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Mamp pro serial 4 free.Primary progressive aphasia: a clinical approach



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Symptoms such as absent or misplaced empathy, social disinhibition and faux pas, a more fatuous sense of humour and pathological sweet tooth are common in both svPPA and behavioural variant frontotemporal dementia [ 29 , 53 — 57 ].

An impoverished concept of self due to diminished awareness of bodily signals may contribute to reduced empathy and an increased rate of suicidality in svPPA relative to other neurodegenerative syndromes [ 61 , 62 ].

Insight and awareness of deficits often appear to be retained, but may be superficial or incomplete. In contrast to nfvPPA, associated neurological signs are not typically found in svPPA, though parkinsonian or motor neuron features may develop later in the course [ 31 , 63 ]. Completing the picture of a highly coherent clinical, anatomical and pathological syndrome, most cases of svPPA have TDP type C pathology at post-mortem [ 12 , 33 , 35 ].

Most cases are sporadic though occasional pathogenic mutations are reported [ 4 ] and may be relatively more likely if motor features are present e. The most recently described of the major PPA syndromes is in more than one sense the most problematic. Interrupted sentences that tend to trail off may give the impression of agrammatism though without the frank syntactic dislocations of nfvPPA [ 18 ].

Speech sound or spelling errors are frequently described. The patient may struggle to understand more complex sentences and to hold verbal information in mind. While language is by definition the leading and dominant issue, there is frequently a history of associated extra-linguistic difficulties extending to the realms of memory e. Generally, phonological speech sound errors can be detected, usually taking the form of syllable misselections that are enunciated clearly and not accompanied by the false starts and distortions that characterise nfvPPA.

Reading aloud is similarly marred by syllabic substitutions, highlighted by sounding out non-words e. Analogous errors of written spelling are often evident Table 3.

The diagnostic feature of lvPPA that distinguishes it from other PPA syndromes is early and disproportionate difficulty repeating heard phrases and sentences versus single words [ 67 ] see Table 2. This signifies an impairment of verbal phonological working memory, also indexed as a reduced auditory span for repetition of random digit strings [ 16 ].

While digit span is often also reduced in nfvPPA, in that syndrome repetition of single words and repetition of phrases are comparably degraded. Other dominant and often, bi-hemispheric posterior cortical signs such as limb apraxia and visual apperceptive agnosia can frequently be elicited in lvPPA.

This extra-linguistic cognitive phenotype tends to be more extensive and severe than in other PPA syndromes at a comparable stage of clinical evolution see Fig. The key neuroimaging association is asymmetric atrophy mainly involving the temporo-parietal junction zone of the dominant hemisphere, appearing as widening of the posterior left Sylvian fissure on a T1-weighted coronal MRI scan [ 68 ] Fig.

This locus potentially accounts for many features of the language phenotype, since posterior superior temporal and inferior parietal cortices are intimately involved in decoding speech sounds and activating phonological representations to link verbal semantic stores to language output [ 10 , 16 , 69 ]. However, there is often extension of atrophy more anteriorly with involvement of other structures notably the hippocampi and the overall extent and pattern of atrophy varies widely between individual patients.

A number of patients with lvPPA exhibit generalised anxiety, irritability and increased clinging emotionally and physically to their primary caregivers [ 29 , 70 , 71 ]. Neurological signs are usually sparse [ 32 ], but include myoclonus, which may be peri-oral. Some patients go on to develop a corticobasal syndrome [ 71 ]. On the other hand, cases of lvPPA lacking Alzheimer markers are consistently represented across series; the pathological substrates have not been clarified, but these may point to separable clinico-anatomical sub-syndromes [ 16 , 68 , 71 — 73 ].

Although lvPPA is generally a sporadic disorder, some caution is called for in cases without Alzheimer markers, since pathogenic progranulin gene mutations have been reported in this subgroup [ 11 , 68 ]. Accurate and early identification of PPA syndromes is essential for clinical counselling and planning appropriate management.

