Feel­ing LAZY? It may be a sign of heart dis­ease — or worse

Daily Mail - - Good Health - By ROGER DOBSON

FROM let­ting dirty dishes pile up to feel­ing list­less about a task at work, al­most ev­ery­one lacks en­thu­si­asm and mo­ti­va­tion now and then. But could longer-term ap­a­thy — a numb­ing loss of en­thu­si­asm, emo­tion and drive — be a di­ag­nos­able health prob­lem?

Tra­di­tion­ally, ap­a­thy has been seen as a sign of de­pres­sion (and, iron­i­cally, can be a side-ef­fect of some an­tide­pres­sants). But sci­en­tists be­lieve it could also be a key sign of dozens of other con­di­tions, in­clud­ing stroke and heart dis­ease.

They are also start­ing to get to the root of what causes ex­treme ap­a­thy in oth­er­wise healthy peo­ple.

‘Many pa­tients with ap­a­thy are wrongly la­belled as just lazy. They are also mis­di­ag­nosed as hav­ing de­pres­sion,’ says Pro­fes­sor Ma­sud Hu­sain, a neu­rol­o­gist at Ox­ford Univer­sity. ‘But while they may sit around all day do­ing very lit­tle, they can be happy, un­like peo­ple with de­pres­sion.

‘It can be found in mild forms in healthy peo­ple. What seem a com­mon fea­ture are changes in cer­tain ar­eas of the brain.’

Last month, neu­rol­o­gists from the Royal Free Hos­pi­tal in Lon­don re­ported that ‘ap­a­thy is an un­der-recog­nised and un­der­es­ti­mated prob­lem in peo­ple with chronic neu­ro­log­i­cal disor­ders [eg, Parkin­son’s].’

De­spite be­ing com­mon and dis­abling, ap­a­thy was a prob­lem that nei­ther pa­tients nor their car­ers tended to raise with their doc­tors, wrote re­searchers in the jour­nal Prac­ti­cal Neu­rol­ogy.

They added that it’s im­por­tant to dis­tin­guish ap­a­thy from de­pres­sion be­cause it re­quires dif­fer­ent treat­ment, such as drugs other than an­tide­pres­sants.

The neu­rol­o­gists de­fined ap­a­thy as re­duced emo­tion (pos­i­tive and neg­a­tive), a lack of con­cern about symp­toms, lack of mo­ti­va­tion and emo­tional empti­ness.

By COM­PAR­I­SON, they de­fined the key clues to de­pres­sion as be­ing sad, tear­ful or guilty, a sense of hope­less­ness about the fu­ture, vari­a­tions in mood and so-called neg­a­tive cog­ni­tive bias — in other words, see­ing the worst side of ev­ery­thing.

The Royal Free re­searchers also noted that, un­like those with de­pres­sion, peo­ple with ap­a­thy can oc­ca­sion­ally be happy.

It is not the only re­search to sug­gest ap­a­thy is more than just part of de­pres­sion. A 2009 study in the U.S. found that ap­a­thy was a symp­tom in 33 con­di­tions.

It af­fected 29 per cent of older peo­ple with heart dis­ease, up to 31 per cent of MS pa­tients and 45 per cent of Parkin­son’s pa­tients.

It was also found in those with Lyme dis­ease, chronic fa­tigue syn­drome, testos­terone de­fi­ciency and vi­ta­min B12 de­fi­ciency.

The ex­act cause of ap­a­thy in these con­di­tions is un­clear, but the ev­i­dence points to changes in ar­eas of the brain as­so­ci­ated with re­ward — namely the pre­frontal cor­tex (at the front of the brain) and the basal gan­glia (a tiny area at the base of the brain).

For in­stance, re­search sug­gests that older peo­ple with heart dis­ease may be af­fected by ap­a­thy be­cause of re­duced blood sup­ply to these ar­eas of the brain be­cause their ar­ter­ies are nar­rowed.

The role of the pre­frontal cor­tex in ap­a­thy was iden­ti­fied by an Ox­ford Univer­sity study pub­lished last month, which ex­am­ined brain scans of healthy peo­ple.

It’s known that nearly all pa­tients with fron­totem­po­ral de­men­tia, which af­fects 16,000 peo­ple in Bri­tain, suf­fer with ap­a­thy.

This form of de­men­tia, char­ac­terised by per­son­al­ity changes, af­fects the frontal lobes of the brain, which are in­volved in lan­guage and con­trol­ling be­hav­iour and emo­tion.

The Ox­ford re­search, led by Pro­fes­sor Hu­sain, found more ac­tiv­ity in the frontal part of the brains of ap­a­thetic peo­ple.

