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Like much of the global biosphere, wildlife species have experienced rapid declines during the Anthropocene. Wildlife ecologists have responded to these crises by developing a range of technologies, techniques, and large datasets, which together have revolutionized the field, provided novel insights into the movements and behaviors of animals, and identified new risks and impacts to wildlife in a human-dominated world. While these advances have been vitally important, wildlife ecology has been slower to recognize and incorporate humans themselves into its new research domains. The chapters of this dissertation explore methods for better incorporating human behaviors, beliefs, actions, and infrastructure into the theories and approaches in wildlife ecology that have flourished in the last two decades. The research presented here demonstrates the importance of linking human beliefs and behaviors to wildlife ecology both by presenting novel findings and by showing the opportunities missed when narrow approaches are applied to complex socio-ecological problems.In Chapter 1, I provide a general introduction on the theories underlying this research, contextualize the research questions in light of the loss and recovery of large predators, and describe the research site where I collected much of the data for this dissertation. In Chapter 2, I apply the methods of movement ecology to some of the first fine-scale telemetry data collected on rifle hunters. I draw conclusions about their individual, site-level, and regional-level hunting behaviors and discuss the broad implications of these findings for hunting management. In Chapter 3, I examine livestock-predator conflict using approaches from both ecology and the social sciences. I describe a form of selection bias that is likely widespread but unreported due to the omission of social data from ecological models of conflict, and I offer guidelines for combining and translating ecological and social research on conflict. In Chapter 4, I explore the ecological impacts of one of the most globally widespread human constructions, the fence. I show for the first time the potential extent of fencing at large scales and discuss the wide variety of ecological effects of fences for both humans and ecosystems. I further highlight biases and gaps in fence research that have thus far limited a complete understanding of the environmental effects of these features. In Chapter 5, I conclude by making recommendations regarding how research might better incorporate human perceptions, decisions, and actions into ecology.

A remembrance of Donald T. Stuss, PhD, OC, OOnt, FRSC, one of the giants of modern neuropsychology, died on September 3, 2019, of complications from pancreatic cancer after a short illness. He was 77.

Studies of symptoms after concussion have been focused heavily on athletic and military populations; generalizability to "civilians" has not recently been demonstrated. We selected cognitive symptoms as an important target to assess because of impact on school and employment. We evaluated cognitive complaints in a highly symptomatic (Rivermead Post-Concussion Symptoms Questionnaire [PCSQ], mean [M] = 29.5) civilian sample (

Concussion is a common problem often managed by nonneurologists. It is often accompanied by headaches, dizziness, sleep disturbance, psychiatric symptoms, and cognitive issues. Here, we outline how to evaluate and manage concussion, including treatment of the most common symptoms.

Objective To determine whether people with moderate-to-severe traumatic brain injury (TBI) can adhere to a minimally supervised, community-based, vigorous aerobic exercise program. Design Prospective trial. Setting Young Men's Christian Association (YMCA) facilities. Participants Community-dwelling volunteers (N=10; 8 men, 2 women; age range, 22–49y) 6 to 15 months after moderate-to-severe TBI. Intervention Participants received memberships to local YMCAs and brief orientations to exercise. They were then asked to independently complete ≥12 weeks of ≥3 training sessions per week, performed at 65% to 85% of maximum heart rate for ≥30 minutes per session. Participants could self-select exercise modality, provided they met intensity and duration targets. Programmable heart rate monitors captured session intensity and duration. Main Outcome Measures Independence with equipment and facility use and compliance with training goals (session frequency, duration, intensity, total weeks of training). Results All participants achieved independence with equipment and facility use. All met at least 2 of 4 training goals; half met all 4 goals. Participants averaged (±SD) 3.3±0.7 sessions per week for 13 weeks (range, 6–24). Average ± SD session duration was 62±23 minutes, of which 51±22 minutes occurred at or above individuals' heart rate training targets. Conclusions People in recovery from moderate-to-severe TBI can, with minimal guidance, perform vigorous, community-based exercise. This suggests that decentralized exercise may be logistically and economically sustainable after TBI, expanding its potential therapeutic utility and rendering longer-duration exercise studies more feasible.

