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J R Hodges

Publications and source records attributed to J R Hodges.

At least 163 records · Page 9Linked to original sources

Recognition and naming of famous faces in Alzheimer's disease: a cognitive analysis.

A Famous Faces Test designed to assess face recognition, spontaneous naming, verbal identification of un-named faces, and cued naming using semantic and phonetic cues was administered to 22 patients with dementia of Alzheimer type (DAT) and 25 matched controls. The DAT patients were significantly impaired in all test conditions with evidence of a temporal gradient for recognition, identification and naming with phonemic cues, but not for spontaneous naming or naming with semantic cues. Analysis of the effects of disease severity showed that performance in all five conditions of the test declined with increasing disease severity, but this did not reach significance for recognition or for naming with phonemic cues. The DAT patients identified and named a significantly smaller proportion of the faces that they recognized than did the controls, and at no stage was identification significantly better than spontaneous naming. These findings indicate that the primary deficit was not one of name access, but an actual loss of stored knowledge about the person represented. In keeping with this observation, semantic cueing did not aid naming. These findings are discussed in the context of contemporary cognitive models of face processing.

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Autobiographical amnesia resulting from bilateral paramedian thalamic infarction. A case study in cognitive neurobiology.

A patient with a chronic amnesic state resulting from bilateral paramedian thalamic infarction showed a pattern of retrograde amnesia not previously reported. Personally relevant autobiographical memory was profoundly impaired, whereas knowledge of famous people and public events was relatively spared. Furthermore, knowledge of famous people, including the ability to make accurate temporal judgements, was less affected than knowledge of public events. In addition, we have documented a severe and systematic distortion of personal memory. These findings are not compatible with current accounts of retrograde amnesia based either upon the type of information stored (e.g. episodic versus semantic memory), or upon simple storage versus access models. We propose an explanation based upon an interactive cognitive model in which the patient shows a disorder at the 'thematic retrieval framework' level of memory organization due to a disconnection of frontal and medial temporal memory systems.

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Contrasting mechanisms of impaired attentional set-shifting in patients with frontal lobe damage or Parkinson's disease.

Tests which assess the ability to shift cognitive set modelled after the Wisconsin Card Sorting Test are particularly sensitive to impairments in patients with Parkinson's disease as well as in patients with frontal lobe damage. However, the underlying mechanisms responsible for the similar deficits observed in the two patient groups are not well understood and may not be identical. For example, an apparent deficit in set-shifting ability may reflect either an impairment in the ability to shift from a perceptual dimension which has previously commanded attention (i.e. 'perseveration'), or in the ability to shift to an alternative perceptual dimension which has previously been irrelevant (i.e. 'learned irrelevance'). In this study, the performance of both medicated and non-medicated patients with Parkinson's disease were compared with a group of neurosurgical patients with localized excisions of the frontal lobes on a novel task designed to assess the relative contribution of 'perseveration' and 'learned irrelevance' to impaired set-shifting ability. Patients with frontal lobe damage were worse than controls in their ability to shift attention from a previously relevant stimulus dimension. Medicated patients with Parkinson's disease were worse at shifting to a previously irrelevant dimension. In contrast to both groups, nonmedicated patients with Parkinson's disease were impaired in both conditions. These results suggest that the gross set-shifting deficits reported in both frontal lobe patients and patients with Parkinson's disease may involve fundamentally different, though related, cognitive processes, and that these may be differentially affected by medication. Specifically, L-dopa therapy may protect Parkinson's disease patients from preservation of attention to a formerly relevant stimulus dimension.

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Neuropsychological and SPECT scan findings during and after transient global amnesia: evidence for the differential impairment of remote episodic memory.

