.Evaluation of the roles of the Leiden Vmutation and ACE I/D polymorphism insubtypes of ischaemic stroke. J Neurol2001;248:75661.

5 Szolnoki Z, Somogyvari F, Kondacs A, et al.

Evaluation of the roles of common geneticmutations in leukoaraiosis. Acta Neurol Scand2001;104:2817.

BOOK REVIEWS

Neurochemistry ofconsciousness: neurotransmittersin mind

Edited by Elaine Perry, Heather Ashton, andAllan Young (Pp 346, EUR65.00). Publishedby John Benjamins Publishing Company,Amsterdam, 2002. ISBN 90-272-5156-8

Consciousness is a portmanteau word, full ofrich and different meanings: contrast Marx-ian, Freudian, and anaesthesiologists use ofthe term. In recent years it has also become afashionable hunting ground for neuroscien-tists, who are rarely troubled by such com-plexities. For them, consciousness is beingawake rather than asleep, being reducible toawareness. Sweeping aside centuries of philo-sophical debate, they ponder over whetherit resides in specific anatomical brainstructures, in microtubules, in patterns ofneurotransmitter release, or whatever. Thepresent book is typical of this type ofcheerfully unsophisticated empiricism: itshuntfor what the editors callNCCsneural

correlates of consciousnessfocuses on neu-rotransmitters, hence the subtitle. However,the concern with mind ceases at that point;this elusive phenomenon finds no place in thebooks index. The central question for the edi-tors seems to be whether the acetylcholine orthe dopaminergic system is the more likelysubstrate for conscious awareness. This reduc-tionism characterises most of the chapters.That on memory, for instance, abandons evenanimal memory for a discussion of a physio-logical phenomenon called long term poten-tiation, and even the psychoanalyst MarkSolms, on dreams, who surely ought to have abroader perspective, confines himself to con-trasting cholinergic and dopaminergic hy-potheses. However, the authors are clearlywriting to an editorial brief: each chapter,in a

book ranging from discussions of attentionand motivation through psychotropic drugmechanisms to mental retardation and au-tism, following a brief nod to marginallywider concerns, offers a neurotransmitter byneurotransmitter list of potential associationsor correlations with states of awareness.Within these limitations many of the chaptersprovide competent student friendly overviewsof their themes. If the books pretensionswerent so much larger this would be fine; asit is, those hoping for a more multilevel ortheoretically informed discussion will bedisappointed.

Steven Rose

Risk control and qualitymanagement in neurosurgery

Edited by H-J Steiger and E Uhl (Pp 227,EUR108.000). Published by Springer VerlagWien, Wien, 2001. ISBN 3-211-83678-0

This is an interesting and timely publication.The book contains a compilation of materialpresented at an international meeting held inOctober 2002. It has been divided into various

sections that take the reader throughgrouped papers and topics and finally aprojection into the future. As would beexpected, the material covers experience andlessons gained in other areas such as aviationand nuclear research. The authors, generallysenior in status, originate from Europe, theUnited States, and the United Kingdom andtherefore offer a diverse collection of views,opinions, and experience relevant to a verywide readership. The increasing requirementsfor quality assessment and competency makethis a very valuable reference book for bothdepartmental and institutional libraries.However, it certainly will be of value to indi-vidual readers. It should be recommendedreading for trainees to understand the princi-ples andthe ongoing thought behindmany of

the practices and control measures that theywill encounter and will need to participate inas their experience and seniority advance.The quality of contributions and the outlineof the information do vary, as would beexpected in such a compilation, but overallvery few pages or chapters do not proveinsightful nor provide useful information andguidelines. It will be of value to all medicaldisciplines, since the principles are universaland the terms of reference or yardsticks usedare convertible or transferable. It is highlyrecommended.

J Van Dellen

Primary progressive multiplesclerosis

Edited by M Filippi and G Comi (Pp 128,EUR47.95). Published by Springer, Milan,2002. ISBN 88-470-0167-6

The field of multiple sclerosis (MS) isawash with literature on every aspect ofthe disease ranging from epidemiology andgenetics to pathology and treatments. It isunusual, therefore, to find a lacuna inthis niche but this book seems to have foundone.

Primary progressive multiple sclerosis is writ-ten to encapsulate the latest evidence onaspects of this condition,which until recentlywas not regarded as important in under-standing demyelinating disease. Filippi andComo have brought together all the impor-tant players in the study of primary progres-

sive MS. Their contributions summarise thelatest information on the epidemiology, ge-netics, immunology, pathology, imaging, andclinical trials and therapies in primaryprogressive MS. This book is meant to be auseful guide to the subject and does not pro-fess to be an authoritative account. However,it occasionally is a little too brief in its expla-nations and definitely lacks pictures, tables,and diagrams in the early part of the book.This makes it a rather bland and dry accountinitially. When the diagrams and scannedimages do appear in the latter parts of thebook, many of them lack definition and it isnot always easy to see the details that arebeing referred to.

All in all this is a good up to date summaryof the latest news in primary progressive MS

and in particular the imaging aspects of thedisease, as would be expected from the inter-ests of theeditors. It wouldbe a useful adjunct

to other literature for those working in thefield of demyelinating disease.

