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NEWSLETTER OF THE NORTH BRITISH PAIN ASSOCIATION - SPRING 2003

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FROM THE EDITOR:

Welcome to the spring edition of Threshold,which, like the last issue, has kindly been sponsored by Janssen Cilag. The winter scientific meetingseems a long time ago now. The long winter monthsare now at an end. Spring is here, heralded by sunnydays, birds singing in the trees and the sound of Threshold dropping through your letter box.Unfortunately, all is not rosy in the world and theseare troubled times. Perhaps, by the time you readthis, the war in Iraq will be over with, we hope, asfew casualties as possible. Current events make thesubject of the Spring Meeting, ‘Pain in Conflict’ allthe more relevant.As I was working on this issue of Threshold, thePain Society newsletter arrived. The new Editor,Stephen Ward, has produced an excellent ‘new look’first issue. Now, being of a competitive nature, I triedtelling myself that we are not rivals butcomplementary publications. I don’t feel pressuredat all, I don’t…. not at all….. absolutely not.I have, in fact formulated bold plans for Threshold, but on consultation with my colleagues Ihave been advised that it would not be proper at this juncture to turn Threshold into the ‘Loaded’magazine of the pain world. Oh well, never mind.The winner of last issue’s caption competition isannounced over the page and for this issue, as wellas the caption competition, Mike Basler has providedus with an interesting anagram competition.As ever, there is much to keep us busy, includingthe Pain Society meeting in Glasgow, the Spring NBPA meeting and of course summer holidays tolook forward to.The deadline for the NBPA essay competition hascome and gone. There has not exactly been a floodof entries but those submitted have been of thehighest standard. The winner will be announced atthe Spring Scientific Meeting. Information on nextyear’s competition will be given in the Autumn issue.If you have an article you would like to submit,a topic you would like covered, or a news item youwould like to be included in the next issue, pleasesend it to the address below. Any photographs,embarrassing or otherwise, suitable for the captioncompetition would be much appreciated. Post themto: -Dr Colin P. Rae,Department of Anaesthesia,Stobhill Hospital,133 Balornock Road,Glasgow,G21 3UW.Tel no: 0141 201 3005.Fax no: 0141 201 4167.Email: colin.rae@northglasgow.scot.nhs.uk NBPA website www.nbpa.org.uk

NEWS FROM NBPA COUNCIL

Clinical Information Subgroup

At the last NBPA Council Meeting, Dr. RobinMcKinlay from Stirling floated the suggestion of forming a Clinical Information Subgroup. The groupwould advise on information technology and auditissues, including the maintenance of the NBPAwebsite. We are all aware of the need to audit our activities and outcomes. There is a generalrecognition that many centres have struggled to setup and utilise the PACS national database for avariety of reasons. The importance of support for this project was recently highlighted in an Editorial in‘Anaesthesia’. It was agreed that Robin wouldapproach three other individual with an interest inthese matters to form the group. If anyone hasexpertise in this field and would like to be involvedthen please speak to Robin at the next meeting inEdinburgh or contact him at Stirling Royal Infirmary.

NBPA Website

There are ongoing discussions about the cost,location and future of the NBPA website which iscurrently located on the University of Newcastleserver. Dr. Semple is to investigate other options andwill report back to council.

DATES FOR YOUR DIARY

NBPA Spring Scientific Meeting Friday 9th May2003 “Pain in Conflict” NBPA Winter Scientific Meeting Friday 21st November 2003 “An Inflammatory View of Pain”

REPORT FROM WINTERSCIENTIFIC MEETING

Friday 22/11/02“Hard nuts to crack”