A patient had neuropsychological testing during, and at two days and seven weeks after a transient global amnesia (TGA) attack. During the attack she exhibited a characteristically profound anterograde amnesia but a limited remote memory loss; the most striking impairment was a deficit in personal episodic memory revealed by her performance on the Autobiographical Memory Interview. Personal and general semantic information was less impaired although there were indications of a temporal gradient in the impairment. When tested after the attack, she demonstrated normal anterograde and retrograde memory. A SPECT scan performed during TGA showed a focal reduction in cerebral perfusion in the postero-medial temporal lobes bilaterally which had resolved after seven weeks.

Amnesia↗

Deterioration of word meaning: implications for reading.

We investigated six patients with progressive focal dementia or progressive aphasia, who showed impairments in knowledge of word meaning ranging from moderate to very severe. In all cases, a test of oral word reading demonstrated preserved reading of words with regular spelling-to-sound correspondences (e.g. MINT), but impaired reading of words with atypical correspondences (e.g. PINT). The level of success on these "exception" words was significantly related to word frequency, and the most common error was the assignment of a more typical spelling-sound correspondence. Various explanations are considered for this common association between loss of word meaning and a surface alexic pattern of reading performance.

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Semantic memory impairment in Alzheimer's disease: failure of access or degraded knowledge?

A battery of neuropsychological tests designed to assess semantic knowledge about the same items both within and across different modalities was administered to a group of 22 patients with dementia of the Alzheimer type (DAT) and 26 matched controls. The DAT patients were impaired on tests of category fluency, picture naming, spoken word-picture matching, picture sorting and generation of verbal definitions. A relative preservation of superordinate knowledge on the sorting and definition tests, as well as a disproportionate reduction in the generation of exemplars from lower order categories was noted. Analysis of the errors made by each patient across the different tests, revealed a significant correspondence between the individual items. These findings offer compelling evidence that the semantic breakdown in DAT is caused by storage degradation.

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Discrepant oral and written spelling after left hemisphere tumour.

Repetition, reading, confrontation naming, and oral and written spelling were studied in a 57 year-old man with a left hemisphere tumour. These tasks were repeated over a period of two weeks when the patient was being treated for brain oedema prior and subsequent to neurosurgical intervention. In the context of intact repetition and good reading, the most striking finding was a significant qualitative and quantitative discrepancy between oral and written spelling, with the latter task more severely affected. The pattern on oral spelling was that of lexical (or surface) agraphia. On written output, however, orthographic errors predominated. The relatively greater impairment of written spelling was not secondary to a motoric or visuo-spatial deficit. The observed patterns are not easily accommodated by current models of writing.

Agraphia↗

Semantic dementia. Progressive fluent aphasia with temporal lobe atrophy.

We report five patients with a stereotyped clinical syndrome characterized by fluent dysphasia with severe anomia, reduced vocabulary and prominent impairment of single-word comprehension, progressing to a stage of virtually complete dissolution of the semantic components of language. A marked reduction in the ability to generate exemplars from restricted semantic categories (e.g. animals, vehicles, etc.) was a consistent and early feature. Tests of semantic memory demonstrated a radically impoverished knowledge about a range of living and man-made items. In contrast, phonology and grammar of spoken language were largely preserved, as was comprehension of complex syntactic commands. Reading showed a pattern of surface dyslexia. Autobiographical and day-to-day (episodic) memory were relatively retained. Non-verbal memory, perceptual and visuospatial abilities were also strikingly preserved. In some cases, behavioural and personality changes may supervene; one patient developed features of the Kluver-Bucy Syndrome. Radiological investigations have shown marked focal temporal atrophy in all five patients, and functional imaging by single positron emission tomography and positron emission tomography (one case) have implicated the dominant temporal lobe in all five. In the older literature, such cases would have been subsumed under the rubric of Pick's disease. Others have been included in series with progressive aphasia. We propose the term semantic dementia, first coined by Snowden et al. (1989), to designate this clinical syndrome.

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Progressive loss of access to spoken word forms in a case of Alzheimer's disease.

