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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.

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.

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.

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.

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.

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

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 …

We examined the hypothesis that, on verbal fluency, clustering (i.e. generating words within subcategories) is related to temporal-lobe functioning, whereas switching (i.e. shifting between subcategories) is related to frontal-lobe functioning. Tests of phonemic and semantic fluency were administered to 53 patients with focal frontal-lobe lesions (FL), 23 patients with unilateral temporal-lobe lesions (TL) and 55 matched controls. Performance by FL patients was consistent with our hypothesis: in comparison to controls, patients with left-dorsolateral or superior-medial frontal lesions switched less frequently and produced normal cluster sizes on both phonemic and semantic fluency. Performance by TL patients was not consistent across fluency tasks and provided partial support for our hypothesis. On phonemic fluency, TL patients were unimpaired on both switching and clustering. On semantic fluency, TL patients were impaired on switching in comparison to controls and left TL patients produced smaller clusters than right TL patients. The best indices for discriminating the patient groups, therefore, were phonemic-fluency switching (impaired only with frontal lesions) and semantic-fluency clustering (impaired only with temporal-lobe lesions).

To characterize the frequency of recovery of arm paresis in patients with traumatic brain injury (TBI) admitted to rehabilitation.Retrospective review identifying a cohort of patients with moderate or severe arm paresis after TBI followed at least 6 months postinjury.Freestanding acute rehabilitation hospital TBI unit.Forty-four patients with moderate to severe arm paresis were selected from 264 consecutive admissions and characterized by injury pathology subtype, injury severity (duration of unconsciousness [loss of consciousness, LOC] and posttraumatic amnesia [PTA]), age, and level of paresis according to Brunnstrom Stages of Recovery (BS 1 to 6). Patient groups with and without arm paresis were compared according to these variables (t tests and chi(2)).Recovery of arm paresis to isolated motor function (BS 5 or 6) and time to achieve recovery. Recovered and nonrecovered patients were compared (Mann-Whitney, t tests, and chi(2)) on injury severity, initial level of paresis, age, time to rehabilitation admission, and pathology subtype. Time to recovery was compared for patients at different levels of initial paresis, ranges of LOC, and pathology subtypes (Mann-Whitney and Kruskal-Wallis tests).Forty-four patients (17%) had moderate (BS 3 to 4) or severe (BS 1 to 2) paresis at rehabilitation admission. They were more severely injured than nonparetic patients based on longer LOC (p.002) and PTA (p.009). Thirty-six patients (82%) recovered by 6 months; 72% of these recovered by 2 months. If still paretic at 2 months, only 56% recovered. Mean recovery time was 6.9 weeks (SD, 6.1) from injury. Time to recovery was best predicted by initial level of paresis and injury severity (r2 = .48), but not age. Patients with diffuse injury tended towards a more protracted recovery (7.9 weeks, SD 6.5) than patients with focal injury (4.2 weeks, SD 3.9) (p = .08) and only those with diffuse injury showed further recovery after 3 months.Arm paresis after TBI is relatively infrequent. Most patients recover by 2 months but later recovery is possible, especially in patients with primarily diffuse brain damage. Recovery is highly related to initial impairment, injury severity, and distribution of brain injury.

Anomalous lateralization of cognitive functions is observed in a small percentage of right-handed patients with unilateral brain damage, either crossed aphasia (aphasia after right brain damage) or “crossed nonaphasia” (left brain damage without aphasia but with visuospatial and other deficits typical of right brain damage). No comprehensive theory of these anomalous cases has been proposed. Nine new right-handed cases (plus one left-handed case) were analyzed and the literature was reviewed. The dramatically anomalous organization of cognitive functions is best explained by random lateralization of all cognitive functions in a small subset of the population. The RS theory of cerebral dominance can account for this pattern of anomalies in right-handers and may account for the most common patterns of dominance observed in left-handers.