Objective: Among survivors of out-of-hospital cardiac arrest (OHCA), the functional outcomes of those with rapid early or with very delayed recoveries are known. For patients between those extremes early recovery is variable, and the probability of longer-term recovery and the implications for quality of life have not been clearly defined. Methods: Twenty-five patients of a consecutive cohort of OHCA survivors with coma duration between 12 h and 7 days and a matched group with acute coronary syndrome underwent cognitive and disability assessments 3 and 12 months after OHCA. Correlations and regression analyses of demographic, clinical arrest variables, and cognitive tests with quality of life outcomes were performed. Results: The OHCA group had impairments in all cognitive domains. There was little cognitive improvement. The OHCA group reported significantly greater health impact and lower quality of life at twelve months than the controls. Longer duration of coma (4–7 versus ≤ 3 days) and greater cognitive impairment at three months, particularly memory impairment, were both associated with reduced late quality of life. Conclusions: These survivors of OHCA had persistent longterm cognitive deficits. Quality of life at one year after OHCA was reduced compared to cardiac controls. Coma duration and memory impairment at three months were harbingers of long term reduced quality of life.

Recognition memory can be subdivided into two processes: recollection (a contextually rich memory) and familiarity (a sense that an item is old). The brain network supporting recognition encompasses frontal, parietal and medial temporal regions. Which specific regions within the frontal lobe are critical for recollection vs. familiarity, however, are unknown; past studies of focal lesion patients have yielded conflicting results. We examined patients with focal lesions confined to medial polar (MP), right dorsal frontal (RDF), right frontotemporal (RFT), left dorsal frontal (LDF), temporal, and parietal regions and matched controls. A series of words and their humorous definitions were presented either auditorily or visually to all participants. Recall, recognition, and source memory were tested at 30 min and 24 h delay, along with “remember/know” judgments for recognized items. The MP, RDF, temporal and parietal groups were impaired on subjectively reported recollection; their intact recognition performance was supported by familiarity. None of the groups were impaired on cued recall, recognition familiarity or source memory. These findings suggest that the MP and RDF regions, along with parietal and temporal regions, are necessary for subjectively-reported recollection, while the LDF and right frontal ventral regions, as those affected in the RTF group, are not.

Regions within the frontal and parietal cortex have been implicated as important neural correlates for cognitive control during conflict resolution. Despite the extensive reciprocal connectivity between the cerebellum and these putatively critical cortical areas, a role for the cerebellum in conflict resolution has never been identified. We used a task-switching paradigm that separates processes related to task-set switching and the management of response conflict independent of motor processing. Eleven patients with chronic, focal lesions to the cerebellum and 11 healthy controls were compared. Patients were slower and less accurate in conditions involving conflict resolution. In the absence of response conflict, however, tasks-witching abilities were not impaired in our patients. The cerebellum may play an important role in coordinating with other areas of cortex to modulate active response states. These results are the first demonstration of impaired conflict resolution following cerebellar lesions in the presence of an intact prefrontal cortex.

Executive dysfunction accounts for significant disability in patients with many types of brain injury in many locations. Clinical reports have described impaired executive functioning after damage to the cerebellum, and anatomical and neuroimaging studies have identified the likely basis for this effect: a cortico—ponto—cerebellar network through which the cerebellum is densely connected to areas of frontal cortex. The patterns of executive impairment attributable to cerebellar damage have been extensively described in the past 15 years, but there has been no assessment of the efficacy of rehabilitation in this patient population. Here, the use of a cognitive rehabilitation technique, Goal Management Training, in a patient with persisting executive dysfunction after a right cerebellar hemorrhage is described. The patient made and maintained modest gains on measures of sustained attention, planning, and organization that translated into significant improvement in real-life functioning. This is the first report on the rehabilitation of impaired executive functioning following focal damage to the cerebellum and in the presence of intact frontal cortex.

