Recovery from aphasia in the first year after stroke.

Most individuals who experience aphasia after a stroke recover to some extent, with the majority of gains taking place in the first year. The nature and time course of this recovery process is only partially understood, especially its dependence on lesion location and extent, which are the most important determinants of outcome. The aim of this study was to provide a comprehensive description of patterns of recovery from aphasia in the first year after stroke. We recruited 334 patients with acute left hemisphere supratentorial ischaemic or haemorrhagic stroke and evaluated their speech and language function within 5 days using the Quick Aphasia Battery (QAB). At this initial time point, 218 patients presented with aphasia. Individuals with aphasia were followed longitudinally, with follow-up evaluations of speech and language at 1 month, 3 months, and 1 year post-stroke, wherever possible. Lesions were manually delineated based on acute clinical MRI or CT imaging. Patients with and without aphasia were divided into 13 groups of individuals with similar, commonly occurring patterns of brain damage. Trajectories of recovery were then investigated as a function of group (i.e. lesion location and extent) and speech/language domain (overall language function, word comprehension, sentence comprehension, word finding, grammatical construction, phonological encoding, speech motor programming, speech motor execution, and reading). We found that aphasia is dynamic, multidimensional, and gradated, with little explanatory role for aphasia subtypes or binary concepts such as fluency. Patients with circumscribed frontal lesions recovered well, consistent with some previous observations. More surprisingly, most patients with larger frontal lesions extending into the parietal or temporal lobes also recovered well, as did patients with relatively circumscribed temporal, temporoparietal, or parietal lesions. Persistent moderate or severe deficits were common only in patients with extensive damage throughout the middle cerebral artery distribution or extensive temporoparietal damage. There were striking differences between speech/language domains in their rates of recovery and relationships to overall language function, suggesting that specific domains differ in the extent to which they are redundantly represented throughout the language network, as opposed to depending on specialized cortical substrates. Our findings have an immediate clinical application in that they will enable clinicians to estimate the likely course of recovery for individual patients, as well as the uncertainty of these predictions, based on acutely observable neurological factors.

Commentary on "Consciousness as a Memory System" by Budson, Richman, and Kensinger (2022).

Consciouness is a phenomenon that has eluded explanation by generations of physicians and scientists. Many discussions, experiments, and theories about consciousness have been published, but none has adequately explained the phenomenon. In the previous issue, Budson and colleagues (2022) present a theory of consciousness based on explicit memory processes, with consciousness developing in the context of memory function. In the authors' view, consciousness accompanying other cortical processes such as language or visual-spatial function developed only later in evolution. The evidence presented for this evolutionary sequence, however, is very limited. Furthermore, no discussion is directed toward the theory that consciousness involves the intersection between external perceptions and internal bodily states. The authors also develop the concept that most of our actions, and even our personality, are conscious only after the fact; immediate decisions are taken by the unconscious mind-the "horse" rather than the "rider." There is empirical evidence that rapid decisions and responses occur before they become conscious. However, Budson and colleagues (2022) extend the concept of unconscious decision-making to virtually all actions; in so doing, not only do they minimize the phenomenon of self-conscious awareness, but their theory has disturbing ethical implications for personal responsibility, criminal law, free will, and personality.

Transient Global Amnesia: Commentary on Trip Gabriel's First-Person Account.

This paper comments on a companion article, a first-person account of an episode of transient global amnesia written by New York Times reporter Trip Gabriel (Gabriel T. 2017. Cogn Behav Neurol. 30:1-4). Mr Gabriel describes having no memories of a cold, rainy day that he had spent on a sailboat competing in two races. The episode may have been triggered by his exposure to water. Afterward, the skipper recalled that Mr Gabriel had functioned fine on the boat, although after returning to shore he needed help finding his car. When he told his wife over the phone that he could not remember where he lived, she got him home and to the hospital. The staff excluded stroke and other causes of amnesia. He felt some awareness after about 9 hours, and the episode ended after about 23 hours. He has been left with a permanent memory gap of 12 hours.The commentary on the case outlines the state of knowledge about transient global amnesia. The diagnosis is well established: a witnessed sudden-onset retrograde and anterograde amnesia lasting <24 hours in a fully conscious person who knows who he/she is and has no other cause for amnesia. Triggers include exposure to water, stress, and sexual intercourse. A normal magnetic resonance imaging scan can help with the often challenging differential diagnosis. Apart from the gap in memory, patients recover fully and only 15% to 20% have recurrences. The underlying pathophysiology has not been explained.