In the current study, we investigated whether standard assessment techniques of visuospatial neglect are sensitive to detecting dissociable subtypes. We administered a battery of tasks commonly used to detect the presence of visuospatial neglect to 120 patients with unilateral right hemisphere infarcts and, in most cases, performed a systematic analysis of their lesions to quantify and localize brain damage. Using a factor analysis, we discovered seven relatively independent constructs, three of which were specifically related to the presence of left hemispatial neglect: Left Attentional Processing, Line Bisection. and Word Reading. Impairments in two of these factors. Left Attentional Processing and Line Bisection, occurred together in most cases but also occurred independently in 38 cases. There were no cases in whom Word Reading was present without concomitant deficits in one or the other two factors. These three factors could not be distinguished neuroanatomically; that is, lesions were equally likely in the temporal/parietal cortex, dorsolateral frontal cortex, or in deep frontal structures. These data confirm the notion that hemispatial neglect is a complex and multifaceted disorder composed of cognitively independent processes. These processes, however, cannot be dissociated neuroanatomically based on currently available assessment techniques. (JINS, 1996, 2, 441–451.)

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

This study compared the post-CVA speech of a patient presenting with the foreign accent syndrome (FAS) to both a premorbid baseline for that patient and to similarly analyzed data from an earlier reported case of FAS. The object of this research was to provide quantitative acoustic data to determine whether: (1) the constellation of phonetic features associated with FAS is the same across patients and (2) a common neural mechanism underlies FAS. Acoustic parameters investigated included features of consonant production (voicing, place and manner of articulation), vowel production (formant frequency and duration), and prosody. Results supported the characterization of FAS patients as having a “generic” foreign accent and the hypothesis that FAS deficits are qualitatively different from that of Broca's aphasia. However, comparison of this case with recent studies revealed the extent to which the constellation of phonetic features may vary among FAS patients, challenging the notion that a general prosodic disturbance is the sole underlying mechanism in FAS.

Word production was examined in four aphasics diagnosed acutely with neologistic jargon and who displayed impairment to the lexical stage of phonological production (Kohn & Smith, 1993, 1994a). To investigate the major source of their nonword errors (i.e., neologisms, phonemic paraphasias), single word production was tested at three different times over the first 6 months postonset, with one subject receiving additional testing at 14 months postonset. Two subjects showed signs of recovery to the phonological output system with respect to: (1) improved word production scores, (2) increased frequency of phonemic paraphasias versus neologisms, and (3) increased production of target phonemes. These subjects also displayed above-chance production of target phonemes and no significant tendency to perseverate phonemes across picture-naming trials. It was argued that this pattern reflects a resolving disturbance in retrieving entries from the phonological lexicon. The other two subjects showed no improvement in word production. They also consistently produced target phonemes at chance levels and had a tendency to perseverate phonemes across picture-naming trials. This static pattern of performance was considered to reflect loss of information from the phonological lexicon. The neuroanatomical damage sustained by each case was consistent with these two recovery patterns.

To demonstrate that the prognosis for patients with traumatic brain injury (TBI) admitted to rehabilitation can be established with use of principled neurologic diagnosis and predictor variables of established value in neurosurgical populations.A cohort of patients with TBI accumulated at rehabilitation admission were followed up for 1 year. Severity measures (Glasgow Coma Scale score, length of coma, and duration of posttraumatic amnesia) and information to generate neuropathologic profiles were gathered retrospectively and prospectively; outcome measures were obtained prospectively.The TBI rehabilitation unit in a freestanding rehabilitation hospital.A consecutive sample of 243 patients with TBI admitted to a rehabilitation unit (age range, 8 through 89 years).Functional outcome measured by the Glasgow Outcome Scale at 6 and 12 months after injury.Posttraumatic amnesia had a clear, predictable relationship to length of coma in patients with diffuse axonal injury (R2 = .58, P.0001). Severity measures, particularly duration of posttraumatic amnesia, correlated with the Glasgow Outcome Scale score at 6 and 12 months after injury (R2 = .45, P.0001, R2 = .48, P.0001), strongly in patients with diffuse axonal injury but poorly in patients with primarily focal brain injury. Age was an important factor in recovery, beginning at age 40 years; older patients had significantly longer posttraumatic amnesia and worse functional outcome at any severity.The early course of recovery and functional outcome in TBI can be characterized in neurorehabilitation populations and is highly dependent on specific neuropathologic diagnosis, severity, and age. Predictions that employ traditional measures of severity are most relevant in patients with diffuse axonal injury. Age has a potent, complex effect on recovery, particularly beyond age 40 years.