Achieving sufficient plasmid delivery is a key unresolved problem in postischemic myocardium for the latest clinical trials whose main objective is to rapidly upregulate potent regenerative mechanisms within a tight therapeutic window (i.e., within 48 hr). The well-documented impediments for efficient plasmid trafficking and subsequent transduction include anatomical-scale, cardiac disease-related comorbidities, and localized immune responses following the acute myocardial infarction event. An appreciation of delivery challenges originated from the first-in-human cardiac surgery gene therapy trial,1 which featured direct intramuscular (IM) injection of adenovirus encoding the vascular endothelial growth factor. Long-term follow-up of this phase I trial yielded no clear evidence of efficacy, likely because of a limited, transient expression profile—but it provided an impetus for improvements in vector, target, and clinical delivery strategies. Since then, numerous regenerative trials such as the stromal cell-derived growth factor 1 have generated significant interest. These strategies seek to repair myocardium through the chemoattraction of endogenous stem cell lineages shortly after myocardial infarction.2 In contrast to viral vector-mediated transgenes, these approaches offer rapid onset gene overexpression through high-dose, yet low-risk vector plasmids. The IM route is attractive for this emerging therapeutic class because of its clinical feasibility through both surgical (Fig. 1A) and catheter-based delivery techniques, but is limited by transfer inefficiency. Despite technical modifications of needle-based delivery in myocardium, these problems persist: poor retention, inconsistent performance per site, and the highly focal resultant delivery profiles. This results in the demand for more injections, thus increasing the risk for additional injury in already-compromised myocardium.3 In addition, recent trial results suggest that the predominant intracoronary infusion route may be even less efficient in patients with significant coronary disease, thus renewing interest in IM delivery. Therefore, a shift toward improvement in the delivery profile featuring clinically applicable drug combination approaches has been explored as a means to increase efficiency per injection site.4

Mild traumatic brain injury (TBI) is common but accurate diagnosis and defining criteria for mild TBI and its clinical consequences have been problematic. Mild TBI causes transient neurophysiologic brain dysfunction, sometimes with structural axonal and neuronal damage. Biomarkers, such as newer imaging technologies and protein markers, are promising indicators of brain injury but are not ready for clinical use. Diagnosis relies on clinical criteria regarding depth and duration of impaired consciousness and amnesia. These criteria are particularly difficult to confirm at the least severe end of the mild TBI continuum, especially when relying on subjective, retrospective accounts. The postconcussive syndrome is a controversial concept because of varying criteria, inconsistent symptom clusters and the evidence that similar symptom profiles occur with other disorders, and even in a proportion of healthy individuals. The clinical consequences of mild TBI can be conceptualized as two multidimensional disorders: (1) a constellation of acute symptoms that might be termed early phase post-traumatic disorder (e.g., headache, dizziness, imbalance, fatigue, sleep disruption, impaired cognition), that typically resolve in days to weeks and are largely related to brain trauma and concomitant injuries; (2) a later set of symptoms, a late phase post-traumatic disorder, evolving out of the early phase in a minority of patients, with a more prolonged (months to years), sometimes worsening set of somatic, emotional, and cognitive symptoms. The later phase disorder is highly influenced by a variety of psychosocial factors and has little specificity for brain injury, although a history of multiple concussions seems to increase the risk of more severe and longer duration symptoms. Effective early phase management may prevent or limit the later phase disorder and should include education about symptoms and expectations for recovery, as well as recommendations for activity modifications. Later phase treatment should be informed by thoughtful differential diagnosis and the multiplicity of premorbid and comorbid conditions that may influence symptoms. Treatment should incorporate a hierarchical, sequential approach to symptom management, prioritizing problems with significant functional impact and effective, available interventions (e.g., headache, depression, anxiety, insomnia, vertigo).

This study examined the performance of 38 normal subjects and 43 patients with focal lesions of the frontal lobes on a simple go-nogo task where the probability of the nogo stimulus was either 75% or 25%. Patients with lesions to the superior medial parts of the frontal lobes, in particular to the left superior portion of Brodmann area 6 (which includes the supplementary motor areas and the premotor areas for the right hand) had an increased number of false alarms (incorrect responses to the nogo stimulus). These results indicate that area 6 is specifically involved in the inhibition of response. Patients with lesions to the right anterior cingulate (areas 24 and 32) were slower and more variable in their reaction time. These findings could be explained by an inability to sustain stimulus-response contingencies. Lesions to the right ventrolateral prefrontal cortex (Brodmann areas 44, 45, 47) also increased the variability of response, perhaps by disrupting monitoring performance.