For the study, 40 healthy vol­un­teers car­ried out psy­cho­log­i­cal tests while un­der­go­ing MRI scans. Those with ap­a­thetic traits had more ac­tiv­ity in an area of the frontal lobes known as the pre­mo­tor cor­tex, which is in­volved in con­trol­ling move­ment and so mak­ing us phys­i­cally take ac­tion.

‘We ex­pected to see less ac­tiv­ity, but we found the op­po­site,’ says Pro­fes­sor Hu­sain. ‘We thought this might be be­cause their brain struc­ture is less ef­fi­cient, so it’s more of an ef­fort for ap­a­thetic peo­ple to turn de­ci­sions into ac­tions.

‘As far as we know, this is the first time any­one has found a bi­o­log­i­cal ba­sis for ap­a­thy in healthy peo­ple.

‘It doesn’t ac­count for ap­a­thy in ev­ery­one, but by giv­ing us more in­for­ma­tion about the brain pro­cesses un­der­ly­ing nor­mal mo­ti­va­tion, it helps us un­der­stand bet­ter how we might find a treat­ment for ex­treme ap­a­thy.’

One pos­si­ble treat­ment is with drugs that act on a key brain chem­i­cal, dopamine.

Dopamine is what makes us feel good when we do things that are ben­e­fi­cial to us — for in­stance, eating. When we eat some­thing we like, nerve cells re­lease dopamine, which makes us feel good.

One sug­ges­tion is that when key ar­eas of the brain in­volved in the re­ward sys­tem are dam­aged by dis­ease, dopamine lev­els are af­fected. ‘Sev­eral lines of ev­i­dence sug­gest that ap­a­thy may be in part due to a dopamine ab­nor­mal­ity,’ said a 2007 report in Cur­rent Treat­ment Op­tions in Neu­rol­ogy.

In other re­search led by Pro­fes­sor Hu­sain, one pa­tient with ap­a­thy — re­sult­ing from a stroke that had dam­aged his basal gan­glia — was given a drug that mim­ics dopamine.

Be­fore his stroke, he had been out­go­ing and con­fi­dent, but he had since be­come ret­i­cent and un­mo­ti­vated, fail­ing to com­plete tasks even when a re­ward was of­fered. Af­ter the dopamine treat­ment, he went out more, found a job and be­came more so­cia­ble.

‘It took about three months to see the ef­fects, but they re­ally were pro­found,’ says Pro­fes­sor Hu­sain. ‘ The treat­ment trans­formed the pa­tient’s life.

‘The find­ings high­light a bi­o­log­i­cal ex­pla­na­tion for lack of mo­ti­va­tion and show that in prin­ci­ple this can be treated with drugs, at least in some pa­tients.’

Dr Adam Perkins, a lec­turer in the neu­ro­bi­ol­ogy of per­son­al­ity at King’s Col­lege Lon­don, says stress can also cause ap­a­thy. ‘Ap­a­thy is tricky to ex­plain be­cause, like a cough, it can be an out­ward symp­tom that could re­sult from a va­ri­ety of dif­fer­ent un­der­ly­ing causes,’ he says.

He agrees that some cases re­sult from dam­age to the pre­frontal cor­tex, but claims: ‘Far more com­mon is where stress causes burnout-re­lated ap­a­thy.

‘This is most com­mon in PTSD (post-trau­matic stress disor­der), which of­ten re­sults in a loss of en­joy­ment and numb­ness.’

He says: ‘Changes that cause PTSD- re­lated ap­a­thy are likely to be rooted in al­ter­ations in the hy­po­thal­a­mus [ a tiny con­trol cen­tre in the brain that man­ages hunger, body tem­per­a­ture and our sleep cy­cles] that oc­cur af­ter a long time dur­ing which stress hor­mones cir­cu­late in the blood.’

Dr Perkins sug­gests that peo­ple who score highly in per­son­al­ity tests for neu­roti­cism — and so may nor­mally be highly mo­ti­vated — could be es­pe­cially at risk of this kind of ap­a­thy be­cause of their high stress hor­mone lev­els.

‘This is be­cause they have a mag­ni­fied per­cep­tion of threat and so are prone to ex­pe­ri­enc­ing large and per­sis­tent stress re­sponses at lower lev­els of threat than an av­er­age per­son.

‘Se­vere and per­sis­tent ap­a­thy aris­ing from con­di­tions such as PTSD shouldn’t be con­fused with day-to-day fluc­tu­a­tions in en­ergy lev­els that most of us ex­pe­ri­ence, which are nor­mal and don’t need any treat­ment.’

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