Beyond clinical characterisation, molecular stratification will become increasingly important with trials of candidate disease-modifying treatments on the horizon [ 35 ]. Some of these less common, atypical variants are in Table 1. In Fig. Structural brain imaging ideally, MRI is essential in all cases of suspected PPA, both to rule out other causes of progressive language failure and more positively, to identify features of particular radiological phenotypes Fig.

Where initial MRI features are borderline notably in nfvPPA and lvPPA it may be helpful to repeat the scan after an interval of a year or so, as directly comparing serial studies of the culprit brain region is often revealing. Functional MRI and FDG-PET in PPA are not in routine clinical use though there is considerable potential interest in applying such techniques to define aberrant and compensatory language network changes, with a view to future therapeutic trials [ 74 , 75 ].

Having arrived at a syndromic diagnosis, it may be appropriate to investigate further to determine the underlying proteinopathy—including CSF examination or amyloid-PET scanning for Alzheimer neurodegeneration markers. These ancillary investigations may be relevant, for example, in deciding to trial a cholinesterase inhibitor in a patient with nfvPPA or more generally, in forecasting the overall outlook of the illness in earlier stage disease.

We discuss the possibility of genetic risk in all younger patients with nfvPPA and genetic screening should be considered in any patient with PPA who has a relevant family history, particularly where there this raises suspicion of a frontotemporal dementia. Discussions in clinic around genetic testing broach a number of sensitive issues and should ideally involve other family members.

All PPA syndromes tend ultimately to give rise to global language failure with mutism or sparse, stereotyped utterances [ 76 ] as well as more widespread cognitive decline. Accordingly, diagnosis later in the course may be more informed by associated neurological features such as Parkinsonism. A related issue concerns the diagnostic relevance of visualised abnormalities; PPA syndromes can be caused by unusual pathologies for example, primary leukodystrophies and prion disease , but most meningiomas and arachnoid cysts will be incidental.

Cerebrovascular changes of small vessel ischaemia are commonly found in older patients but seldom if ever cause a canonical PPA syndrome though word-finding difficulty commonly accompanies vascular cognitive impairment. Accurate diagnosis is worthwhile, given the quite different management issues that these groups present. Interpretation of apparent language deficits should be cautious in older patients with a history of developmental dyslexia or longstanding peripheral hearing loss, especially when the recent symptoms target phonology or articulation and if additional cognitive involvement is subtle.

Often a period of follow-up will establish the nature of the deficit. Performance on language tests should always be calibrated for premorbid literacy skills in the test language. Word-finding difficulty is a very common complaint in patients attending memory clinics [ 10 ]. Many will be experiencing the effects of normal ageing and intercurrent stressors; they typically describe inefficiency in recalling names or clearly expressing their thoughts when preoccupied or fatigued and have no evidence of language deficits on objective testing.

Our patients with nfvPPA and occasional cases of primary progressive dysprosodia have exhibited degraded native accents or loss of a previously competent second language accent, rather than developing a facsimile foreign accent. An expert second opinion may be useful and the passage of time and lack of clinical and radiological evolution often clarifies the situation. Patients with PPA generally live for a number of years following diagnosis, with evolving deficits and specific needs at each stage of the illness.

Widely accepted clinical staging markers are presently lacking, however, the major PPA syndromes collectively raise similar management challenges and these broadly require the integration of non-pharmacological and pharmacological approaches.

Management begins with diagnosis; this is often delayed due to the lack of experience with these conditions in the wider medical community and the value of a clear explanation for patients and families should never be underestimated. Diagnosis supports future planning including discussions around end-of-life care and mobilisation of appropriate social services. Supportive care is still the mainspring of management for all PPA syndromes. Patients and caregivers need clear advice about driving safety, work arrangements, safeguarding and finances particularly in younger patients who may have dependent children or elderly relatives.