We report the results of a longitudinal study of a progressive anomia in a patient with dementia of the Alzheimer type (DAT). The anomia cannot be attributed to a deficit within the semantic system, but appears instead to arise from impaired access to the phonological lexicon at a post-semantic stage of the naming process: a deficit that hitherto has not been reported in DAT. Specific naming responses were affected consistently by the disorder, showing that disorders of access are not invariably associated with inconsistent responding. Before specific responses disappeared from spontaneous use, there appeared to be an intervening stage at which some responses could be elicited by an initial phoneme cue, suggesting a low level of spontaneous activity of insufficient strength to elicit a response unaided. The frequency of the name affected naming performance, but did not appear to interact with the severity of the naming disorder, suggesting that the parameters of the normal naming system were unaffected. It is claimed that important new insights into the characteristics of progressive anomia have been obtained by taking a longitudinal approach.

Alzheimer Disease↗

Pure apraxic agraphia with recovery after drainage of a left frontal cyst.

A case is reported of isolated apraxia of writing in which general limb praxis was spared. Spontaneous writing, writing to dictation and copying were equally affected. Letter selection and spelling were preserved and other language functions intact. A CT scan revealed a left frontal arachnoid cyst. After surgical drainage the agraphia resolved. The anatomical basis of the disorder is discussed in the light of modern information processing models of writing.

Agraphia↗

Amnesia following damage to the left fornix and to other sites. A comparative study.

Two memory-impaired patients, who had suffered damage to the left or both fornix columns during removal of a ventricular cyst, were compared with 3 others having left-sided hippocampal or thalamic lesions, and with normal controls. The tests used were nonverbal--scene recognition, delayed matching-to-sample and concurrent pattern and object discrimination learning. The last two are differentially sensitive to fornix transection and to hippocampal or thalamic ablations in monkeys; however, the patients with fornix damage did not show a distinctive pattern of impairment. The reasons for this discrepancy are discussed. The study adds to the evidence that fornix transection can cause wide-ranging memory disturbances in man.

Adult↗

The nature of the naming deficit in Alzheimer's and Huntington's disease.

A comparison of naming performance, on the Boston Naming Test, of 52 patients with dementia of Alzheimer's type (DAT), 16 patients with Huntington's disease (HD) and 52 normal control subjects was performed using a comprehensive classification of error types. Spontaneous and cued naming scores were significantly impaired both in the DAT and HD groups, but performance in the DAT patients was significantly worse than that of the HD patients. Normal controls made predominantly semantic-category and circumlocutory errors. The HD group differed from normal only in the proportion of visually based errors, which was greater in the patient group. By contrast, the DAT patients made a significantly greater proportion of semantic-superordinate and semantic-associative errors. The same pattern of naming errors was found when a group of DAT and HD patients matched for overall naming ability was compared. A subgroup of 22 DAT patients was followed longitudinally over 3 y. Their deterioration in overall naming performance was accompanied by a consistent change in the profile of naming errors: the proportion of semantic-associative errors increased significantly as did the proportion of visual errors. These results are considered in the light of current cognitive models of naming. They suggest that in HD, naming deficits initially involve disruption of perceptual analysis, whereas in DAT such impairments in the early stages reflect a breakdown in semantic processes. However, as DAT progresses, perceptual problems also begin to contribute to the patients' naming difficulties. Postlexical (phonemic) processes remain relatively intact throughout in both diseases.

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Anterograde amnesia with fornix damage following removal of IIIrd ventricle colloid cyst.

Two patients developed anterograde amnesia following the apparently uncomplicated transcallosal-transventricular removal of a colloid cyst. Damage to the fornical columns was demonstrated on CT and MRI scans, whilst other memory related structures were entirely normal. Longitudinal neuropsychological evaluation, over 12-24 months, has revealed a very similar pattern of deficit in the two cases: verbal memory has remained persistently impaired whilst nonverbal anterograde memory has improved to some degree. Formal tests of remote public (famous faces and events) and personal autobiographical memory have supported the clinical impression that neither patient has a temporally extensive retrograde amnesia. These findings address the role of the fornix, and the dissociation of memory processes in humans.