The Inflammatory Form of Cerebral Amyloid Angiopathy or "Cerebral Amyloid Angiopathy-Related Inflammation" (CAARI).

Cerebral amyloid angiopathy-related inflammation (CAARI) is a recently recognized syndrome of reversible encephalopathy seen in a subset of patients with cerebral amyloid angiopathy (CAA). CAA is a disorder of the elderly in which amyloid peptides are deposited in the walls of cerebral arteries, leading to microhemorrhages, macrohemorrhages, and eventually dementia. In a few cases, the amyloid deposition is accompanied by inflammation or edema. The clinical syndrome of CAARI is distinguished by subacute neurobehavioral symptoms, headaches, seizures, and stroke-like signs, contrasting the acute intracranial hemorrhage typically seen in CAA. Magnetic resonance imaging findings may be symmetric or asymmetric and involve patchy or confluent T2 hyperintense lesions in the cortex and subcortical white matter. Recent diagnostic criteria have been proposed which help distinguish CAARI from alternative diagnoses. Improvement has been reported in most cases with immunosuppression, although a few cases have had recurrent symptoms. Here, we review the clinical and radiologic features of CAARI and compare these with CAA.

ADHD drugs and serious cardiovascular events in children and young adults.

BACKGROUND: Adverse-event reports from North America have raised concern that the use of drugs for attention deficit-hyperactivity disorder (ADHD) increases the risk of serious cardiovascular events. METHODS: We conducted a retrospective cohort study with automated data from four health plans (Tennessee Medicaid, Washington State Medicaid, Kaiser Permanente California, and OptumInsight Epidemiology), with 1,200,438 children and young adults between the ages of 2 and 24 years and 2,579,104 person-years of follow-up, including 373,667 person-years of current use of ADHD drugs. We identified serious cardiovascular events (sudden cardiac death, acute myocardial infarction, and stroke) from health-plan data and vital records, with end points validated by medical-record review. We estimated the relative risk of end points among current users, as compared with nonusers, with hazard ratios from Cox regression models. RESULTS: Cohort members had 81 serious cardiovascular events (3.1 per 100,000 person-years). Current users of ADHD drugs were not at increased risk for serious cardiovascular events (adjusted hazard ratio, 0.75; 95% confidence interval [CI], 0.31 to 1.85). Risk was not increased for any of the individual end points, or for current users as compared with former users (adjusted hazard ratio, 0.70; 95% CI, 0.29 to 1.72). Alternative analyses addressing several study assumptions also showed no significant association between the use of an ADHD drug and the risk of a study end point. CONCLUSIONS: This large study showed no evidence that current use of an ADHD drug was associated with an increased risk of serious cardiovascular events, although the upper limit of the 95% confidence interval indicated that a doubling of the risk could not be ruled out. However, the absolute magnitude of such an increased risk would be low. (Funded by the Agency for Healthcare Research and Quality and the Food and Drug Administration.).

Hashimoto's encephalopathy: a brief review.

Hashimoto's encephalopathy (HE) is a syndrome of altered mental status, hallucinations, delusional thinking, and often, epileptic seizures. It is diagnosed by the clinical syndrome, the presence of elevated titers of antithyroid antibodies, the lack of another diagnosis based on clinical evaluation, and the response to corticosteroid and other immunosuppressant treatment. This review discusses the symptoms, pathophysiology, and treatment of HE. The disorder is important to recognize because aggressive treatment may bring about a favorable clinical outcome. The disorder has a relatively benign prognosis, compared with many of the entities for which it can be mistaken.

Multivariate lesion symptom mapping for predicting trajectories of recovery from aphasia.