Patients should also be monitored for the emergence of other motor and neurological features that impact on mobility and activities of daily life. Early detection of physical deficits is key because these tend to herald a step change in functional status and care requirements. Support and respite for caregivers are often overlooked, but vital to maintaining patients in the community.

Speech and language therapy in PPA has an important role in providing communication aids and strategies. Even simple measures such as picture books and cards listing frequent and important words and phrases that the patient can carry may be of great practical value particularly in nfvPPA. More structured therapy aims to provide person-centred and goal directed interventions to alleviate impairment e. These can in principle be tailored to the particular PPA syndrome: for example, word-relearning techniques might focus on object features use, location, appearance in patients with svPPA or phonology rhyming, first and last sound identification in lvPPA [ 84 ], while orthographic cues to word production can be targeted in nfvPPA [ 85 ].

In practice, however, combined approaches have often been used [ 84 ]. Communication skills training is informed by experience in stroke aphasia and aims to enhance strategies that facilitate communication e. Augmentative and alternative communication devices may help patients with nfvPPA and limited verbal output, but preserved comprehension [ 86 ].

Adapting everyday technology such as smartphones and total communication strategies incorporating photos and pictures may enable continuation of daily activities such as shopping or cooking [ 87 , 88 ]. Unfortunately, gains from non-pharmacological therapies are usually modest and there is little evidence for generalisation of effects or lasting benefit in daily life [ 83 , 84 ].

It is important that new approaches continue to be developed and are assessed in adequately powered and controlled studies, with a view to a future where cognitive rehabilitation may be deployed in conjunction with disease modifying pharmacotherapy. There are currently no disease modifying treatments for PPA and evidence for efficacy of symptomatic treatments is scant.

Selective serotonin reuptake inhibitors should be considered in patients with comorbid depression or anxiety and may help to settle behavioural symptoms such as impulsivity and aggression, particularly in svPPA [ 92 ].

Newer generation neuroleptics may be indicated to manage severe agitation or psychotic symptoms later in the illness. Recognition of the major PPA syndromes has transformed our understanding of the language system and given us a new picture of selective neural vulnerability in degenerative brain disease.

However, this dramatic progress should not obscure the many remaining difficulties surrounding these conditions. Ultimately, effective treatment of PPA will depend on both earlier and more accurate diagnosis improved syndrome characterisation , more accurate disease and disability staging and identification of new biomarkers that can target tissue pathology and track therapeutic effects dynamically, in advance of irrecoverable brain atrophy improved signalling of underlying proteinopathy [ 93 ].

A successful PPA biomarker will need to encompass substantial individual variation within syndromic categories see, e. Emerging evidence suggests that generic disorders of nonverbal auditory information processing may underpin the canonical PPA syndromes [ 40 , 94 — 96 ] and that these syndromes may further be stratified by profiles of autonomic reactivity to emotional and other salient stimuli [ 61 , 97 , 98 ].

This evidence dovetails with the recent finding that implicit auditory sequence learning is retained in nfvPPA [ 99 ]. Such observations could motivate novel biomarkers and treatment strategies that do not depend on specific language capacities a practical advantage in mounting large-scale, international trials in PPA.

There is currently considerable interest in the application of molecular ligand neuroimaging techniques including new tracers that can demonstrate tissue deposition of pathogenic proteins other than beta-amyloid in PPA and other dementias [ ]. Such techniques promise to delineate proteinopathies in vivo more reliably than is currently feasible; multivariate approaches combining ligand imaging with pathophysiological indices may constitute a powerful and dynamic signal of the underlying disease.

The authors thank Dr Thomas Cope, Prof. Chris Butler and Prof. Tim Griffiths for helpful discussion. Charles R. Marshall and Chris J. Hardy contributed equally to the work. Electronic supplementary material. Marshall, Phone: 44 , Email: ku. Jason D. Warren, Phone: 44 , Email: ku. Journal of Neurology. J Neurol. Published online Feb 1. Marshall , 1 Chris J. Hardy , 1 Anna Volkmer , 2 Lucy L. Russell , 1 Rebecca L.

