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Background: Investigations of cognitive deficits after frontal lobe damage have commonly relied on multidimensional tests and relatively coarse specification of lesion anatomy. Some form of impairment in attention is often asserted to cause the revealed deficits.Objective: To describe a disorder of attention in patients with frontal damage using a theoretical model of the fundamental cognitive processes that underlie attention.Methods: The ability to perform a task of concentrated responding was studied in 43 patients with well-defined chronic frontal lesions and 38 control subjects using a continuous reaction time (RT) test. Performance measures were mean RT, RT across blocks of the test, and errors. Lesion measures were coarse localization and a hot-spot analysis to detect finer grained lesion effects.Results: Only patients with lesions in the right superomedial (SM) frontal regions had significantly prolonged RT consistently across the entire test. The critical lesion was in Brodmann’s areas 24, 32, 9, and 46 days and in the adjacent corpus callosum. Patients with lesions in left lateral frontal (LL) regions made significantly more errors on the 20% of trials in the first block. The critical lesion was in areas 44, 45, and 47/12.Conclusion: Concentrating attention to respond is affected by lesions in two different frontal regions for reasons that reflect impairments in different cognitive processes. Right superomedial lesions cause an insufficient energizing of attention to respond. Left lateral lesions cause defective setting of specific stimulus-response contingencies. Constrained tests of attention can demonstrate impairments in specific cognitive operations following lesions to different regions of the frontal lobes.

Background: Although cardiac arrest (CA) is commonly cited as a cause of amnesia, patients referred to the authors’ center with a diagnosis of “amnesia” after CA rarely have isolated memory deficits. Objective: To determine whether CA is a cause of pure amnesia and to assess patterns of cognitive deficits after CA. Methods: The authors used cognitive assessment of 11 consecutive patients referred for memory deficits after CA, targeted at deficit domains identified in the literature reviews, and analysis of specific case reports and prospective studies of cognition after CA. Results: The most common pattern of impairment in their patients was a combination of memory and motor deficits with variable executive impairment. No patient had isolated memory impairment. The case reports do not support the claim that isolated amnesia is a residual of CA; most cases of isolated amnesia are caused by subacute episodes of anoxia or excitotoxic injury. The prospective reports identify highly variable patterns of impairment, but isolated amnesia remains rare. Conclusions: Diffuse, sudden ischemic-hypoxic injury caused by cardiac arrest (CA) does not preferentially damage memory systems. Subacute or stepwise hypoxic or excitotoxic injury may cause isolated hippocampal injury and amnesia. The common pattern of impairment in the postacute phase after CA is a combination of memory, subtle motor, and variable executive deficits.

Whiplash is the commonly applied term for sprain or strain of the cervical region caused by sudden flexion-extension movements, most typically as a result of rear-end collisions. A specific diagnosis such as fracture, dislocation, herniated disc, root or plexus injury, or spinal cord injury overrides a diagnosis of whiplash. Thus, patients with whiplash do not have overt structural abnormalities. The forceful flexion-extension injury may damage cervical muscles, longitudinal vertebral ligaments, capsules of the facet joints, or the intervertebral discs. Whiplash causes neck pain, headache, and a variety of upper extremity regional pain or paresthetic symptoms either referred or possibly due to plexus compression by injured muscles. In most patients, pain gradually decreases over days to weeks, and by 6 months most patients are asymptomatic.1 Early treatment may utilize brief immobilization (collar), a short course of muscle relaxants, anti-inflammatory analgesics (aspirin or nonsteroidal anti-inflammatory drugs [NSAIDs]), heat and ultrasound begun after a few days, massage, gradual mobilization, and strengthening. A cervical pillow may prevent inadvertent exacerbation due to poor positioning during sleep. A variety of nontraditional treatments are often used, mostly chiropractic and acupuncture. The exact, best treatment is not known. A minority of patients have persistent or worsening pain despite treatment. The causes of persistent symptoms-chronic whiplash-are unknown. Pearce waded into this controversy in an editorial in Neurology in 1994, concluding that there was little evidence for a structural basis for chronic whiplash.2 Subsequent correspondence was vitriolic: polemics, doctrines, promotion of confusion, liars, malingerers, hysterics, neurotics, and egregious errors were mentioned. In his response, Dr. Pearce parried these thrusts skillfully, although there must have been some superficial flesh wounds.3 Chronic whiplash may "evolve" into fibromyalgia, a diagnosis by committee that inflames the extremists and leaves no unscorched ground for the moderates.4,5 Some patients also have cognitive …

