Naltrexone: effects on motor function, speech, and activities of daily living in a patient with traumatic brain injury.

Evidence from many studies has suggested that endogenous opioid peptides participate in a number of pathophysiological responses to brain injury. This provides the rationale for the use of opioid antagonists for the enhancement of neural recovery after brain injury. A case is presented of an 18-year-old male who had loss of consciousness for 1 month after a severe brain injury. Three months of intensive rehabilitative therapies did not change his functional status. A trial of naltrexone was given while his performance in mobility, speech and overall Functional Independence Measure (FIM) scores were monitored. Results indicate an accelerated improvement in functional status and statistically improved FIM score.

Predicting hand preference with performance on motor tasks.

Handedness may be defined as preference or hand-differences in task performance. The strength and significance of the relationship between hand preference and hand performance asymmetries have been contested. To evaluate this relationship, we administered the Edinburgh Handedness Inventory and measured asymmetries in finger tapping, Purdue Pegboard, and grip strength in 30 subjects who prefer their right hand and 30 subjects who prefer their left hand. Hand asymmetries in finger tapping, Purdue Pegboard, and grip strength each predicted hand preference scores. However, a multiple regression equation best predicted hand preference by using performance of each task. Hand asymmetries in finger tapping correlated strongly with asymmetries in Purdue Pegboard performance, but neither of these asymmetries correlated strongly with asymmetries in grip strength. These findings indicate that hand preference and asymmetries in motor proficiency are strongly related, but suggest that preference and proficiency for different aspects of motor performance may be independently lateralized.

Treatment with amantadine potentiated motor learning in a patient with traumatic brain injury of 15 years' duration.

This study sought to determine whether pharmacotherapy with amantadine potentiates motor recovery in an 18-year-old man with traumatic brain injury (TBI) of 15 years' duration. This uncontrolled single-case multiple-baseline design allowed preliminary evaluation of amantadine within the context of standard data-collection procedures on the TBI unit. Measurements tracked speed of wheelchair propulsion, wheelchair transfer, donning shirt, and inserting pegs into holes. Data were collected during a 3-week practice period, followed by a 6-week period of practice plus daily treatment with amantadine. The rate at which performance improved was significantly increased with drug treatment in the wheelchair transfer task. There was a statistically insignificant trend toward improvement in donning shirt. Amantadine did not appear to potentiate recovery in the wheelchair propulsion or peg placement tasks. The results suggest that amantadine facilitates some measures of motor recovery in chronic brain injury. Further trials are warranted to investigate this issue.

Effects of dopaminergic combination therapy for frontal lobe dysfunction in traumatic brain injury rehabilitation.

Traumatic brain injury poses significant and diverse challenges to rehabilitation efforts. Neurobehavioural deficits represent a particularly difficult barrier to rehabilitative progress and societal reintegration. Early studies have identified dopaminergic drugs such as amantadine, bromocriptine and sinemet as potentially assistive in countering these deficits. To date, side effect profiles have been relatively benign, noted most frequently in small-scale case trials. The case of a 40-year-old patient with bilateral frontal traumatic brain injuries, and previous arteriovenous malformation (AVM) bleed with significant ataxia, dysarthria and neurobehavioural deficits is presented. This long range study demonstrates, through multiple varied dosing schedules, a trade off between the benefits and side effects of dopaminergic therapy, with implications for a larger brain injury population.

Transcranial magnetic stimulation reveals a hemispheric asymmetry correlate of intermanual differences in motor performance.

Hemispheric asymmetries in the threshold for eliciting motor evoked potentials (MEPs) with transcranial magnetic stimulation (TMS) are associated with hand preference. We posited that hemispheric asymmetries in TMS thresholds may be strongly correlated with some hand-differences in motor performance. MEPs result from the activation of neuronal networks targeting large cortical motoneurons. Thus, MEP thresholds might reflect physiological features of the corticospinal motor system. Considering the role of corticospinal pathways in the control of independent finger movement, we hypothesized that MEP thresholds would better predict speed and dexterity than strength. In 30 right-handers and 30 left-handers, we correlated right and left hand-differences in the threshold for eliciting MEPs with hand-differences in the performance of three manual tasks: finger-tapping speed, pegboard dexterity, and grip strength. Correlations of hand-differences in TMS thresholds with hand-differences in performance indicated that a lower TMS threshold for one hand is strongly associated with greater ability with that hand. The correlations of hand-differences in TMS thresholds with hand-differences in finger-tapping and pegboard dexterity were significantly larger than the correlation of hand-differences in TMS thresholds with hand-differences in grip strength. Our results indicate that hemispheric asymmetries in MEP thresholds may have functional significance related to basic parameters of movement. These results are consistent with the critical role of the corticospinal motor system in the control of independent finger movement. Furthermore, they imply that asymmetry in the corticospinal motor system may be an important substrate for asymmetries in hand preference and performance.