The meeting was kindly sponsored by Merck Sharp and Dohme, Napp Pharmaceuticals, Pfizer andJanssen Cilag.The day started with an excellent lecture given by Dr Roger E Cull, Consultant & Senior Lecturer in Neurophysiology, Western General Hospital,Edinburgh. The title of his lecture was “Diagnosisof migraine and other headaches”.Migraine is defined as: - “A familial periodicdisorder characterised by recurrent attacks of headache in which the pain is often unilateral, pulsating in quality and usually accompanied byanorexia, nausea and vomiting.” In some cases, itmay be preceded or accompanied by focalneurological, especially visual, symptoms. Thelifetime risk of suffering from migraine is 25% andthe prevalence in the general population is 10% -15%. It is 2 – 3 times more common in women thanmen, especially during the reproductive years. Thecommonest age of onset is in the second or thirddecade. A positive family history is present in 70%of cases and other risk factors include female sex,age, menstruation, early pregnancy, stress, diet,sleep, travel, exercise, head injury, SLE and certaindrugs.Migraine can be sub-divided into different types.The commonest is migraine without aura affecting80%-90% of sufferers, followed by migraine withaura affecting 10% - 20%. Migraine with aura can be further subdivided into basilar artery migraine,which causes double vision and speech slurring,hemi-plegic, dysphasic/dysmnesic and dysphoric.Migraine without aura generally lasts between 4and 72 hours. The headache should have two of thefollowing four features: --Unilateral-Throbbing-Moderate to severe intensity-Exacerbation by physical activityThere may be associated symptoms of photophobia, nausea and vomiting.Typical features of migraine with aura includethose for migraine without aura with at least threeof the following characteristics: --One or more fully reversible aura symptoms-Aura symptoms develop over more than four minutes-Aura lasts less than 60 minutes-Type of aura may change during attack -Headache follows within 60 minutes-Visual prodomata including teichopsia andscintillating scotoma