Urinary incontinence (UI) after stroke is common and associated with overall poor functional outcomes.There is controversy regarding which factors contribute to incontinence after stroke and which factors may be predictive of recovery of continence. This study investigated consecutive stroke admissions to an inpatient rehabilitation hospital and evaluated the impact of several pre-selected factors on the presence of UI and its recovery. We also studied the impact of UI on outcome in terms of functional abilities with the Functional Independence Measure (FIM) and in terms of disposition. UI on admission was associated with severe functional impairment with large infarctions and was probably caused by general severity rather than specific impairment of neuromicturition control. Patients with less impairment (admission FIM >60) and small vessel strokes were likely to recover continence. UI on admission had a negative impact on outcome.NEUROLOGY 1996;47: 659-663

Accurate outcome prediction following stroke is important for proper delivery of poststroke care.It has been difficult to determine specific factors that provide reliable and accurate predictions of outcome, particularly for patients with intermediate deficit severities. Age and severity of deficit have repeatedly been found to be most reliable, but only as rough estimates and for patients at either extreme of the disability spectrum. This paper reports a prospective study of consecutive rehabilitation admissions (N = 536) to determine the influence of preselected factors. Outcome was analyzed in terms of functional improvement and disposition. Patients younger than 55 years or with an admission Functional Independence Measure (FIM) greater than 80 almost universally went home. Admission FIMs less than 40 were associated with nearly certain nursing home discharge. The comprehensive FIM score was a stronger predictor of outcome than motor impairment in isolation. An admission FIM of 60 or greater was associated with a higher probability of functional improvement during rehabilitation. Small-vessel strokes had the best outcome. Intracerebral hemorrhages improved more than ischemic strokes but more slowly. Right hemisphere lesions did worse than left. Comorbidities influenced outcome only when several conditions accumulated. The absence of a committed caregiver at home increased the risk of nursing home discharge. Suggestions for rehabilitation triage are given.NEUROLOGY 1996;47: 388-392

Article abstract-Numerous reports of aphasia after subcortical lesions have produced incomplete agreement about basic clinico-anatomic correlations. Some disagreement has arisen from methodologic differences. To control for some of the common differences, we analyzed 13 patients with left putaminal hemorrhage controlled for location--subcortical but not thalamic, and for time postonset--studied in both acute and postacute epochs. There was no apparent correlation between lesion site and acute language profiles. During the postacute epoch, there were several distinct correlations between lesion site (postacute decreased CT density) and specific aphasia dimensions--nonfluency, impaired comprehension, and perhaps impaired repetition. Our correlations were compatible with comparably controlled cases in the literature. A corollary result of this study is that patients fluent during the early epoch are likely to have a better outcome, and those initially nonfluent have a poor prognosis for language recovery.NEUROLOGY 1995;45: 38-41

Background: Lesions of the frontal lobes may impair the capacity of patients to control otherwise intact cognitive operations in the face of ambiguous sensory input or conflicting possible responses. Objective: To address the question of whether focal lesions in different regions of the frontal lobes produced specific impairments in cognitive control. Methods: We evaluated 42 patients with chronic frontal lesions and 38 control subjects on a modified Stroop test that allowed measurement of reaction times and errors. Planned, stratified analyses permitted identification of discrete frontal lesions that are critical for impaired performance. Results: Lesions of the left ventrolateral region produced an increased number of incorrect responses to distractors. Lesions of a large portion of the right superior medial region, including anterior cingulate, supplementary motor area (SMA), pre-SMA, and dorsolateral areas, caused a slow reaction time and a decreased number of correct responses to targets. Conclusion: Lesions in two distinct frontal regions impair cognitive control for a Stroop task, and the mechanisms of impairment are specific to the region of injury. This is support for a general proposal that the supervisory system is constructed of distinct subsystems.

Emotional synesthesia is a condition in which specific sensory stimuli are consistently and involuntarily associated with emotional responses.1 There is a very small number of reports of subjects with these stereotyped emotion-sensation pairings. One report described a subject in whom tactile stimulation from different textures (e.g., denim) elicited affective experiences (e.g., feelings of depression).2 Others have described emotional synesthetic associations to grapheme-color perceptions3 and to written names of acquaintances.1 Because there is such a small amount of literature, all in normal subjects with long histories of synesthesia, the neural substrates are unknown. There is a single report of acquired synesthesia: a tingling sensation elicited by sounds, but without emotional synesthesia, after a thalamic infarction.4 We report on the only known case of acquired emotional synesthesia after a focal thalamic lesion, providing a possible window into the neural substrate of this condition.