Production of complex discourse—lengthy, open-ended utterances and narratives—requires intact basic language operations, but it also requires a series of learned procedures for construction of complex, goal-directed communications. The progression of clinical disorders from transcortical motor aphasia to dynamic aphasia to discourse impairments represents a progression of procedural deficits from basic morpho-syntax to complex grammatical structures to narrative and a progression of lesions from posterior frontal to polar and/or lateral frontal to medial frontal. Two cases of impaired utilization of language exemplify the range of impairments from clearly aphasic agrammatic, nonfluency to less and less “aphasic” and more and more executive impairments from transcortical motor aphasia to dynamic aphasia to narrative discourse disorder. The clinical phenomenology of these disorders gradually comes to be more accurately defined in the terminology of executive deficits than that of aphasia. The executive deficits are, in turn, based on impairments in various components of attention. Specific impairments in energizing attention and setting response criteria associated, respectively, with lesions in superior medial and left ventrolateral frontal regions may cause defective recruitment of the procedures of complex language assembly. (JINS, 2006,12, 236–247.)

To describe the functional outcome of 19 patients with anterior communicating artery aneurysm following the completion of an inter-disciplinary out-patient rehabilitation programme.Retrospective descriptive study.Community-based inter-disciplinary outpatient programme.n = 19; consecutive referred sample, mean 182 days post-onset; in-patient rehabilitation completed.Inter-disciplinary treatment of functional activities; 2-5 hours/day, 3-5 days/week; mean duration: 55-57 days.Supervision rating scale (SRS) and change in prevalence at admission and discharge of executive impairments, memory, confabulation, apathy, initiation, social inappropriateness and incontinence.Sixty per cent of the patients showed a clinically significant improvement in their SRS from requiring full-time supervision to part-time supervision. Change in SRS was correlated with change in the impairments of executive function, memory and confabulation.Although pervasive impairments associated with this disorder may limit capacity for even moderate independence, substantial reduction in direct supervision by family members may be achieved.

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.

There has long been controversy about the function of the frontal lobes in memory. Historically, in lesion studies, the frontal lobes were discussed as if they represented a single functional unit, and little attention was paid to possible regional differences. In a series of experiments involving patients with focal frontal lobe lesions, we have demonstrated that different frontal regions affect strategic memory processes in unique ways. In addition, some regions of the frontal lobes are involved in nonstrategic memory encoding, likely through actual involvement of the limbic memory regions or through the impact of processing deficits related to the specific mode of the information to be learned (e.g., language). These findings converge with those of functional imaging studies showing the dissociation of memory processes within the frontal lobes, and are indicative of the complex roles subserved by the frontal lobes. Future research will need to explore how the different functions within the frontal lobes influence other dynamic cognitive systems.

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.

Katz DI, White DK, Alexander MP, Klein RB. Recovery of ambulation after traumatic brain injury. Arch Phys Med Rehabil 2004;85:865–9. Objectives To identify variables that are predictive of independent ambulation after traumatic brain injury (TBI) and to define the time course of recovery. Design Retrospective review of consecutive admissions of patients with severe TBI over a 32-month period. Setting Brain injury unit in an acute, inpatient rehabilitation hospital. Participants Of 264 patients screened, 116 met criteria that included the ability to participate in motor and functional evaluation on admission to acute rehabilitation, and the absence of other neurologic disorders or fractures that affect one's ability to ambulate. Intervention Inpatient rehabilitation on a specialized TBI unit by an interdisciplinary team. Main outcome measures Recovery of independent ambulation and time to recover independent ambulation. Results Of eligible patients, 73.3% achieved independent ambulation by latest follow-up (up to 5.1mo). Patients who achieved independent ambulation were significantly younger ( P P P =.058)—than those who did not ambulate independently. There were no differences in recovery based on neuropathologic profile. Mean time to independent ambulation ± standard deviation was 5.7±4.3 weeks; of those achieving independent ambulation, 82.4% did so by 2 months and 94.1% by 3 months. If not independent by 3 months postinjury, patients had a 13.9% chance of recovery. Multivariate regression analysis generated prediction models for time to independent ambulation, using admission FIM instrument scores and age (38% of variance); initial gait score, loss of consciousness, and age (40% of variance); or initial gait score and PTA (58% of variance), when restricted to just those patients with diffuse axonal injury. Conclusions Most patients with severe TBI achieved independent ambulation; the vast majority did so within 3 months postinjury. Functional measures, injury severity measures, and age can help guide prognosis and expectations for time to recover.

