Martin L. Albert

A simple test of visual neglect.

“Every man takes the limits of his own field of vision for the limits of the world.” SCHOPENHAUER, Psychological Observations: Studies in Pessimism . The primary purpose of this paper is to explain a simple, clinically useful test for visual neglect. The results of this test, which was standardized with normal subjects and presented to patients with unilateral cerebral lesions, shed light on the nature of visual neglect. In this paper the term “visual neglect” refers to a defective and, therefore, a reduced ability to attend to one or more components of the visual world.

The "subcortical dementia" of progressive supranuclear palsy.

Progressive supranuclear palsy (Steele et al.) has a characteristic pattern of dementia: (1) forgetfulness, (2) slowing of thought processes, (3) emotional or personality changes (apathy or depression with occasional outbursts of irritability), and (4) impaired ability to manipulate acquired knowledge. In many neurological disease states associated with subcortical pathology a similar pattern of dementia exists. The neurobehavioural changes of progressive supranuclear palsy thus typify a clinical pattern which may be referred to as subcortical dementia. The subcortical dementias have a striking clinical resemblance to the dementia which occurs after bifrontal lobe disease. However, the subcortical dementias can be clearly distinguished clinically from cortical dementias, other than frontal dementias. We propose as a tentative hypothesis that there may be common pathophysiological mechanisms underlying the subcortical dementias—in particular, disturbances of timing and activation. There are immediate practical implications of this hypothesis: drugs which have an effect on subcortical timing and activating mechanisms may be useful in the treatment of subcortical dementias.

Naming errors in healthy aging and dementia of the Alzheimer type.

Naming errors were analyzed for healthy younger and older adults and patients with a diagnosis of senile dementia of the Alzheimer type (SDAT). Three types of errors were identified, varying in relatedness to the target word: near synonyms; semantically related naming errors; and unrelated naming errors. Older adults made relatively more related errors than did younger adults. SDAT patients were distinguished by the number of unrelated responses given. In addition, SDAT patients who scored within the normal range were identified by the high number of response attempts relative to the number of initial errors. We suggest that error patterns on naming tasks may potentially serve as clinical markers to distinguish healthy older persons with mild naming disorders from patients with SDAT.

Speech monitoring skills in Alzheimer's disease, Parkinson's disease, and normal aging

We examined the abilities of 15 patients with dementia of the Alzheimer type (DAT), 22 patients with Parkinsons Disease (PD), and 141 healthy subjects (ranging in age from 30 to 79 years) to detect and correct their own speech errors. Each subject was shown the Cookie Theft picture of the BDAE (Goodglass & Kaplan, 1972. The assessment of aphasia and related disorders. Philadelphia: Lea & Febiger.) and instructed to tell the examiner the ...story of whats happening in the picture. Self-monitoring performance was assessed by tabulating the number of uncorrected errors as well as repaired errors. We divided repairs into two types based on the psycholinguistics literature (van Wijk & Kempen, 1987. Cognitive Psychology, 19, 403-440). Speech corrections were judged to be lemma repairs when the reparandum was a single word, and reformulation repairs when a new syntactic constituent was added to the reparandum. Patients with DAT corrected only 24% of their total errors and patients with PD only 25%. Healthy subjects, by contrast, corrected from 72 to 92% of their total errors. Patients with DAT tended to rely on reformulation repairs while patients with PD used both repair types about equally often. While healthy elderly Ss (in the 70s group) utilized lemma repairs more often than the reformulation strategy, all other healthy Ss used both strategies about equally often. Across all groups naming performance correlated negatively with numbers of undetected errors. Results point to a previously unrecognized communication disorder associated with PD and DAT and manifested by an impairment in the ability to correct output errors. This impairment may be related to attentional and frontal dysfunction in the two patient groups.

Hemianopic colour blindness.

A man developed cortical blindness after cerebral infarction in the distribution of both posterior cerebral arteries. When he recovered from this condition, he was found to be colour blind in the left visual field, but not in the right. This unusual situation resulted in apparently contradictory performances on hemifield and free-field tasks of colour discrimination, naming, and recognition. The contradictions may be explained by interhemispheric competition between a hemisphere which could discriminate colours and a hemisphere which was colour blind.