A patient is reported who suffered hypoxic-ischemic injury causing isolated and eventually partially reversible semantic memory loss. Despite normal MRI findings, single-photon emission CT demonstrated dysfunction in posterior cortical association areas. Semantic memory is the sum of categorical, perceptual, and conceptual knowledge. While not localized in the brain in a strict sense like visual fields, semantic memory is thought to be broadly organized in the posterior association cortices, with a particular focus in the inferior temporal regions. Evidence for this has come from patients with herpes simplex encephalitis, temporo-occipital infarctions, and dementias. This case confirms the importance of these cortical regions for semantic memory. The rapid recovery in this case, as opposed to the encephalitis or infarction cases, suggests an important role for preservation of white matter connections in the region for reconstitution of function. NEUROLOGY 1997;48: 165-173

Verbal material may be processed by semantic and phonologic systems.Damage to these language systems may also impair memory. We classified 16 mildly aphasic patients according to phonologic and lexicosemantic abilities, tested them on a variety of short- and long-term memory measures, and correlated behavioral deficits with lesion location. Aphasia impaired both short- and long-term memory. Phonologic impairment affected only digit span performance. Lexicosemantic deficits impaired self-organized encoding of word lists. Memory impairment was not associated with specific lesion locations. Persistent verbal-memory impairments accompanying even mild residual aphasia may be responsible for much of the difficulty mildly aphasic patients experience returning to vocational, academic, and social life. Co-occurrence of these deficits probably reflects their underlying dependence on similar processing systems.NEUROLOGY 1996;47: 795-801

We administered two experimental tasks to 16 patients with neglect following unilateral right hemisphere strokes, designed to probe processing of information in the neglected left visual field. A semantic priming/lexical decision task examined implicit processing of stimuli presented to the neglected field, and a discrimination task required explicit recognition of the same stimuli. We grouped patients according to three patterns of performance: (1) poor discrimination in the left visual field but intact priming, (2) normal priming and discrimination in both fields, and (3) normal priming but poor discrimination in both fields. Although patients in group 1 had posterior lesions, patients in groups 2 and 3 had extensive deep anterior lesions. These results suggest that the clinical phenomenon of unilateral visual neglect can be the surface manifestation of deficits in two different and interacting processes--attentional processes (group 1) and intentional processes (group 2)--or it may be a global attentional disturbance superimposed on these deficits (group 3).

We report 9 cases of aphasia following lesions in the region of the left frontal operculum. It is not possible to capture their variety of clinical manifestations with the simple labels of "Broca's area aphasia." or "Broca's area aphasia." Analysis of the breakdown of various components of speech and language in these cases suggests that the operculum, lower motor cortex, and subjacent subcortical and periventricular white matter contain critical parts of different language systems. These systems can be independently impaired. There are several common language syndromes that follow damage that includes the left frontal operculum. These syndromes reflect the effects of the direction and extent of the lesion in the various language systems.

Neuropsychiatry, Neuropsychology, and Clinical Neuroscience edited by Rhawn Joseph , 864 pp., ill., Baltimore, Williams & Wilkins, 1996, 2nd ed. 1990, $69.00 This book represents a remarkable effort: 751 pages of text and 80 pages of references from one author covering an enormous range of topics in neuroscience and behavioral science. Consider the book's subtitle: "Emotion, Evolution, Cognition, Language, Memory, Brain Damage, and Abnormal Behavior." Other texts that attempt such a breadth of material usually have contributors numbering in the tens, if not the hundreds, all determined to review the same material from their own viewpoints. Written by a single person, this text benefits from coherence of narrative; there is only one author's story to be told. And at $69 (at a local Boston …

Reply from the Author: Dr. Peterson has accused me of one of the few failings from which I truly thought I was immune: providing aid and comfort to “those who file false and exaggerated claims of head injury.” I was apparently led to this failing by three factors. Mild TBI does not produce DAI “unless there is a period of loss of consciousness of at least many minutes and perhaps hours in duration.” “Many” is in the eye of the beholder. In Gennarelli et al. 2 (Table 5), grade 1 DAI was reported in animals unconscious for 16 to 119 minutes. At milder levels, the injury may not cause actual axonal disruption and subsequent classic neuropathologic findings. Disruption of axonal transport may be the key pathophysiologic disturbance. 10 In any case, relatively mild TBI can produce overt DAI in humans. 11 Animals unconscious for less than 15 minutes had no DAI 2 …