Language after frontal injury is usually not overtly aphasic, i.e, the essential instrumentalities of language ? phonology, lexical-semantics, and most aspects of grammar ? are intact. Patients with frontal lobe lesions are impaired at level of assembly of complex language. This impairment has three prototypical forms although there is substantial overlap between the prototypes, both in the language procedures recruited and in the clinical phenomenology. Transcortical motor aphasia is impairment at the level of complex sentence construction. Dynamic aphasia is impairment at the level of schema assembly. Discourse disorder is an impairment of script assembly, reflected as deficient narrative capacity. One model for understanding these disorders is the “action planning” model. The capacity to utilize language instrumentalities to produce goal-directed communications requires the on-line recruitment of a number of procedures (schemas) at various levels of complexity. These procedures are learned within cultural constraints across the lifespan. They may be the single most practiced and over-learned capacities of humans.

The hypothesis that prefrontal cortex plays a critical role in accurate predictions of episodic memory performance was tested using the feeling-of-knowing (FOK) paradigm. Fourteen patients with a broad spectrum of damage to the frontal cortex and matched controls read sentences and later were tested for recall memory, confidence judgments, and FOK accuracy using as cues the sentences with the final word missing. While frontal patients were impaired at recall and recognition memory, they were able to make accurate confidence judgments about their recall attempts. By contrast, as a group, the patients were markedly impaired in the accuracy of their prospective FOK judgments. Lesion analysis of frontal patients with clear FOK impairment revealed an overlapping region of damage in right medial prefrontal cortex. These findings provide functional and anatomical evidence for a dissociation between recall confidence and prospective memory monitoring and are discussed in terms of familiarity and access theories of FOK predictions.

The causes of variability of performance by individual subjects have rarely been investigated, although excessive variability or inconsistency may be a functionally significant factor for many real-life activities. Our objective was to determine whether patients with focal frontal brain lesions have excessive individual performance variability. Thirty-six patients with focal frontal (n=25) or non-frontal (n=11) lesions were compared with 12 control subjects on different measures of intra-individual variability: dispersion within a testing session; and consistency across testing sessions. Four reaction time tasks, varying in levels of complexity and based on a model of detection using feature integration, were administered. Following the first test session, 22 patients and 10 controls returned for two subsequent test sessions, which permitted the assessment of consistency of performance. Measures of abnormal dispersion of performance on these tests were observed in frontal patients only (except those with exclusively inferior medial damage). Disturbances in consistency of performance were observed primarily in patients with frontal lesions. Damage to the frontal lobes impairs the stability of cognitive performance. Damage to different frontal regions causes different profiles of abnormal variability. Fluctuations in performance of a task may underlie some of the reported difficulties in daily tasks reported by patients with frontal injuries.

Riluzole is the only therapy proven in clinical trials to prolong amyotrophic lateral sclerosis (ALS) survival (approximately three months). Questions remain concerning riluzole's effectiveness in everyday practice, the appropriate duration of treatment, which certain subtypes of ALS specifically benefit from the medication, and whether early administration prolongs survival in ALS patients. We report the results of a population-based outcome study of riluzole in the Irish ALS population over a five-year period. Using data from the Irish ALS Register, we examined the survival of patients diagnosed with ALS between 1 January 1996 and 31 December 2000 who attended a general neurology clinic (n = 264 patients, MD = 16). An intention to treat analysis is employed. 149 (61 %) patients were prescribed riluzole and the remaining 99 (39 %) were not. Riluzole therapy reduced mortality rate by 23 % and 15 % at 6 and 12 months respectively and prolonged survival by approximately four months. This beneficial effect was lost in prolonged follow-up. Suspected or possible ALS patients receiving riluzole experienced similar improvement in survival as the overall cohort. Survival benefit was more marked among patients with bulbar-onset disease. Multivariate analysis did not show riluzole to be an independent predictor of survival. We conclude that riluzole therapy improves ALS survival in everyday clinical practice by a short period of time. This beneficial effect is transient and stopping the medication in advanced ALS should be reconsidered. Bulbar-onset patients appear to particularly benefit from riluzole for unclear reasons. Our initial observations support riluzole use in early ALS.