Physiological motor asymmetry in human handedness: evidence from transcranial magnetic stimulation.

We hypothesized that human handedness might be associated with measurable differences in the excitability of the motor system. We compared the thresholds for electromyographic activation of the left and right abductor pollicis brevis (APB) and biceps muscles in 30 left-handers and 30 right-handers, by varying the direction of a brief monophasic pulse in a circular electromagnetic coil centered over the vertex of the scalp. In right-handers, we found that the threshold for activation of muscles in the right arm was lower than the threshold for activation of corresponding muscles in the left arm. In left-handers, the reverse was true. Threshold asymmetry was influenced significantly by the consistency with which each subject used the writing hand to perform other motor tasks, and was not significant between non-consistent left-handers and right-handers. Our results indicate that human handedness, and in particular, consistency of hand preference, are associated with lateralized differences in the excitability of motor system projections activated by transcranial magnetic stimulation. Our findings might reflect physiological differences in corticospinal tract function or cortical motor representation.

Elements of cognitive rehabilitation after right hemisphere stroke.

There are two basic approaches to cognitive training: (1) impairment training and (2) task specific training. Impairment training addresses impairments common to a number of tasks and attempts to offer a general benefit to all of the tasks at once. Task specific training focuses on the impairments that arise in a single task and attempts to improve performance on that task. Impairment training of spatial disorders following right hemisphere stroke has shown some success when curricula are properly designed. The success, however, is quite limited because of normal cognitive constraints and those occurring after brain damage. Task specific training in conjunction with the combined application of various cognitive principles appears more promising, but as yet, only a few studies exist. The neurologic factors are likely to be the same factors that influence recovery. The factors that influence trainability are lesion topography (size and location of the focus plus premorbid atrophy), lesion chronicity, and the presence of additional cognitive impairments (anosognosia, confusion, and abulia). Other interventions that may be beneficial, even for training resistant patients, include behavior modification, cognitive prostheses, and drugs.

The pathogenesis of anosognosia for hemiplegia.

We compared patients with unawareness of hemiplegia lasting more than 1 month after right hemisphere stroke with other patients with right hemisphere stroke who became aware of hemiplegia within a few days after onset. Patients with persistent unawareness invariably had severe left hemisensory loss and usually had severe left spatial neglect. They were almost always apathetic; their thought lacked direction, clarity, and flexibility, and they had at least moderate impairment of intellect and memory. Their right hemisphere strokes were large and always affected the central gyri or their thalamic connections and capsular pathways. In addition, there was evidence of at least mild left hemisphere damage, most commonly caused by age-associated atrophy. The pathogenesis of anosognosia for hemiplegia may involve failure to discover paralysis because proprioceptive mechanisms that ordinarily inform an individual about the position and movement of limbs are damaged, and the patient, because of additional cognitive defects, lacks the capacity to make the necessary observations and inferences to diagnose the paralysis. We discuss the implications of this "discovery" theory and contrast it with other explanations of anosognosia.

Reappearance of the visual percept after intentional blinking in a patient with Balint's syndrome.

We present a patient with Balint's syndrome who complained of fading of the scenes under visual fixation. When he intentionally blinked, the faded visual percept reappeared. The disappearance of the visual percept may be explained as the result of either unstable visual fixation or of saturation of the visual pathways. The role of blinking in reviving the visual percept may be explained accordingly as causing a refixation of the target under visual fixation or as resetting the visual pathways for visual processing.

Prosopagnosia: a defect in visual configural processing.

A patient with severe, lasting prosopagnosia could not get an immediate overview of a face sufficiently specific for successful identification. He also failed completely in tasks of visual closure despite adequate performances on numerous other tests of visual perception and memory. We conclude that prosopagnosia represents a loss of visual "configural processing"--a learned skill enabling immediate identification of individual members of a class without conscious visuospatial analysis or remembering. Prosopagnosia and agnosic alexia represent two distinct defects of configural processing: Alexics cannot identify items with distinctive features that are themselves identifiable. Prosopagnosics cannot identify objects whose critical distinguishing features have no independent identities.

A case study of mental imagery deficit.