Chapter 7 – Naming in Normal Aging and Dementia of the Alzheimer's Type

Publisher Summary nThis chapter focuses on age-related difficulties that are faced by people in remembering names of a particular entity. Elderly people often complain of inability to remember names of people, places, and things. One of the numerous cognitive impairments that are demonstrated by individuals with dementia of the Alzheimers type (AD) is a disturbance in naming. The chapter explores the phenomenon of age-related difficulties in finding the right word at the right time. The chapter documents changes in the ability to retrieve words linked to processes of normal aging, and it examines how these naming problems affect everyday communication. It also examines the observed language behaviors in the context of contemporary models of naming and attempts to analyze psycholinguistic aspects of naming in normal aging. Focus is laid on the changes in naming ability associated with AD. In particular, it discusses research implicating a disturbance of semantic memory as the underlying mechanism of the naming impairment in subjects with AD. The chapter also focuses on investigations of naming in AD with respect to naming errors, response to cues and consistency of naming responses. The relationship between dementia severity and naming disturbance in AD is also discussed.

Wernicke and Alzheimer on the language disturbances of dementia and aphasia.

Signs of language dysfunction in dementia of the Alzheimers type (DAT) and in the aphasic syndromes of transcortical sensory aphasia and Wernickes aphasia are superficially similar. The unresolved question concerning the extent to which the language disturbances of DAT are aphasic is linked to a more fundamental question concerning the relation of language to thought, given that aphasia is often defined as language disturbance without disturbance of intellect, and dementia as dissolution of intellectual function, of which language forms an integral part. In this paper we explore the historical roots of todays debate by analyzing the original case studies of Wernicke (1874) and Alzheimer (1907, 1911). Although each of these neurologists described similar patterns of language disturbance, they drew different conclusions. Wernicke argued for a distinction between language and thought and between the language disturbances of aphasia and those of dementia. Alzheimer continued the then dominant paradigm of aphasia in describing the language disturbances of his demented patients as aphasic. Paradoxically his conclusion makes him appear, in contrast to Wernicke, to argue for the identity of the language disturbances of aphasia and dementia. Yet he himself acknowledged that the presence of focal language symptoms arising from diffuse degenerative pathology was indeed problematic. We conclude that todays discussion could profitably be refocused on the question which emerges from the original works of Wernicke and Alzheimer, which Alzheimer himself asked, and which remains unanswered: How can diffuse cerebral pathology give rise to a pattern of language deficit virtually identical to that of a focal lesion?

Enlargement of the Sylvian aqueduct: a sequel of head injuries.

A review of pneumoencephalography and clinical data in a large group of patients has shown that severe head injury may be followed by a consistent clinical-radiological syndrome. A prolonged period of unconsciousness is a characteristic initial feature of this syndrome. Clinically there is ataxia and dysarthria and, often, abnormal movements and oculomotor dysfunction. The characteristic radiological feature is an enlargement of the aqueduct of Sylvius. The clinical picture, together with the enlargement of the aqueduct, suggests that loss of neuronal and axonal substance in the midbrain is the probable pathology.

Variability in aphasia research: aphasia subject selection in group studies.

Subject selection criteria and descriptive data were compiled from 15 consecutive aphasia group studies published in Brain and Language from its inception (1974-1976) and two decades later. While some measures remain constant (aphasia type and lesion site are most commonly used in both periods), additional measures are reported only or more frequently in the recent period (e.g., age, handedness, bilingualism, language spoken, multiple vs. single lesions). Of interest is the decrease in the total number of subjects included in aphasia group studies from the early to the current period.

General Clinical Considerations

Language is a means by which people communicate with each other using verbal symbols. Dysphasia may be defined as a disorder of language due to brain damage. This monograph deals with disorders of language, not disorders of speech. Speech refers to the mechanical process of articulation, which can be disturbed by weakness, slowness, or incoordination of the muscles of the glossopharyngeal apparatus. Such disturbances would be termed dysarthria, dysphonia, or mutism. The term dysphasia is applied to a neurological disorder resulting from damage to those regions of the cerebral hemispheres which form the anatomical basis for the human capacity for language.