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

An anterior disconnection syndrome was first described over 100 years ago by Liepmann and Maas1 and brought back to clinical awareness 50 years ago by Geschwind and Kaplan.2 Damage to the corpus callosum has been confirmed by postmortem analysis but precise anatomic along with its functional characterization has not been accomplished. We report a patient with the anterior disconnection syndrome after stroke. Diffusion tensor imaging (DTI) tractography and transcallosal neurophysiologic recordings confirmed the exact transcallosal disconnection.

A total of 20 stroke patients received acupuncture, including 10 chronic and 10 acute patients; 19 of the 20 patients (95%) could be correctly classified regarding beneficial response to acupuncture, versus poor response, based on CT scan lesion site data, alone. Patients with beneficial response had damage to less than half of the motor pathway areas on CT scan, especially in the periventricular white matter area (PVWM) at the level of the body of the lateral ventricle. Overall, 8 of the 20 patients receiving acupuncture had beneficial response with measurable objective improvement in motor function, including 3 of the 10 chronic patients treated at > 3 months poststroke, and 5 of the 10 acute patients treated at < 3 months poststroke. Among the 8 patients with beneficial response, significant improvements were observed in knee flexion, knee extension, and shoulder abduction. Neither age, nor months poststroke when acupuncture was begun, was significantly correlated with the total number of improved tests, post-acupuncture. Two chronic patients with beneficial response first began receiving acupuncture at 3 years and 6 years poststroke. Most improvements were sustained for at least 4 months after the last acupuncture treatment.

The nature of residual cognitive deficits after out of hospital cardiac arrest (OHCA) is incompletely described and has never been defined against a cardiac control (CC) group. The objective of this study is to examine neuropsychological outcomes 3 months after OHCA in patients in a “middle range” of acute severity. Thirty prospective OHCA admissions with coma >1 day and responsive but confused at 1 week, and 30 non-OHCA coronary care admissions were administered standard tests in five cognitive domains. OHCA subjects fell into two deficit profiles. One group (N= 20) had mild memory deficits and borderline psychomotor deficits compared to the CC group; 40% had returned to work. The other group (N= 10) had severe impairments in all domains. Coma duration was associated with group. Neither group had a high prevalence of depression. For most patients within the “middle range” of acute severity of OHCA, cognitive and functional outcomes at 3 months were encouraging. (JINS, 2011,17, 364–368)

Impairment on verbal fluency tasks has been one of the more consistently reported neuropsychological findings after cerebellar lesions, but it has not been uniformly observed and the possible underlying cognitive basis has not been investigated. We tested twenty-two patients with chronic, unilateral cerebellar lesions (12 Left, 10 Right) and thirty controls on phonemic and semantic fluency tasks. We measured total words produced, words produced in the initial 15 seconds, errors and strategy switches. In the phonemic fluency task, the right cerebellar lesion (RC) group produced significantly fewer words compared to the left cerebellar lesion (LC) group and healthy controls, particularly over the first 15 seconds of the task with no increase in errors and significantly fewer switches over the entire task. In the semantic fluency task there was only a modest decrease in total words in the RC group compared to controls. RC lesions impair fluency with many of the same performance characteristics as left prefrontal lesions. This supports the hypotheses of a prefrontal-lateral cerebellar system for modulation of attention/executive or strategy demanding tasks.