Abstract: The objectives of this review paper were to demonstrate whether there are separable attentional processes related to the frontal lobes, and to illustrate procedures on how to examine this question. Distinctions among frontal lobe attentional processes can be achieved if cognitive processes are adequately differentiated and if a sufficient number of patients are assessed to allow investigation of the relation of these distinct processes to different frontal lobe regions. The first section summarizes early evidence for the fractionation of the anterior attentional system using clinical tests. The second section extends these findings using experimental tests such as feature integration reaction time tasks. Different attentional processes include activation, task setting, shifting, and differentiating among relevant and irrelevant information. Although there are multiple anterior attentional processes related to different frontal brain regions, such anterior attentional processes likely interact with posterior attentional processes, with task demands altering the relationship among brain regions involved.

Mild traumatic brain injury (TBI) is common but accurate diagnosis and defining criteria for mild TBI and its clinical consequences have been problematic. Mild TBI causes transient neurophysiologic brain dysfunction, sometimes with structural axonal and neuronal damage. Biomarkers, such as newer imaging technologies and protein markers, are promising indicators of brain injury but are not ready for clinical use. Diagnosis relies on clinical criteria regarding depth and duration of impaired consciousness and amnesia. These criteria are particularly difficult to confirm at the least severe end of the mild TBI continuum, especially when relying on subjective, retrospective accounts. The postconcussive syndrome is a controversial concept because of varying criteria, inconsistent symptom clusters and the evidence that similar symptom profiles occur with other disorders, and even in a proportion of healthy individuals. The clinical consequences of mild TBI can be conceptualized as two multidimensional disorders: (1) a constellation of acute symptoms that might be termed early phase post-traumatic disorder (e.g., headache, dizziness, imbalance, fatigue, sleep disruption, impaired cognition), that typically resolve in days to weeks and are largely related to brain trauma and concomitant injuries; (2) a later set of symptoms, a late phase post-traumatic disorder, evolving out of the early phase in a minority of patients, with a more prolonged (months to years), sometimes worsening set of somatic, emotional, and cognitive symptoms. The later phase disorder is highly influenced by a variety of psychosocial factors and has little specificity for brain injury, although a history of multiple concussions seems to increase the risk of more severe and longer duration symptoms. Effective early phase management may prevent or limit the later phase disorder and should include education about symptoms and expectations for recovery, as well as recommendations for activity modifications. Later phase treatment should be informed by thoughtful differential diagnosis and the multiplicity of premorbid and comorbid conditions that may influence symptoms. Treatment should incorporate a hierarchical, sequential approach to symptom management, prioritizing problems with significant functional impact and effective, available interventions (e.g., headache, depression, anxiety, insomnia, vertigo).

To retrospectively evaluate gastrostomy placement in patients with amyotrophic lateral sclerosis (ALS) to determine the insertion method of choice.During 3(1/2) years, 36 patients with ALS (19 men, 17 women; mean age, 54 years; age range, 37-69 years) underwent gastrostomy. Twenty patients were primarily referred for percutaneous endoscopic gastrostomy (PEG) and 16 for percutaneous radiologic gastrostomy (PRG). Gastrostomy method, success rate of each technique, and reason for procedure failure were reviewed in each patient. Forced vital capacity (FVC) prior to gastrostomy was recorded. PEG was performed with a pull-through technique after transillumination of the abdominal wall. PRG was performed with fluoroscopic guidance and T-fastener gastropexy. A log-rank test was used to compare survival rates after PRG and PEG, and a Wilcoxon rank sum test was used to evaluate the influence of declining FVC on PEG success. The Kaplan-Meier product limit method was used to estimate survival probabilities.Of the 20 patients referred for PEG, 11 had successful results. The nine failures (45%) resulted from failure to transilluminate the abdominal wall. All 16 patients primarily referred for PRG underwent successful gastrostomy. The nine patients in whom PEG failed underwent subsequent successful PRG. In patients with diaphragmatic palsy and a high subcostal stomach, an angled subcostal approach (n = 6) or intercostal approach (n = 2) was required at PRG. One death occurred in the PEG group (9%) because of procedure-related aspiration, and a second patient from the PEG group required laparotomy for postprocedural peritonitis. One death occurred in the PRG group (4%) because of inadvertent placement of the feeding tube in the peritoneal cavity. There was no significant difference between PEG and PRG in patient survival. FVC did not have a statistically significant influence on PEG failure.Results show PRG to be the method of choice.

