Biomedical subjects
Publications and source records attributed to D F Benson.
Although often considered to be a relatively new subdivision of neurology, behavioral studies actually have a long and colorful history. The events that led originally to a consideration of behavior as a neurologic subspecialty are outlined, followed by a listing of some of the major occurrences and key figures that have produced the considerable growth of behavioral neurology over the past two decades.
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A patient with persistent amnesia after bilateral medial temporal and left inferotemporo-occipital infarction could not match colors to objects in verbal, visual, or visuoverbal tasks. A severe naming disorder for objects was present but the patient could name colors and point to colors whose name was given. The matching disorder appeared to be a deficit in the semantic classification of objects rather than a problem in identifying colors.
A 54-year-old, right-handed male suffered three sequential infarcts. The first two destroyed much of the right posterior parietal area, the posterior-medial portion of the right temporal lobe and virtually the entire right occipital lobe producing left homonymous hemianopsia and left visual neglect but no prosopagnosia. A third vascular accident involved the left parieto-occipital lobe and immediately produced prosopagnosia that has persisted. The sequential correlations of lesion and symptomatology in this case demonstrate that development of persistent prosopagnosia occurred only after bilateral damage.
Twenty one unselected patients with an acute whiplash injury of the neck had neurological and neuropsychological assessment, cervical x rays, EEG, BAEP, MRI, and an otoneurological examination within two weeks of the injury. Subjectively, 13 patients reported concentration deficits, 18 reported sleep disturbances, 9 had symptoms of depression, and 7 female patients told of menstrual irregularities. Neuropsychological examination revealed significantly lower performance in tests related to attention and concentration compared to sex, age and educational matched control subjects. Otoneurological examination showed abnormalities in 9 of 17 whiplash subjects. EEG showed questionable changes in 8 of 18 recordings. MRI and BAEP were normal in all patients. Repeat neuropsychological testing in 15 patients at three months showed that attention deficits had improved but were still shown in 12 of 14 and the concentration deficits in 8 of 13 patients. At one year all patients had returned to work, 16 to full and 5 to part time employment. In 4, cognitive dysfunction remained the only significant problem. These findings are discussed as being compatible with possible damage to basal frontal and upper brain stem structures after whiplash injury of the neck.
We studied the MRI and clinical factors associated with dementia following stroke by quantifying ventricle-to-brain ratio (VBR), anatomic region of infarction, and cortical, subcortical, and white matter areas of infarction in 24 stroke patients with dementia and 29 nondemented stroke patients. The factors that most strongly correlated with dementia were total white matter lesion (WML) area, left WML, VBR, right WML, age, left cortical infarction area, left parietal infarction area, and total infarction area. Using discriminant analysis, these factors correctly classified 28 of 29 nondemented patients and 18 of 24 demented patients. Both cortical and white matter total infarction area measurements were strongly associated with dementia in stroke patients, suggesting that these factors strongly influenced the development of dementia following stroke. There was a strong association between dementia and left- but not right-hemisphere infarction area. The only demographic factor that strongly associated with dementia was age.
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Among diverse populations concerning the etiology of attention deficit hyperactivity disorder (ADHD), frontal dysfunction remains strong. The influences of frontal systems on attention, particularly the elements of higher mental control postulated as prefrontal functions, are illustrated through presentation of a number of syndromes of abnormal mental awareness associated with prefrontal brain damage. Against this background, a theory explaining part (but not all) of the problem seen in ADHD children is postulated, and a firm stand for prefrontal dysfunction as one element in the disorder is presented.
A characteristic personality syndrome consisting of circumstantiality (excessive verbal output, stickiness, hypergraphia), altered sexuality (usually hyposexuality), and intensified mental life (deepened cognitive and emotional responses) is present in some epilepsy patients. For identification, the term "Geschwind syndrome" has been suggested as a name for this group of behavioral phenomena. Support for, and criticism against, the existence of this syndrome as a specific personality disorder has produced more fire than substance, but the presence of an unsettled, ongoing controversy has been acknowledged. At present, the strongest support stems from the many clinicians who have described and attempted to manage seizure patients with these personality features. Carefully directed studies are needed to confirm or deny that the Geschwind syndrome represents a specific epilepsy/psychiatric disorder.
Various recently developed brain imaging techniques used to assist in the diagnosis of dementia are reviewed. The methods reviewed are x-ray computed tomography scan imaging, magnetic resonance imaging, positron emission tomography, and the older techniques of pneumoencephalography and radioisotope cisternography. It was concluded that while these techniques often offer excellent diagnostic information, none of them provides a definitive characteristic image for Alzheimer's disease.
The presence of delusions, a significant feature of many schizophrenic patients, implies a disturbance of reality testing. Through descriptions of a number of organic delusion syndromes featuring frontal damage, and a theory of prefrontal functions, a correlation of schizophrenic delusions and prefrontal malfunctions is postulated.
Three cases of slowly progressive speech and language disturbance were studied at various points post onset (three, five and 15 years respectively). Language, neuropsychological and brain imaging (computer tomography and positron emission tomography) evaluations were completed on all three patients. The data suggest that the syndrome of "progressive aphasia": 1) does not involve a uniform symptom complex; 2) does not necessarily develop into a full blown dementia syndrome; 3) varies greatly in rate of progression from case to case; 4) is associated with normal brain structure (on computer tomography); and 5) is associated with abnormal left temporal lobe metabolism as measured by fluorodeoxyglucose (FDG) positron emission tomography (PET). One patient had histological findings consistent with Alzheimer's disease at necropsy.
The authors present case reports of three patients with temporal lobe epilepsy who developed anorexia nervosa. All three patients showed both affective disorder and dysmorphic delusions, which were probable contributors to the appearance of the eating disorder.
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Numerous theories discuss the neuropsychological functions of the frontal lobes, most based on some concept of supramodality, and an extensive literature presents the phenomenology and semiology of language and communication deficits after focal brain lesions involving the frontal lobes. Despite this, few attempts have been made to link the clinical phenomenology to a theory. This paper presents (1) a general theory of frontal functions; (2) a brief summary of experimental and anatomical literatures in support of defined frontal functional systems; (3) clinical observations that delineate these functional systems for the specific modalities of language and communication; (4) a review of the available literature supporting the idea of specific modal and supramodal language and communication capacities; (5) hypotheses about the distributed anatomy of these functional systems; and (6) implications for traditional clinical notions of aphasia, particularly in relation to a general theory of frontal lobe functions.
Sixty-one inpatients manifesting chronic aphasic syndromes were reviewed. Most aphasic patients with behavioral abnormalities sufficiently severe to require hospitalization had posterior hemispheric lesions and fluent disorders. Thirty-eight (62%) had fluent aphasia, eight (13%) had nonfluent aphasia, and 15 (25%) had anomic, global, or transcortical aphasic syndromes. Delusions were more common among patients with fluent aphasias (58%), whereas depression was the most common psychiatric disorder among patients with anterior lesions (63%). Elation occurred in 12 patients, 11 with posterior lesions and 1 with a nonlocalizing syndrome. Neuropsychiatric disturbances in patients with chronic aphasia syndromes correlate with the type of language disorder and with the location of the associated lesion.
In a prospective study of late-life onset psychosis, five of the first 27 patients studied had extensive white-matter lesions demonstrated by MRI and/or CT. None of 60 age-matched psychiatrically healthy controls demonstrated such lesions. All five patients had a mild dementia and a frontal behavioural syndrome. In addition, every patient performed poorly on neuropsychological tests of frontal function. Dysfunction of the frontal cortex associated with white-matter lesions appears to contribute to the clinical picture of some cases of late-life psychosis.