Dr Roger Cull and Dr Charlotte Feinmann

Various trigger factors for migraine have beenidentified and include:-Relief of stress-Hormonal changes-Physical exertion-Change of routine-Visual glare, vivid patterns-Weather and atmospheric pressure changes-Foods and alcoholic drinksThe differential diagnosis of migraine include:1.Tension type headache. These affect 70% - 80%of the population, have a variable duration withmild to moderate pain, often bilateral which istight, pressing or band-like. The headache isoften frontal, temporal or occipital, there isusually no nausea, vomiting or photophobia andit is often triggered by stress and relieved byrelaxing.2.Cervicogenic headache. These are less wellestablished than tension type headache. Theytend to occur daily, with occipital headacheassociated with neck pain that may radiate to thetemporal region. The headache is worse withcertain postures and there are limited and painfulneck movements.3.Cluster headache (Migrainous Neuralgia). Thisaffects men 5 – 8 times more commonly thanwomen. It is a rare disorder affectingapproximately 1 in 1000 people.Characteristically, there are clusters of one or more daily headaches over a period of severalweeks, followed by painfree periods. They arecommoner in smokers. They are characterised by severe retro-orbital pain, lasting 15 – 90minutes. Attacks are often nocturnal andassociated with epiphora, nasal congestion andHorner’s syndrome. In contrast to migrainesufferers, people with cluster headache tend towalk around and may be aggressive.4.Temporal arteritis. This condition should also beconsidered in older patients with a new headachewhether uni or bilateral. There may be associatedtenderness over the temporal region or in theoccipital area and there may be systemicsymptoms including malaise, weight loss, fever, polymyalgia and visual loss. If there is asuspicion of temporal arteritis, an ESR should be taken to confirm or exclude the diagnosis.5.Raised intra-cranial pressure headache. Thisheadache is characterised by diffuse pain that isworse on bending. Vomiting may occur (withoutnausea). There may be visual obscuration,seizures, focal neurological symptoms, optic discswelling and daily morning headache.6.Sub-arachnoid haemorrhage. This ischaracterised by sudden onset, blow-like painoften to the back of the head. It may radiate tothe neck and be associated with collapse,vomiting and neck stiffness. The latter sign may be absent early. Exertion is a trigger for sub-arachnoid haemorrhage and patients may havealteration in their conscious level withirritability, drowsiness and focal neurologicalsigns. Examination of the optic fundi may revealsub-hyaloid haemorrhages. Urgent CT scanningis indicated.7.Cranio-vertebral anomalies. There may becongenital anomalous development at the baseof the skull with descent of the inferior cerebellum. This is associated with cough-induced headache and cerebellar, brain stem and pyramidal signs. The diagnosis is confirmed byMRI scan. Treatment is surgical decompression.8.Benign occipital epilepsy. This normally presentsin childhood with idiopathic focal seizuresaccompanied by visual hallucinations that areoften described as being circular in shape andmulti-coloured. EEG demonstrates occipitalspike wave discharges and the condition respondswell to treatment with anti-convulsants.Dr Cull concluded by emphasising theimportance of taking a detailed history, thoroughlyexamining the patient and undertaking investigationsif the history is suspicious, clinical signs are presentor the headache cannot be categorised. He advisedextra caution when dealing with patients with a previous neoplasm and also older patients with a newheadache.Dr Charlotte Feinmann, Reader in Psychiatry,Behavioural Sciences and Dentistry, Eastman DentalInstitute and Royal Free and University CollegeMedical School, gave the second lecture. The subjectof the talk was “Oro-facial Pain”.associated with a suppression or mis-attribution of mood”.The basis of treatment is to consider thefunctional somatic symptoms together. A psychosocial approach with an empathic interviewer may help the patient to recognise the problem. Health beliefs can be explored and appropriate reassurancegiven although premature reassurance may not havethe desired effect. The aim of management is tochange the patient’s focus of attention.The pain team at the Eastman Dental Instituteincludes psychiatrists, psychologists, nursing practitioners, restorative specialists, neurologists andan anaesthetist. Treatments include the use of antidepressants, cognitive behavioural therapy,informed reassurance, hypnosis, relaxation and splinttherapy. Clinicians must take a full history in anattempt to make a diagnosis. Investigations and physical treatments, however, may make pain moredifficult to treat, can exacerbate anxiety anddepression and frustrate both patient and clinician.In conclusion, Dr Feinmann stressed theimportance of adequate assessment, informedreassurance, team management, antidepressants, theuse of cognitive behavioural therapy and hypnosis.There followed the usual high quality lunch inthe conservatory.Dr Feinmann started by giving an overview of the complexity of pain. Melzack and Wall were thefirst to describe pain as the result of afferent upstream processes within the spinal cord with downstreammodulation. We are aware that the brain can generate pain in the absence of input from peripheralnociceptors, for example in phantom limb pain. Sheemphasised the cognitive model of pain which takesinto account both physical and psychosocial aspectsand described the common problem of being able toexplain to a patient what is not wrong with them butnot what is wrong with them.She then reported the results of a series of studies. In 1985, Bridges and Goldberg, found thatone in five new consultations in primary care are for medically unexplainable symptoms. One third of these persist and cause distress and disability.In 2002, MacFarlane et al published a population based cross sectional survey of 2504 adults aged between 18 and 65 in the journal Pain. It reportedthat 23% of patients questioned described oro-facial pain, 6% described widespread pain only and 4%described both. There were high levels of psychosocial distress.Predictors of chronic facial pain are: -1.Widespread pain within the facial region.2.Widespread pain outside the facial region.3.Inactivity.An outpatient three year retrospective case notereview study published by Koenke and Mangelsdorf in 1989 reported an incidence of 30% in women and21% in men of facial pain. The highest incidencewas in the 18 – 25 age group and the lowest in the56 – 65 age group. Only 46% of people sought helpwith 17% taking time from work. Less than 2% of patients received an organic diagnosis.In patients with chronic temporo-mandibular joint pain, there is no relationship between earlysigns and symptoms and severity of physicalabnormalities in the joints. There is, however, astrong relationship with depression, anxiety andsomatisation. Often there will be a history of highlevels of health care use and of other chronically painful conditions.Simon and Von Korff in 1991 demonstrated that patients may misattribute normal bodily functions as pain. We are aware that experience of pain isinfluenced by childhood exposure to illness, possiblerecall of physical or sexual abuse, depression, anxietyand phobias.The definition of somatisation is: -“An amplification of normal bodily sensationsDr Mike Basler from Glasgow Royal Infirmarychaired the afternoon session. Dr Tom Brown,Consultant Liaison Psychiatrist based at the Westernand Gartnavel Hospitals in Glasgow started theafternoon. The title of his lecture was “Chronicfatigue syndrome and its management”.

Dr Andrea Harvey and Dr Charlotte Feinmann Drs Carlin Thomas, Tom McCubbinand Joanne Wood enjoy lunch

The lecture started with a very entertainingSimpson’s video which nicely demonstrated people’sfear of being thought to be “at it”. One of the problems of patient doctor interaction is that patients present to doctors with illness (behaviour) anddoctors diagnose and treat diseases. He discussedthe classification of chronic fatigue syndrome andits relationship to other disorders such as irritable bowel syndrome, atypical chest pain,hyperventilation syndrome, non-epileptic seizures.There is also a marked overlap between chronicfatigue syndrome and fibromyalgia.The prevalence of chronic fatigue symptom is0.4% to 2.6% of the general population. It is twiceas common in women than in men and is commonest between the ages of 20 and 40. It has been suggested

