Evidence map›Paper›PMID 39387948›Full record

ArticleJournal of neurology2024

Apraxia phenotypes and frontotemporal lobar degeneration.

Tobias C Langheinrich, Jennifer C Thompson, Matthew Jones, Anna M T Richardson, David M A Mann, Julie S Snowden

Abstract read
In one paragraph

Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Tobias C LangheinrichCerebral Function Unit, Manchester Centre for Clinical Neurosciences, Northern Care AllianceNHS Foundation Trust, Salford, UK. tobias.langheinrich@nca.nhs.uk.ORCID http://orcid.org/0000-0002-4714-8657
Jennifer C ThompsonCerebral Function Unit, Manchester Centre for Clinical Neurosciences, Northern Care AllianceNHS Foundation Trust, Salford, UK.ORCID http://orcid.org/0000-0002-7512-7570
Matthew JonesCerebral Function Unit, Manchester Centre for Clinical Neurosciences, Northern Care AllianceNHS Foundation Trust, Salford, UK.
Anna M T RichardsonCerebral Function Unit, Manchester Centre for Clinical Neurosciences, Northern Care AllianceNHS Foundation Trust, Salford, UK.ORCID http://orcid.org/0000-0001-9848-7571
David M A MannDivision of Neuroscience, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK.
Julie S SnowdenCerebral Function Unit, Manchester Centre for Clinical Neurosciences, Northern Care AllianceNHS Foundation Trust, Salford, UK.ORCID http://orcid.org/0000-0002-3976-4310

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApraxia has been identified in all clinical forms of frontotemporal lobar degeneration (FTLD). The characteristics of apraxia symptoms and their underlying cognitive/motor basis are not fully understood. This study investigated apraxia in pathological subtypes of FTLD.

methodsThe study constituted a retrospective review of 115 pathologically confirmed cases of FTLD from a single cognitive neurology centre. Patients in whom apraxia had been documented as a notable clinical characteristic were identified. Apraxia features, demographic, cognitive, neurological, and imaging findings were recorded.

resultsEighteen patients were identified: 12 with FTLD-tau pathology (7 corticobasal degeneration (CBD), four Pick type and one progressive supranuclear palsy (PSP)) and six with FTLD-TDP pathology, all type A and four linked to progranulin gene mutations. Apraxia as a dominant presenting feature was typically associated with tau pathologies, whereas it emerged in the context of aphasia in TDP pathology. Apraxia typically predominated in one body part (face or limb) in tau but not TDP pathology. Relatively preserved activities in daily life were associated with TDP. Apraxia of speech was associated with tau pathology. Pick-type pathology was linked to symmetrical atrophy and late development of limb rigidity.

conclusionApraxia in FTLD subtypes has variable characteristics. Apraxia associated with CBD pathology conformed to criteria for probable corticobasal syndrome (CBS), whereas apraxia with Pick-type pathology did not. Apraxia in patients with TDP-A pathology was interpreted as one manifestation of their generalised communication disorder. Apraxia in FTLD may have distinct cognitive and motor substrates that require prospective investigation.

Indexed as

ApraxiasFrontotemporal Lobar DegenerationPhenotypeAgedAged, 80 and overBrainDNA-Binding ProteinsFemaleHumansMaleMiddle AgedProgranulinsRetrospective Studiestau ProteinsDNA-Binding ProteinsProgranulinstau ProteinsApraxiaCorticobasal syndromeProgranulinProgressive aphasiaTau pathologyTDP pathology

Identifiers

PMID39387948
PMCPMC11588949

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.