Objective: Patients with left neglect on line bisection show normal implicit sensitivity to manipulations of both the stimulus and the visual background. Three experiments were designed to define this sensitivity more exactly. Methods: Normal controls and patients with left neglect performed a series of horizontal line bisection tasks. Independent variables were the configurations of the backgrounds for the line—rectangle, square, circle, left and right pointing isosceles triangles—and whether the background was the shape of the piece of paper or an outline drawn on a standard piece of paper. In a separate experiment different components of the triangle were outlined on a piece of paper. Deviation from true midpoint was calculated. Results: Simply placing the target lines in a symmetric background such as a square or circle did not reliably reduce neglect. A triangle asymmetric in the horizontal plane caused a shift in bisection away from the triangle9s vertex. With right pointing triangles the perceived midpoint shifted to the left of true centre (crossed over). The effects of the triangles were comparable in the patients and the controls when controlled for baseline bisection bias. The critical components of the triangles were the angular legs. This effect of background was not influenced by lesion site or by hemianopia. Conclusions: Patients with left visual neglect remain sensitive to covert manipulations of the visual background that implicitly shift the perceived midpoint of a horizontal line. This effect is strong enough to eliminate neglect on a bisection task. The mechanism of this effect is expressed through preattentive visual capacities.

This article reviews the clinical profiles of memory disorders that are commonly encountered on neurorehabilitation units. Memory is comprised of several dissociable processes and is subserved by a distributed network of brain regions. The cognitive and neuroanatomical bases of memory provide the foundation for clinicians to evaluate and treat patients with memory disorders. Memory disorders occur with disparate etiologies including stroke, aneurysms, head injury, encephalitis and anoxia. Recovery of memory function is dependent on several clinical factors such as etiology and lesion location. There is no direct treatment of amnesia, but memory rehabilitation with pharmacotherapy or cognitive remediation is often attempted. The relative strengths and weaknesses of each therapy strategy must be known.

Objective: Akinetic mutism (AKM) is an uncommon disorder with a complex neuropathology. There is no generally accepted treatment, and it is not known if late treatments are effective. The relationship between AKM and abulia is uncertain. Methods: The effects of dopaminergic treatment of a patient with chronic AKM after discrete bilateral infarctions of the mesencephalic ventral tegmental area and the lat eral hypothalamus were studied with motor measures, the Functional Independence Measure (FIM), and neuropsychological tests. Results: Treatment with a combination of carbidopa/levodopa and pergolide produced prompt amelioration of AKM with dra matic and rapid improvement in FIM. An apathetic, amotivational state persisted de spite resolution of akinesia and normal frontal executive functions. Conclusions: AKM may respond to dopaminergic treatment even after months of severe akinesia. The mechanism of abulia is more complex than simply a partial dopaminergic deficiency state and may persist even when AKM is treated and frontal cognitive functions are normal. Key Words: Akinetic mutism—Dopamine—Abulia.