Dr Tom Brown, Consultant Liaison Psychiatrist, Glasgow

that disturbance of the hypothalamic pituitary axiswith associated low levels of cortisol and enhancedserotonin function is important in its pathophysiology. This is in contrast to depressionwhere there is reduced serotonin function.Effective interventions in chronic fatiguesyndrome can be categorised into behavioural,immunological, antiviral, pharmacological anddietary.Of four randomised control trials of cognitive behavioural therapy, benefit was shown in three.There was improvement in fatigue, physicalfunctioning and global measures of well-being.There were no differences in depression. A five-year follow up in one study demonstrated thatimprovement was generally maintained.Other treatments used include graded exercise programmes, immunological therapies such as IgGand drug treatments such as Interferon, Acyclovir and Gamcyclovir. There is no evidence for the beneficial effect of antidepressants or steroids.Lisa Manchanda, Specialist Registrar inAnaesthesia at the Western Infirmary, Glasgow, gavethe next talk. She presented her winning entry tothe North British Pain Association EssayCompetition, Spring 2002.Below is a transcript of her winning essay.

The North British Pain AssociationEssay Competition Spring 2002

Is Surgery The Answer?

Dr Lisa Manchanda SpR,Western Infirmary, GlasgowIntroduction

During an evening of pre-assessments, I noticedan unusual entry on the normally routine renalsurgery list. As I was unfamiliar with the procedure – a renal auto-transplantation – I discussed the casewith the attending surgeon.The patient was a young female who had sufferedchronic loin pain for over ten years. She was toundergo this surgical procedure in an attempt toalleviate her pain, which mainly affected the left side but was occasionally bilateral. She also experiencedspontaneous exacerbations of severe pain and nothingwould alleviate her symptoms. The pain greatlyaffected her daily activities and as a result she hadsuffered psychological distress. After years of extensive negative investigations she was finallydiagnosed as having loin pain haematuria syndrome(LPHS).renal capsule and cortex follow the same pathwayand most fibres terminate in the sympathetic systemwith some following the vagus nerve.Visceral renal pain may be experienced as achingand non-specific in the area of the costovertebralangle and may be due to inflammation of the kidneysor acute ischaemia due to thrombus in the renalvasculature. Patients without this pathology may alsoexperience a similar type of pain and may in fact haveloin pain haematuria syndrome.

Loin Pain Haematuria Syndrome

Loin pain haematuria syndrome (LPHS) was firstdescribed by

Little et al

in 1967. Patients often present with recurrent episodes of loin pain(unilateral or bilateral) and some degree of microscopic or gross haematuria, which may beintermittent. The onset of pain may precede the presence of haematuria. The pain is often severe anddebilitating and may radiate to the abdomen, thighor groin. Although the majority of patients withLPHS are female and present between the ages of twenty and forty, it can also occur in children.LPHS is rare and unfortunately the syndromeremains a diagnosis of exclusion reached whenurological investigations do not reveal adequate pathology to account for the symptoms. As a result, patients should be assessed by a renal physician withexperience of LPHS and should have adequateinvestigations including an ultrasound, intravenous pyelogram, cystoscopy and renal isotopescintigraphy. Ureteroscopy, angiography and renal biopsy should also be considered.Abnormalities detected following a renal biopsyhave included mesangial proliferation and immunecomplementation C3 deposition in the arterioles. Oneseries showed that nearly 50% of patients had thinglomerular basement membrane disease. Changes inintrarenal arterioles, the presence of cortical infarctsand the occurrence of microaneursyms have beendetected on renal angiography. Decreased heparin-thrombin clotting time and elevated plasma serotoninconcentration suggests evidence of a platelet or coagulation disorder.These abnormalities provide evidence thatsuggests the presence of a vascular disorder.However, surprisingly, these patients do not go onto develop impaired renal function. Serum creatinineand renal concentrating ability remain normal.

Psychological Factors

In the original description of LPHS, some patients were described as anxious, demanding of medical attention, and inclined to fabricate medicalevidence. Furthermore,

Lucas et al

proposed asrecently as 1995 that LPHS was a psychogenic painand a form of somatisation. This idea has further perpetuated the belief that the syndrome had a primary psychological aetiology.In contrast,

Bultitude et al

published a study in

Pain

in 1998, showing that psychological disabilityimproves as the pain symptoms improve. Theyassessed 26 patients before and after a recognisedtreatment option and found that the psychologicaldistress is secondary to the pain and the disability itcauses.