Omar Malik

Multiple sclerosis: a guide forthe newly diagnosed, 2nd edn

By N J Holland, T J Murray, and S C Reingold(Pp 160, US$21.95). Published by DemosMedical Publishing Inc, New York, 2002.ISBN 1-888799-60-9

This book is an invaluable guide for patientswith multiple sclerosis (MS), as well as theirfriends and families. The fact that a second

edition has become necessary is extremelyencouraging for those involved with MS andhighlights the recent therapeutic advances forthis still devastating diagnosis. Most people

who develop MS are desperate for infor-mation about their new disease and manyturn to the internet to find this. Unfortu-

nately, they are then f aced with misleading orsimply incorrect information, which can leavepatients confused or disillusioned.

The authors present detailedinformation in

the first two chapters covering the pathologi-cal processes causing the symptoms of MSand the diagnostic tests in use. Uncertainties

in both these fields are explained. The nexttwo chapters deal with treatments, includingconventional and alternative or complemen-tary therapies; the text is clear about the lack

of a cure for MS but discusses all the optionsincluding steroids for acute attacks, diseasemodifying drugs, and symptomatic treat-

ments. There is a whole chapter on the impor-tant issues of lifestylediet, rest, sexual func-

tion, pregnancy, etcthat help patients tocontrol their condition. A further chapterconcentrates on the psychological impact of adiagnosis of MS and its effect on relation-ships.Employment issues are deservedly dealt

with on their own, with practical advice onwhen and how to disclose the diagnosis andthe legal implications of disclosure both at

work and on application forms such as thosefor health and life insurance.

The latter part of the book deals with clini-cal and research trials in MS that will help

patients to understand how trials are de-signed and why treatments are offered topatients with specific disease types. The many

fields in which MS research is ongoing aredescribed and the questions being asked byinvestigators are well presented.

The book ends with more practical adviceon how to get further information about spe-cific topics; however, this is predominantlyaimed at the North American readership withemphasis on the MS societies of the UnitedStates and Canada.

In summary, this is an excellent book,which presents all the facts in a straightfor-ward but sympathetic way. As well as themedical facts about the disease, it is full ofpractical advice covering all life topics, areasthat are often neglected by busy physicians. Itis highly recommended to all those whoselives have been affected by this disease.

Valerie Stevenson

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Disordered mind and brain: theneural basis of mental symptoms

By Peter F Liddle (Pp 320, 40.00). Publishedby Gaskell, London, 2001. ISBN 1-901242-65-X

The premise of this book is that the key tounderstanding the neural basis of the majormental disorders is an understanding of theorigin of five symptom clusters or dimensionscommon to these disorders. These are realitydistortion (hallucinations and delusions);disorganisation (of thought and behaviour);psychomotor poverty and excitation; depres-sion and elation; and anxiety. Thus, there arefive chapters each devoted to a description ofa specific dimension and an exposition of howit is correlated with cognitive abnormalitiesderived from the dysfunction of specific neu-ral processes.

These central chapters are preceded by fivechapters describing the neuroscience of brainsystems thought to be involved in generatingthe various symptom clusters. These are briefand the literature reviews are in no way com-prehensive. Nevertheless, they serve the pur-pose of informing the reader of the basic neu-roanatomical and neurophysiologicalconcepts that underpin Professor Liddlesapproach to understanding mental illness.

The final four chapters summarise the cur-rent evidence regarding the neurobiology ofschizophrenia, bipolar affective disorder, ob-sessive compulsive disorder, and psychopathy.

Each ends with a synthesis that integratesthis with the previous account of how thesymptom clusters arise.

The explanatory power of Professor Liddlesthesis concerning the neural basis of mentalsymptoms is stronger for some symptomdimensions, such as reality distortion, thanothers, such as distortion. But it is the generalunifying approach that is the major strengthof this bookthe detail will certainly behoned over the next decade. Another strengthis that this is a self contained book! It assumesno neuroscientific or medical knowledgeother than the most basic. There are manyexcellent colour illustrations. Therefore, thisbook can be highly recommended to anybodyinterested in the disordered mind and brain.

Eileen Joyce

CORRECTIONS

Rosso SM, van Swieten JC, Roks G, et al.Apoliproprotein E4 in the temporal variant offrontotemporal dementia. J Neurol NeurosurgPsychiatry 2002;72:820.

Due to the style used in house for listingauthors affiliations in the Letters section ofthe journal, the authors names have beenincorrectly listed. The correct order shouldread as follows:

Rosso SM, Roks G, Cruts M, van Broeck-hoven C, Heutink P, van Duijn CM, vanSwieten JC

This also applies to:Lnemann JD, Kassim N, Zschenderlein

R, et al. Rhabdomyolysis during interferon-1a treatment. J Neurol Neurosurg Psychiatry2002;2:274.

The correct order of the authors is: Lne-mann JD, Schwarzenberger B, Kassim N,Zschenderlein R, Zipp F.

Aarsland D et al. Donepezil for cognitiveimpairment in Parkinsons disease: a ran-domised controlled study. J Neurol Neurosurg

Psychiatry 2002;72:70812. An error occurredin the production process in which the codesof the two lines were erroneously inter-changed. The correct figure appears below:

Figure 2 Change in mini mental stateexamination (MMSE) score from baselineover the two treatment sequences. Values aremean (SE).

30

25

20

15

1020

Time (weeks)

Donepezil-placeboPlacebo-donepezil

Crossover

MMSEscore

0 18161412108642

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doi: 10.1136/jnnp.73.3.3532002 73: 353J Neurol Neurosurg Psychiatry

Steven Rose90-272-5156-8Publishing Company, Amsterdam, 2002. ISBN

346, EUR65.00). Published by John BenjaminsPerry, Heather Ashton, and Allan Young (Ppneurotransmitters in mind : Edited by ElaineNeurochemistry of consciousness:

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