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and a simple spatial-attention task,the researchers measured the brainactivity from the acute stroke phase to9 months after stroke.

Patients with lesions localised in theright frontal lobe had altered brainactivity in several nodes in the dorsal,ventral parietal, frontal networkinvolved in attention. In the acutephase there was hyperactivity in thecontralateral hemisphere and reducedactivity in the attention network in thelesioned hemisphere, over time,unusual patterns of activity becameless prominent. These changes incortical activity coincided withfunctional recovery. In anaccompanying commentary, YalçinAbdullaev and Michael I Posner write“the most striking change was that thedorsal right parietal lobe, which wasnot activated at all during the acutephase, was now strongly activated in

the chronic phase” (Nat Neurosci 2005;8: 1424–25).

“We show that spatial attentiondeficits and their recovery do notdepend just on the structural damagein the stroke area, but on thefunctional effects of this lesion on theactivity pattern in distant areas”,Corbetta told The Lancet Neurology.

Declining activity in the contralateralhemisphere from the acute to thechronic phase and the concomitantdecrease in neglect seems to dependlargely on recovery in a right parietalarea. This asymmetrical dominance ofattention helps to explain why left-sided neglect is more common thanright-sided neglect.

Corbetta says that their findingsraise several question about howlesions in different brain regions affectneglect, whether hyperactivity in theintact hemisphere is associated with

degree of neglect, and whethersuppression of activity withtranscranial magnetic stimulationmight aid functional recovery.

Peter Hayward

http://neurology.thelancet.com Vol 4 December 2005 801

Mutations that cause structuraldamage to a protein encoded onchromosome 13, or that reduce theproduction of the functional version,could be partly responsible forTourette’s syndrome (Science 2005;310: 317–20).

People with Tourette’s syndromehave motor tics and involuntaryvocalisations, usually accompanied byother problems ranging fromobsessive-compulsive disorder toimpulse control difficulties. Althoughthe disorder has a genetic component,researchers have been unable topinpoint the genes involved.

“Knowing where to draw the linebetween Tourette’s syndrome andrelated disorders, like obsessivecompulsive disorder, can be difficult”,explains study leader Matthew State(Yale University, New Haven, CT,USA). “This, plus the likelycontribution of many genes,gene–environment interactions, andother confounding factors havehindered gene mapping through

genetic linkage or associationstudies.”

In an alternative approach, State’steam genetically screened a child withTourette’s syndrome whose familyhad no history of the disorder, andidentified an inversion onchromosome 13. “We reasoned thatthis patient’s problems might becaused by disruption of gene structureor function at the breakage point”,explains State.

Indeed, the researchers identifiedthe gene SLITRK1 in the breakageregion, the product of which isnormally expressed in large quantitiesin areas of the brain thought to beaffected in Tourette’s syndrome,although the coding region was notdamaged. However, when theresearchers looked at another 174people with the disorder they foundone with a clear mutation in thisarea—a frameshift rendering theSLITRK1 product useless—and twoothers with a mutation just outsidethe coding region in an area regulating

the production of the functionalprotein. This latter mutation affectedthe binding of a microRNA, inhibitingthe final synthesis of SLITRK1.

“In further experiments we saw thatSLITRK1’s protein was involved indendrite growth”, explains State, “andthat cells [with mutations] producedless of it. So, any mutation reducingprotein formation would potentiallypromote Tourette’s syndrome in somepeople.”

“Although this gene abnormalityaccounts for only a small percentageof patients with Tourette’s syndrome,this finding is certainly a move in theright direction”, remarked JosephJankovic (Baylor College of Medicine,Houston, TX, USA). “But this disorderalmost certainly has a polygenicaetiology. Working out which genesaffect which people [with whichphenotype], and how to transfer thisknowledge into clinical advances willbe a long process.”

Adrian Burton

SLITRK1 trouble in Tourette’s syndrome

Dorsal parietal regions direct attention to imagesthat we expect to impress

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