Reply from the Author : I had two goals in my review of minor brain injury. First, I wanted to emphasize-to an audience of neurologists-that the natural history of concussion is complex. Neurologic disturbances (predominantly of attention and memory) last longer and are more disabling than is often recognized. Second, I attempted a clinical analysis of the patients who seem symptomatic and disabled out of proportion to the apparent injury. For this group, I proposed that some were probably hurt more severely than appreciated, but that most were suffering chronic pain and depression, both certainly related to the injury but not to direct central …

edited by JACQUELINE MONTGOMERY, 219 pp., ill., New York, Churchill Livingstone, 1995. $59.95 This book is written by and directed at physical therapists who work with patients who have suffered traumatic brain injury. In the preface, the editor states that the book is designed for \``the neophyte as well as the practicing clinician,'' and she describes the chapters as \`\`contemporary, state-of-the-art,'' with \`\`original applications'' and \``unique approaches.'' There is nothing of intrinsic neurologic interest in this book. Most of the neurology is schematic and simplified. The medical and surgical discussions are presented so undigested …

There has been disagreement about the precise characteristics of "subcortical aphasia." We evaluated 14 patients with aphasia after subcortical lesions and controlled for duration, general anatomic site of lesions (capsulostriatal only), and etiology. The clinical profiles of the patients were quite similar, varying in severity in rough proportion to lesion size and varying in quality in proportion to anterior paraventricular extent. Large lesions were associated with impaired "executive" and "generative" language functions. Similar aphasia profiles in patients with deep frontal and paraventricular white matter lesions suggest that damage to a frontal-caudate functional system underlies a "core" aphasia profile in these patients.

The position of the auditory pathways in the human corpus callosum has not been defined by modern imaging techniques. We report a case with a discrete hemorrhagic lesion in the posterior body of the corpus callosum. The only signs of disturbed callosal function were limited to the auditory system--suppression of left ear stimuli with dichotic listening and neglect of left-sided auditory simultaneous stimuli.

In pure alexia, acquired inability to read contrasts with normal speech and handwriting. Rare cases of right hemisphere lesions causing this syndrome are usually attributed to right hemisphere dominance for language. After infarction of the right occipital lobe and thalamus, a fully right-handed man became allelic, but language and spontaneous and dictated writing were intact. Left hemispatial neglect and constructional disturbances were marked, and we suggest that pure alexia was mimicked by the impairment in visuospatial perception. Injury of the no dominant hemisphere and thalamus together may have been important in causing these deficits.

We studied 9 patients with severe, chronic Parkinson disease and complications of long-term L-DOPA therapy. After a "holiday" of 3 to 21 days, excess dopamine effects improved in all patients, and the baseline parkinsonian picture emerged. After reinstitution of L-DOPA therapy, often at lower doses than had been used previously, parkinsonian signs improved. Complications of immobility were seen in two patients; one had deep vein thrombophlebitis, and the other became depressed. In treating the individual patient, the risks of immobility despite aggressive attempts to prevent complications should be weighed against the possible improvement of parkinsonism. These findings suggest that a holiday from L-DOPA therapy may extent the drug's usefulness in treating Parkinson disease, perhaps by resensitizing striatal dopamine receptors in patients receiving the drug for prolonged periods.

We describe five patients with spontaneous, persistent confabulation. While the basis of confabulation in general is not known, the evidence in this specific group of patients with spectacular, impulsive, and spontaneous confabulation suggests a marked deficit in frontal function, superimposed upon a basic defect in memory, as a possible mechanism.

We studied 11 patients with amnesia and personality change after surgical repair of ruptured anterior communicating artery ( ACoA ) aneurysm. CT and clinical evidence suggested that infarction in the territory of the ACoA was responsible for amnesia and personality change. The medial septal nuclei, the paraventricular nucleus of the anterior hypothalamus, and the medial forebrain bundle are the primary areas of potential interest in these cases. Gross infarction in the frontal lobes is not a requirement for the syndrome.