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Persistent memory impairment following transient global amnesia.

A controlled neuropsychological study of 41 patients tested at 6 months after attacks of transient global amnesia (TGA) revealed no evidence of general intellectual, immediate (short-term) memory or nonverbal memory impairment. The patient group's performance was, however, significantly worse than that of the control's on measures of verbal memory notably immediate, 30-minute and 24-hour delayed paragraph recall. In addition, tests of public and personal remote memory revealed significant impairment of naming and recognition of famous faces, and of dating famous events without evidence of a temporal gradient, and impairment of cued recall of autobiographical memories on the Modified Crovitz Test. These findings suggest that following TGA there is persistent, albeit mild, hippocampal-diencephalic dysfunction which appears to involve left-sided structures preferentially. This impairment probably results from the attack, although a pre-existent deficit cannot be excluded.

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The aetiology of transient global amnesia. A case-control study of 114 cases with prospective follow-up.

A case-control comparison of 114 transient global amnesia (TGA) patients using both normal community-based controls (n = 109) and transient ischaemic attack (TIA) controls (n = 212) showed no evidence of an increased risk of TGA associated with any of the conventional risk factors for cerebrovascular disease. However, migraine was significantly more common in the TGA patients than in either control group. A prospective longitudinal study using actuarial (life table) analysis confirmed that the prognosis of the TGA patients was strikingly better than that of the TIA controls. An important minority (7%) of TGA cases developed epilepsy, usually within one year of presentation. On the basis of this evidence, a thromboembolic aetiology for TGA can be confidently rejected, at least for the vast majority of cases. There are good theoretical reasons to link migraine and TGA casually, and occasionally epilepsy may masquerade as TGA. In the remaining cases the cause remains unknown.

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Syndromes of transient amnesia: towards a classification. A study of 153 cases.

Of 153 patients presenting with acute transient amnesia, 114 fulfilled the proposed strict diagnostic criteria for transient global amnesia (TGA). The prognosis of this group was excellent with the exception of a small subgroup (7%), largely identifiable because of atypically brief or recurrent attacks, who developed epilepsy of temporal lobe type on follow up. Computerised tomography (CT) scans performed on 95 patients were normal, evidence for covert alcoholism was lacking and there was a familial incidence of approximately 2%. By contrast, the group of 39 patients who did not meet the criteria for TGA had a significantly worse prognosis with a high incidence of major vascular events. The groups could not be distinguished on the basis of behavioural characteristics during the attack. The following classification was proposed: 1) pure TGA--attacks fulfilling the strict criteria, and of more than one hour in duration which do not require detailed investigation, 2) probable epileptic amnesia--attacks of less than an hour or rapidly recurrent, 3) probable transient ischaemic amnesia, a minority of cases with additional focal neurological deficits during the attack.

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Differential impairment of semantic and episodic memory in Alzheimer's and Huntington's diseases: a controlled prospective study.

A controlled prospective study compared the performance of 14 patients with dementia of Alzheimer type (DAT) and 14 patients with Huntington's Disease (HD), who were matched for overall level of dementia, on a battery of semantic and episodic memory tests. The DAT patients were significantly more impaired on measures of delayed verbal and figural episodic memory, and in addition showed a more rapid rate of decline on tests which depend upon the integrity of semantic knowledge (naming, number information, similarities and category fluency). In contrast, the HD patients were significantly worse, and showed a more rapid decline on the letter fluency test, a task especially sensitive to deficiencies in retrieval. The HD patients were also more impaired than DAT patients on a vocabulary test and on copying geometric figures. The observed double dissociations offer compelling evidence that aetiologically distinct forms of dementing illness result in different patterns of cognitive impairment.

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