There were three primary objectives: to examine the usefulness of the Stroop interference effect as a measure of frontal lobe function; to investigate the possibility of distinct lesion effects for word reading or color naming; and to specifically determine the brain regions necessary for the performance of the incongruent condition. Fifty-one patients with single focal brain lesions in frontal and non-frontal regions and 26 normal control subjects (CTL) were administered the word reading, color naming and incongruent conditions of the Stroop task. Only frontal lesions produced significant impairment. Patients with posterior lesions were not significantly deficient in any condition. Damage to the left dorsolateral frontal lobe resulted in increased errors and slowness in response speed for color naming. Contrary to Perret (Neuropsychology, 1974; 12: 323-330), lesions of the left frontal lobe did not result in a selective interference deficit on the Stroop incongruent condition. Rather, bilateral superior medial frontal damage was associated with increased errors and slowness in response time for the incongruent condition. This result is interpreted as failure of maintenance of consistent activation of the intended response in the incongruent Stroop condition. The results and conclusion are compatible with the prevalent theories of both the Stroop effect and the role of the superior medial frontal regions. The role of the anterior cingulate cortex on performance of the Stroop task is likely related to task and patient context.

The relationship of the Trail Making Test (TMT) to the frontal lobes was tested by comparing patients with damage to the frontal and nonfrontal regions to control participants. Although the analysis of time measurements, both raw and transformed, showed notable slowing of frontal groups, error analysis proved to be a more useful method of categorizing performance. Analysis of errors on Part B indicated that all patients who made more than 1 error had frontal lesions. Dividing the frontal damaged patients into subgroups on the basis of the number of errors yielded specificity of brain-behavior relations within the frontal lobes. Patients with damage in dorsolateral frontal areas were most impaired. Those with inferior medial damage to the frontal lobes were not significantly affected in TMT Part B performance.

Within the broad discipline of psychology, clinical psychology has estab-lished a tradition of providing services in the assessment and treatment ofbehavioral disorders. More recently, clinical neuropsychology emerged inresponse to a need to describe neurocognitive impairment associated withbrain damage and relate deficits to specific forms of brain dysfunction. Asthe field developed, interest in rehabilitation increased and programs aimedat directly improving basic cognitive function began to appear.The most frequent complaints of patients with brain damage are memory

Two patients with pure alexia were studied with tachistoscopically presented stimuli to examine factors influencing their ability to distinguish words from nonwords and to derive semantic information at exposures too brief for explicit letter identification. Both patients had profound right hemianopia and computerized tomography (CT) evidence of splenial destruction. Both patients were successful in making word/nonword decisions for high-frequency, but not low-frequency, words. They could judge semantic class membership reliably for such common categories as animals and vegetables, but not for arbitrarily selected categories, such as office-related items. Judgments about the gender of people's names and place versus person name distinctions were made with high reliability. Results are interpreted as evidence for limited word recognition and semantic-processing capacity in the right hemisphere.

The neurology of frontal lobe disorders can be summarized in descriptions of behavioral problems (apathy, etc.), of cognitive impairments (poor planning, etc.), and of motor deficits (grasp reflex, etc.). Reviews of this sort do not indicate, however, any regional specificity to the deficit profiles or identify any of the component processes of the complex deficits-what exactly is "poor planning"? In this review we present specific steps that assist in overcoming the limitations: (1) identify weaknesses in current understanding, (2) operationally define the processes to be analyzed, (3) review some methodologies that allow parsing of discreet processes into specific frontal regions, (4) review the unique advantages and disadvantages of the various neurological disorders that provide us with subjects for study, and (5) propose approaches to advance further a useful clinical neurology of frontal lobe disorders as well as a more finely grained scientific description of core frontal processes.

A location-based ('select-what, respond-where') priming task was used to examine three measures of selective attention (interference (INT), negative priming (NP), and inhibition of return (IOR)) as a function of focal brain pathology and the complexity of target selection. Control subjects showed different patterns of performance for the three attentional measures as a function of complexity, suggesting some independence among INT, NP, and IOR. Brain-damaged subjects showed significant response slowing, as well as a number of lesion-specific attentional abnormalities. Right frontal (including bifrontal) damage resulted in proportionally increased interference related to task complexity. Left posterior damage increased IOR in the most complex task, while left frontal damage reversed the control pattern of IOR as a function of complexity. Right hemisphere (right posterior and right frontal damage) pathology resulted in a virtual loss of negative priming at all levels of task complexity; left and bifrontal damage resulted in diminished NP only related to increases in the complexity of selection. INT, NP, and IOR are mediated by different brain regions and their expression can be modulated by the complexity of the selection task.

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 …