We describe a patient with a deficit in imagery ability, following a left posterior cerebral artery infarction and possible anoxic episode. This deficit was inferred from the patient's performance on several tasks, including one in which normal adults are known to rely on imagery and two that tested imagery nonverbally, allowing us to examine the possibility of a language-imagery disconnection. In addition, we queried the patient on some cognitive capacities related to visual imagery: dreaming, geographical knowledge, and introspection regarding visual and auditory imagery. Hypotheses concerning the critical lesion site and underlying cognitive mechanism of image generation deficits are discussed in relation to this and other recent cases of impaired imagery ability with intact recognition ability, and the relevance of this deficit to the "imagery debate" is discussed.

Pure agraphia and Gerstmann's syndrome as a visuospatial-language dissociation: an experimental case study.

A right-handed man suffered a left parieto-occipital cerebral infarction, causing agraphia with Gerstmann's syndrome but without major aphasia, alexia, or apraxia. Oral spelling was superior to written spelling. Experiments were performed involving (1) analysis of errors in writing, (2) tasks of visual imagery, and (3) identifying letters drawn without leaving a visual trace. The results suggest that the agraphia and Gerstmann's syndrome are due to a dissociation of language skills and visuospatial skills caused by a dominant parieto-occipital lesion.

Left visual spatial neglect is both environment-centered and body-centered.

To determine whether the left space that is neglected after right hemisphere lesions is body centered or environment centered, we asked patients with right hemisphere stroke and normal controls to report the contents of spatial arrays of objects or words, either while seated or while reclining on their side. The reclining posture eliminated the alignment of the vertical axis of the body with the vertical axis of the environment. Patients made fewer reports to the body left, but also fewer reports to the environment left, independent of body position. This suggest that a cerebral hemisphere directs attention not only relative to the body midline axis, but also relative to an environmental reference frame.

Left spatial neglect: effects of lesion size and premorbid brain atrophy on severity and recovery following right cerebral infarction.

We measured the severity of left spatial neglect in 29 patients, 2 to 4 weeks after right cerebral infarction. The severity of neglect increased with both the size of the lesion and the degree of premorbid diffuse cortical atrophy. Recovery over 3 to 5 months from an initially moderate to severe neglect was less complete in patients with cortical atrophy. The importance of lesion size shows that spared areas of the right hemisphere limit the severity and duration of left neglect. The importance of premorbid atrophy suggests that the integrity of the left hemisphere is also essential.

Dementia after surgery for cerebellar stroke: an unrecognized complication of acute hydrocephalus?

Three patients became demented after surgery for cerebellar hemorrhage or infarction with acute hydrocephalus. All were inattentive, perseverative, and disoriented. They had difficulty with memory, and trouble solving arithmetic problems or copying geometric figures. None showed aphasia, apraxia, or agnosia, although one had word-finding difficulty. One improved substantially in 6 months; one improved slightly in 1 year, and one did not change. None had persistent hydrocephalus. Acute hydrocephalus may have damaged the periventricular white matter to cause the dementia.

Language in the absence of inner speech.

A 54-year-old man abruptly became mute with mild right hemiparesis. Written expression, comprehension of speech and print, calculating ability, and verbal short-term recall, although slow, were largely preserved. Extensive studies demonstrated complete loss of inner speech. He was unable to speak to himself and unable to appreciate the phonological structure of words. Instead, his preserved language skills were based on a highly developed visual imagery. This case greatly extends the range of language skills previously thought possible in individuals who suffer the loss of inner speech.

Acquired learning disability for reading after left temporal lobe damage in childhood.

A 6-year-old boy developed hemorrhage in the left temporal lobe and subsequently underwent left temporal lobectomy. Afterwards, he was completely unable to learn to read or write. Psychological tests showed impairment in verbal learning and memory, with right ear and right visual field superiority in verbal perception. A Wada test showed no aphasia after right carotid injection. We conclude that damage to the speech-dominant temporal lobe resulted in the inability to learn to read or write. Despite the lesion, speech remained strongly lateralized to the left hemisphere, accounting for the right-sided advantage in verbal perception. Some patients with developmental dyslexia may have dysfunction of a strongly dominant left hemisphere rather than a delay or incompleteness of language lateralization.

Visual discrimination after lesion of the posterior corpus callosum.

Visual discrimination was studied in each visual field of a patient with surgical section of the posterior corpus callosum. Light-detection thresholds were increased nearly equally in right and left visual fields, suggesting that normal thresholds require the cooperative activity of both posterior cerebral hemispheres, mediated by the corpus callosum. In contrast, there was superiority in the right visual field in naming, coping, and matching letter, number, and colors, but not unfamiliar shapes. The results are attributed to a differential effect of experience on perception in each visual field. The right-visual-field superiority in learning to perceive arrays on letters, numbers, and colors may result directly from the superiority of the left hemisphere in speech.