Bond , 1 Phillip D. Fletcher , 1 Camilla N. Clark , 1 Catherine J. Mummery , 1 Jonathan M. Schott , 1 Martin N. Rossor , 1 Nick C. Fox , 1 Sebastian J. Crutch , 1 Jonathan D. Rohrer , 1 and Jason D.

Warren 1. Chris J. Lucy L. Rebecca L. Phillip D. Camilla N. Catherine J. Jonathan M. Martin N. Nick C. Sebastian J. Jonathan D. Author information Article notes Copyright and License information Disclaimer. Corresponding author. This article has been cited by other articles in PMC. Supplementary material 2 MP3 kb. Supplementary material 3 MP3 kb. Supplementary material 4 MP3 kb.

Supplementary material 5 DOCX 14 kb. Electronic supplementary material The online version of this article Introduction The primary progressive aphasias PPA are a diverse group of disorders that collectively present with relatively focal degeneration of the brain systems that govern language. Table 1 Summary of key language features and cognitive, neurological, neuroanatomical and neuropathological associations in syndromes of primary progressive aphasia.

Open in a separate window. Table 2 A framework for assessment of language functions, directed particularly to progressive aphasias. Communication task Cognitive process Key history Clinical test Neuropsychological test SYND Message production Idea Generating verbal idea Reduced initiation of conversation a Describe a recent vacation; generating words by initial letter e.

Edmunds h Dabul Apraxia battery for adults. Second, Pro-Ed: Austin i Kay et al. Table 3 Examples of spoken and written language output in patients with canonical syndromes of primary progressive aphasia. Syndrome Speech transcriptions Written sentences nfvPPA: prominent speech apraxia The lady is drying a the plate, which she has washed. The man a boy um a cookie is on there. Um a daughter a no no um sister… And when she gonna throwen on them.

And they broken and book on there on there stool on round by them. And lady and she was having a washing on there and they be taps on them and drain is come on the floor one there. And um…And this man are there bear maybe going in the went on there… working out the window. With water running down. The lvPPA cases show marked word retrieval difficulty impaired message content reflected in prolonged pauses when speaking and trailing off of written sentences and in addition, incorrect syllable selection impaired message structure; underlined despite intact sentence construction; the speech sample of the lvPPA case here illustrates the challenge of reliably assessing spoken grammar in the setting of severe word-finding difficulty lvPPA logopenic variant primary progressive aphasia, nfvPPA nonfluent—agrammatic variant primary progressive aphasia, svPPA semantic variant primary progressive aphasia.

This Table presents some clinical observations that are not currently emphasised in standard diagnostic formulations but which we have found useful in the bedside diagnosis of the major syndromes of primary progressive aphasia lvPPA logopenic variant primary progressive aphasia, nfvPPA nonfluent—agrammatic variant primary progressive aphasia, svPPA semantic variant primary progressive aphasia.

A clinical framework for assessing language functions in primary progressive aphasia When confronted by an aphasic patient, it is important firstly to establish the context of the language disturbance. Canonical syndromes of primary progressive aphasia: nonfluent—agrammatic Clinical presentation Patients with nfvPPA present with slow, effortful, hesitant and distorted speech Table 3 ; Supplementary sound files 1 and 2.

Key associations General intellect is often remarkably well preserved, though a degree of executive dysfunction is usual and may be accompanied behaviourally by apathy or impulsivity [ 29 , 30 ]. Canonical syndromes of primary progressive aphasia: semantic Clinical presentation In striking contrast to nfvPPA, patients with svPPA exhibit well structured, well articulated language that is relentlessly bereft of substance Table 3 ; Supplementary sound file 3.

Neuroanatomy On neuroimaging, svPPA has a hallmark pattern of asymmetric, focal cerebral atrophy chiefly involving the dominant anteroinferior and mesial temporal lobe, including amygdala and anterior hippocampus [ 9 , 48 ].



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