Introduction It has been asserted that damage to the cerebellum produces a specific pattern of cognitive deficits, but clinical studies have had ambiguous results. There remains particular uncertainty about the effects of focal cerebellar injuries on cognition in adults. Clinical reports and anatomical connectivity studies have suggested a possible functional convergence of frontal lobes and cerebellum. This investigation was designed to assess whether focal cerebellar injuries in adults would cause impairment on tasks previously demonstrated to be sensitive to prefrontal lesions. Method We investigated this question in 32 adults with either stroke or resection of benign tumours and 36 healthy control subjects. Patients underwent standard and experimental cognitive testing and an assessment of general health and well-being at least 3 months post onset. Results The group with right cerebellar lesions had lower performance on some tests of response control and verbal fluency than the controls and also the patients with left cerebellar lesions. On most tests, including most of the experimental tests sensitive to prefrontal lesions, the patients had no significant difference from the controls. The patient groups reported no health or functional decline. Conclusions These results and the bulk of the clinical literature suggest that damage to some cerebellar sites may have specific cognitive consequences, but the cognitive impairment after focal cerebellar injury in adults is mild or transient. After the acute epoch, demonstration of deficits may require more demanding probes of specific domains of cognition.

Background and Purpose— Previous studies have shown motor impairment after a stroke relates to lesion size and location, but unexplained variability in recovery still exists. In this study, we used lesion-mapping techniques in combination with diffusion tensor imaging to quantitatively test the hypothesis that motor recovery in patients with chronic stroke is inversely related to the proportion of the corticospinal tract (CST) affected by the lesion. Methods— We studied 50 patients with chronic stroke, all of whom presented with moderate to severe motor impairments in the acute stage, using high-resolution anatomic MRI. We evaluated the degree of motor impairment with the Upper Extremity module of the Fugl-Meyer Assessment. To analyze the relationship between CST damage and impairment scores, we calculated a CST-lesion load for each patient by overlaying the patient’s lesion map with a probabilistic tract derived from diffusion tensor images of age-matched healthy subjects. Results— CST-lesion load was a significant predictor of motor deficit. Infarct size, despite correlating with motor scores, did not significantly predict impairment. Conclusions— Our results show the degree of functional motor deficit after a stroke is highly dependent on the overlap of the lesion with the CST and not lesion size per se. In the future, automated calculation of CST-lesion load may allow more precise prediction of motor impairment after stroke.

Phonological agraphia is a neurolinguistically specific profile of spelling impairment. It is characterized by an impairment in spelling pronounceable pseudowords (‘sild’) and by an impairment in spelling real words related to their familiarity, length, and often, part of speech (Shallice, 1981 ; Roeltgen, 1985 ; Bub & Chertkow, 1988) . We report two cases of phonological agraphia, each with a different lesion profile. Analysis of the small number of published cases that include lesion data, plus our own cases, suggests that phonological agraphia can be produced by lesions in a wide range of perisylvian cortical regions that have in common some role in central phonological processes.

Outcome studies from post-acute cognitive rehabilitation programmes vary widely and mostly emphasize changes in neuropsychological measures. More recently, the functional outcomes of patients following cognitive rehabilitation have been reported. This study describes the functional outcomes of 42 traumatically brain-injured patients (29 male, 13 female: average age 28.6 years, time post-injury 50.3 months) following treatment in a structured out-patient post-acute cognitive rehabilitation programme. The programme consisted of a minimum of 6 weeks of treatment and emphasized improvement of the patients' real-life functional abilities and psychological support. The treatment goals were individually established for each patient. Patient improvement was determined by the accomplishment of treatment goals and differences in pre- and post-treatment functional measures and speech pathology cognitive measures. Follow-up at 6, 12 and 18 months determined the maintenance of treatment effects. There was a significant improvement on patients' functional measures after treatment. Cognitive measures were not significantly different after treatment, but there was a trend towards improvement. Functional improvements were independent of age, neuropathological category, injury severity and time post-injury. It is concluded that post-acute traumatic brain injury treatment aimed at retraining real-life functional abilities exclusive of specific cognitive remediation can lead to long-term improvements in independence.

We evaluated whether prior semantic knowledge would enhance episodic learning in amnesia. Subjects studied prices that are either congruent or incongruent with prior price knowledge for grocery and household items and then performed a forced-choice recognition test for the studied prices. Consistent with a previous report, healthy controls' performance was enhanced by price knowledge congruency; however, only a subset of amnesic patients experienced the same benefit. Whereas patients with relatively intact semantic systems, as measured by an anatomical measure (i.e., lesion involvement of anterior and lateral temporal lobes), experienced a significant congruency benefit, patients with compromised semantic systems did not experience a congruency benefit. Our findings suggest that when prior knowledge structures are intact, they can support acquisition of new episodic information by providing frameworks into which such information can be incorporated.