Pain Management

Patients diagnosed with LPHS are often verychallenging to manage. They commonly experiencesevere pain requiring high dose opioid medication.On review of our Pain Management Clinic database,it was found that the management of patients, who presented with similar symptoms, included treatmentwith opioid analgesics, tricyclic antidepressants,TENS application and local anaesthetic nerve blocks.The success of treatment was usually of a limitedduration and varied across the patient population.Regional techniques used for the treatment of LPHS include intercostal, interpleural, paravertebraland epidural local anaesthetic nerve blocks. Lumbar sympathetic and splanchnic nerve blocks have also been described in case literature. Implant able devicesreleasing intrathecal opioids have also been used.In 1995 Bultitude first described the use of acapsaicin solution for the treatment of LPHS. Itinvolved ureteric catheterization with instillation of a capsaicin solution into the renal calyx and ureter, performed under general anaesthesia and required prolonged epidural anaesthesia. In humans the nervesupply to the renal pelvis and ureter is proportionallyrich in C fibres. Capsaicin is said to cause intensestimulation of these nerves with release andsubsequent depletion of substance P from thenociceptors of the urothelium. It has been reportedto give 65% of patients short to medium term painrelief. However questions have been raised over thesafety of its use. In one study two patients developeddeterioration in their renal function followingcapsaicin treatment. Capsaicin could not be excludedfrom contributing to this complication. Another patient suffered mucosal ulceration in the bladder after extravasation of the solution.

Surgical interventions

Surgery is rarely appropriate for the managementof chronic pain conditions. It can worsen the patient’ssymptoms and cause further chronic postoperative pain. However, surgical techniques have now beendeveloped for the treatment of LPHS and are aimedat denervating the kidney. They include renal nerveexcision, surgical sympathectomy, removal of therenal capsule, nephrectomy and renal auto-transplantation. Renal nerve excision has providedtemporary pain relief, however case studies report ahigher incidence of pain recurrence compared to autotransplantation. In an extreme example of asuccessful outcome, a patient was able to return toemployment following a bilateral nephrectomydespite the need for dialysis.Renal auto transplantation surgery was firstdescribed by

Aber and Higgins

in 1982 and isextremely rare is this country. It is performed as aform of nephron-sparing denervation therapy. This procedure involves removing the affected kidneyfrom the loin and retransplanting it in the iliac fossa.Most of the available literature on renal autotransplantations is from small case studies. In 1998

Chin et al

looked at the results of 26 patients whohad undergone renal auto transplantation for LPHS.The mean follow-up time was 7 years withapproximately 70% of patients having sustained painrelief and returning to normal activities. The procedure however carries the significant risks of major renal surgery including graft failure and acuterenal failure. Other complications includerecurrence of the pain in the graft site and areassumed to be due to renal reinnervation. Thistheory is probably too simplistic to explain therecurrence of pain. The procedure may be carried out bilaterally as new pain can develop on thecontralateral side years later.The risks of performing surgery as an isolatedtreatment option for chronic pain are huge and mayactually worsen the patient’s symptoms and function.This approach perpetuates a patient’s belief that thedoctor will alleviate chronic pain rather than assistthe patient in managing their symptoms in order toimprove their functions of daily living. It is thereforecritical to meticulously screen surgical candidatesincluding a full psychological assessment. Ignoringthe multifactorial biopsychosocial model of any patient with chronic pain will decrease the chancesof successful management.Giving the varying long-term success together with the risks and complications, the decision to perform surgery is often taken at a late stage intreatment and may be the last resort.

Case History

Following diagnosis, the patient described in the beginning, was managed with oral opioid analgesiawith little improvement in her symptoms. She wasreferred to the Pain Management Team who treatedher with tricyclic antidepressant medication as anadjunct to her opioid medication. This unfortunatelyhad no effect on her symptoms. Other managementincluded a trial of transcutaneous electrical nervestimulation, which had a beneficial effect for alimited duration only. Over the years she hadnumerous paravertebral nerve blocks with varyingdegrees of success.

Renal Pain

Pain due to a renal aetiology is often elusive anddifficult to explain. This is partly due to the complexinnervation of the renal system. The kidney isinnervated by the renal plexus that is situated behindthe origin of each renal artery at the level of T12 toL2. There is an autonomic contribution from thecoeliac ganglia, aorticorenal ganglion, the aortic plexus and the first lumbar splanchnic nerve. Thesefibres follow the renal artery into the kidney hilussupplying the vessels, glomerular structures andtubules. Afferent fibres arising in the region of the

Lisa Manchanda, Sarah Morrisand Kenneth Pollock