Individuals with post-stroke aphasia tend to recover their language to some extent; however, it remains challenging to reliably predict the nature and extent of recovery that will occur in the long term. The aim of this study was to quantitatively predict language outcomes in the first year of recovery from aphasia across multiple domains of language and at multiple timepoints post-stroke. We recruited 217 patients with aphasia following acute left hemisphere ischaemic or haemorrhagic stroke and evaluated their speech and language function using the Quick Aphasia Battery acutely and then acquired longitudinal follow-up data at up to three timepoints post-stroke: 1 month (n = 102), 3 months (n = 98) and 1 year (n = 74). We used support vector regression to predict language outcomes at each timepoint using acute clinical imaging data, demographic variables and initial aphasia severity as input. We found that ∼60% of the variance in long-term (1 year) aphasia severity could be predicted using these models, with detailed information about lesion location importantly contributing to these predictions. Predictions at the 1- and 3-month timepoints were somewhat less accurate based on lesion location alone, but reached comparable accuracy to predictions at the 1-year timepoint when initial aphasia severity was included in the models. Specific subdomains of language besides overall severity were predicted with varying but often similar degrees of accuracy. Our findings demonstrate the feasibility of using support vector regression models with leave-one-out cross-validation to make personalized predictions about long-term recovery from aphasia and provide a valuable neuroanatomical baseline upon which to build future models incorporating information beyond neuroanatomical and demographic predictors.

Determination of mental competency, a neurological perspective.

This article discusses the evaluation of the capacity of a person to make informed decisions about financial matters, independent living, and informed consent for medical treatment and research. Determination of capacity is a function for which most physicians have little training. The determination of competency for a general medical patient may be assessed by a combination of a bedside mental status examination such as the MMSE and a questionnaire such as the Aid To Capacity Evaluation (ACE 1999). For patients with focal neurological deficits such as aphasia, further evaluation of specific cognitive and language functions is needed; Alexander (Arch Neurol 45:23-6, 1988) suggested 7 specific functions to be assessed. Finally, in dementing illnesses, evaluation by the MMSE and a questionnaire such as the CCTI, or Capacity to Consent to Treatment Instrument (Marson et al. Arch Neurol 52:949-54, 1995) is needed. Dementia includes several separate syndromes of neurodegenerative disease, and in many of these conditions, focal deficits such as aphasia may necessitate a more thorough neuropsychological evaluation.

Primary progressive aphasia and Alzheimer's disease: brief history, recent evidence.

Primary progressive aphasia (PPA) has been recognized as a syndrome distinct from the usual pattern of language deterioration in Alzheimer's disease and typically more related to the pathology of frontotemporal dementia (FTD). In recent years, however, the syndromes of primary progressive aphasia have become more complex, divided into the three subtypes of progressive nonfluent aphasia (PNFA), semantic dementia (SD), and logopenic/phonological progressive aphasia (LPA). These syndromes have not only made the linguistic analysis more complex, but the associated pathologies have also become more variable. In particular, PNFA is usually, but not always, associated with FTD pathology and often evidence of a tau mutation, but rarely AD; SD is usually associated with FTD of the ubiquitin staining or progranulin (TAR-DNA) mutation type, but, again, occasionally AD; LPA is typically associated with AD pathology. Patterns of atrophy on magnetic resonance imaging (MRI) generally conform to these subtypes, with PNFA associated with left frontal and insular atophy, SD associated with bilateral temporal atrophy, and LPA associated with L superior-posterior temporal and parietal atrophy. These patterns can also be seen on positron emission (PET) scanning with fluorodeoxyglucose. The newer amyloid binding ligand PET technologies are less useful for detecting regional atrophy patterns but more useful for indication of the underlying pathology. We can thus speak of syndromes of PPA or underlying pathological bases of PPA.

Transient global amnesia: a brief review and update.

Transient global amnesia (TGA) is a transitory syndrome of memory loss, lasting less than 24 h. Although there are many known causes of transient amnesia, the syndrome of TGA remains of unknown etiology. Known causes of transient amnesia, theories of pathogenesis of TGA, and recommended evaluation and treatment are discussed.