That the left prefrontal cortex has a critical role setting response criteria for numerous tasks has been well established, but gaps remain in our understanding of the brain mechanisms of task-setting. We aimed at (i) testing the involvement of this region in setting the criteria for a non-response and (ii) assessing functional connectivity between this and other brain regions involved in task-setting. Fourteen young participants performed a go/nogo task during functional magnetic resonance imaging. The task included two nogo visual stimuli which elicit a high (distractor) or a low (other) tendency to respond, respectively. Two task blocks were examined to assess learning the criteria. First, a multivariate Partial Least Squares (PLS) analysis identified brain regions that co-varied with task conditions, as expressed by two significant Latent Variables (LVs). One LV distinguished go and nogo stimuli. The other LV identified regions involved in the first block when the criteria not to respond to distractors were established. The left prefrontal region was prominently involved. Second, a left ventrolateral prefrontal area was selected from this LV as a seed region to perform functional connectivity using a multi-block PLS analysis. Results showed a distributed network functionally connected with the seed, including superior medial prefrontal and left superior parietal regions. These findings extend our understanding of task-setting along the following dimensions: 1) even when a task requires withholding a response, the left prefrontal cortex has a critical role in setting criteria, and 2) this region responds to the task demands within a distinctive functional network.

Memory impairments are common after stroke, and the anatomical basis for impairments may be quite variable. To determine the range of stroke-related memory impairment, we identified all case reports and group studies through the Medline database and the Science Citation Index. There is no hypothesis about memory that is unique to stroke, but there are several important facets of memory impairment after stroke: (1) Every node of the limbic system implicated in memory may be damaged by stroke but very rarely in isolation and the combination of amnesia with the associated deficits often illuminates additional aspects of memory functions. (2) Stroke produces amnesia by damage to critical convergence white matter connections of the limbic system, and stroke is the only etiology of amnesia that can delineate the entire pathway of memory and critical convergence points. (3) Stroke also impairs memory, without causing classical amnesia, by damaging brain regions responsible for cognitive processes, some modality specific and some more generally strategic, that are essential for normal learning and recall.

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.

The role of the frontal lobes has often been described as a ‘paradox’ or a ‘riddle’. Ascribed to this region has been the loftiest of functions (e.g. executive; seat of wisdom); others contested that the frontal lobes played no special role. There has also been controversy about the unity or diversity of functions related to the frontal lobes. Based on the analysis of the effects of lesions of the frontal lobes, we propose that there are discrete categories of functions within the frontal lobes, of which ‘executive’ functioning is one. Within the executive category, the data do not support the concept of an undifferentiated central executive/supervisory system. The results are better explained as impairments in a collection of anatomically and functionally independent but interrelated attentional control processes. Evidence for three separate frontal attentional processes is presented. For each process, we present an operational description, the data supporting the distinctiveness of each process and the evidence for impairments of each process after lesions in specific frontal regions. These processes and their coarse frontal localizations are energization — superior medial , task setting — left lateral and monitoring — right lateral . The strength of the findings lies in replication: across different tasks; across different cognitive modalities (e.g. reaction time paradigms, memory); and across different patient groups. This convergence minimizes the possibility that any of the findings are limited to a specific task or to a specific set of patients. Although distinct, these processes are flexibly assembled in response to context, complexity and intention over real time into different networks within the frontal regions and between frontal and posterior regions.

PUBLISHED, This study provides an introduction to, and overview of, several papers that resulted from a randomized control trial that evaluated a new cognitive rehabilitation protocol. The program was designed to improve general strategic abilities in ways that would be expressed in a broad range of functional domains. The trial, which was conducted on a sample of older adults who had experienced normal age-related cognitive decline, assessed performance in the following domains: memory, goal management, and psychosocial status. The general rationale for the trial, the overall experimental design, and the approach to statistical analyses that are relevant to each paper are described here. The results for each functional domain are reported in separate papers in this series (JINS, 2007, 13, 120?131.)