We studied eight children with acquired aphasia. All had left hemisphere lesions. In most, the correlation between the CT lesion site and the resulting aphasic syndrome duplicated an anatomic-clinical correlation described in adults. Rapid recovery of language fluency distinguished the children from reported adults. Late follow-up indicated poor scholastic achievements, reflecting an acquired handicap in new learning. Anatomic-clinical correlates and recovery patterns suggest that brain organization for language is similar but not identical in children and adults.

A patient recovering from a severe head injury developed a prolonged Capgras syndrome in which he believed his wife and five children had been replaced by nearly identical substitutes. Although this phenomenon is considered a functional disorder in the psychiatric literature, recent reports postulate an organic basis. Recent studies of the comparable neurologic disorder, reduplicative paramnesia, have stressed the importance of bilateral frontal and right hemisphere pathology. Neuropsychologic and neuroradiologic data in our patient revealed this combination, suggesting that the Capgras syndrome may be a form of reduplicative paramnesia with the same pathologic substrate.

Patients who exhibited frank confabulation were examined with four tests designed to elucidate the nature of confabulation in a structured situation, test the ability of confabulators to use cues, and examine the degree to which certain cognitive deficits are associated with confabulation. Two groups of confabulators emerged: mild and severe. Severity of confabulation was associated with perseveration, impaired self-monitoring facility, and failure to inhibit incorrect responses. Attenuation of these cognitive deficits with resolution of confabulation in a single patient suggested that the two levels of confabulation represented different levels of impairment of the same disorder.

Progressive aphasia without dementia (primary progressive aphasia) is increasingly recognized as an important neurobehavioral syndrome. Clinical diagnosis of progressive aphasia is difficult early in its course, and the differential diagnosis is usually said to include Alzheimer's and Pick's diseases. We report a 61-year-old man with autopsy-proven Creutzfeldt-Jakob disease (CJD) whose major initial manifestation was a progressive, fluent aphasia. Myoclonus was absent, and characteristic EEG abnormalities appeared relatively late. We believe that this case of CJD is unique in its presentation of profound and isolated aphasia. CJD should be considered in the differential diagnosis of the progressive aphasia syndrome.

The function of subcortical nuclear structures in language is uncertain, and language disorders after injury to these structures are described incompletely. We report 15 patients with left putaminal or thalamic hemorrhage, describe the range of language and behavioral disorders produced, and review the potential mechanisms of these disorders. Clinicoanatomic correlations revealed no definite differences between aphasia after hemorrhage in putamen or in thalamus.

We studied a patient with severe on-off phenomena that complicated chronic L-dopa treatment of Parkinson disease. Neuropsychologic testing was performed in both the on and the off states. Compared with the profound changes in motor status, the neuropsychologic alterations were modest: general disinhibition of language, worsened memory, and perseveration.

Analysis of language profiles and CT anatomy in transcortical motor aphasia (TCMA) suggests that the essential lesion is disruption of connections at sites between the supplementary motor area and the frontal perisylvian speech zone. If the lesion is extended, there may also be poor articulation (lesion deep to motor strip for face), impaired auditory comprehension (lesion in anterior head of caudate, anterior limb internal capsule, anterior putamen, and anterior portion of external capsule, claustrum, extreme capsule, and insula), or stuttering (lesion in pars opercularis and lower third of premotor region). This concept unifies disparate anatomic and psychophysiologic observations about three syndromes: classical TCMA, aphasia after left medial frontal infarction, and TCMA during recovery from Broca's aphasia.

Traumatic basal ganglia hemorrhage (TBGH) is probably secondary to rupture of lenticulostriate or anterior choroidal arteries. We evaluated 6 consecutive cases of this entity to define its clinical and pathologic dimensions. Relative frequency of TBGH was 3% (3 left, 3 right) in this acute rehabilitation population. Lesion size and associated pathology varied. Contralateral hemiparesis, present in all, recovered to varying extents, apparently related to lesion location (posterior limb, internal capsule, or midperiventricular white matter), not size. Prolonged muteness occurred in 4 of 6; these 4 patients also had severe diffuse axonal injury. Clinical findings corresponded with previously recognized subcortical hemisphere profiles. All achieved a moderate disability or good recovery rating on the Glasgow Outcome Scale. Rather than any features of the TBGH itself, duration of coma and/or associated temporal herniation predicted slower recovery and worse outcome. In conclusion, TBGH is a rare entity compatible with a favorable recovery, especially when occurring in isolation. The hemorrhage itself determines clinical signs related to particular subcortical structures involved and the side of the lesion. Overall cognitive impairment and speed and quality of recovery are more related to associated cerebral damage.