To understand better which brain regions support emotional empathy.Emotional empathy, the ability to interpret and share the affective states of others, is a key component in human social interaction. Previous research has suggested that emotional empathy relies on several distinct brain regions, although further evidence from human lesion studies is needed to determine which regions are critical.We studied 192 male Vietnam combat veterans who had sustained focal penetrating traumatic brain injuries, and 54 non-brain-injured veterans. We used voxel-based lesion-symptom mapping on computed tomographic scans to elucidate the neural bases of self-reported emotional empathy as measured by the Balanced Emotional Empathy Scale.Damage in several brain regions, particularly the ventrolateral prefrontal cortex, left and right posterior temporal lobes, and insula, was associated with diminished emotional empathy.These findings provide further insight into the neural substrates of emotional empathy, and are consistent with the notion that emotional empathy is supported by a distributed network of brain regions. Additional work may advance our understanding of the empathic deficits commonly observed in patients with neurologic and psychiatric disorders.

Although a role for right hemisphere dysfunction has been hypothesized in Cotard delusion, it remains unclear which functions are disturbed. We report here the first known patient with unilateral right hemisphere lesions and delusions of death (1 of the 2 types of Cotard delusion). This man began to believe that he was dead after suffering a right hemisphere infarction involving the frontal, temporal, and parietal lobes, as well as the thalamus. He had delusions of death in the context of both depersonalization/derealization and delusional misidentifications of people and places. Neuropsychological testing revealed left hemispatial neglect and deficits in general attention. The patient's sense of body ownership and face recognition abilities were preserved. This case suggests that abnormal feelings of familiarity, which have been implicated in several delusional misidentification syndromes, contribute significantly to the development of delusions of death. If this is true, affective processes involved in the identification of people and places and in the feeling of being alive may partially overlap, and these affective processes may be supported by the right hemisphere.

Conceptual apraxia (CA), a feature of Alzheimer disease (AD), can be detected by asking participants to identify the correct tool to act on an object. Assessment can be based on either learned associations (a tool selection test) or the mechanical properties that the tool needs to alter the target object (an alternative tool selection test).We wanted to determine whether knowledge of semantic taxonomic relations (intrinsic properties shared by items) correlated with performance on tests for CA in people with AD or amnestic mild cognitive impairment (aMCI).We tested 10 participants with AD, 12 with aMCI, and 18 healthy older adults for CA using an alternative tool selection test, a tool selection test, and a test of taxonomic relations.The aMCI group did not differ from the control group on the CA tests. The patients with AD were impaired on all tests except tool selection; their performance on the alternative tool selection test correlated significantly with their performance on the taxonomic relations test.The correlation between performances on the alternative tool selection test and the taxonomic relations test in AD suggests a common pathophysiologic substrate, either impairment in accessing conceptual-semantic representations or a degradation of these representations.

Cognitive, emotional, and behavioral characterizations have been reported for patients with a few chromosomal imbalances, but not for patients with a 13q deletion. We report the neuropsychological profile and specific linguistic, visual, spatial, constructional, and behavioral disabilities of a young man with a de novo chromosome 13 deletion (13)(q21.32)(q31.1). Karyotyping at 550 G-band resolution showed that the patient's parents did not share the deletion. According to array-comparative genomic hybridization, the deletion spanned about 14 Mb and included 27 genes. A fluorescence in situ hybridization assay revealed an intact 13q telomere on the partially deleted chromosome. The patient had multiple morphologic and ophthalmologic anomalies. A brain magnetic resonance imaging study did not show gross brain defects. Neuropsychological testing showed an acceptable use of everyday language, but mild mental retardation, executive dysfunction, and very poor performance on visual, visuospatial, and constructional tasks. Establishing a neuropsychological profile for a patient with a specific genetic defect can help clinicians, parents, and teachers work to meet the patient's medical, academic, and behavioral needs.

: Hyposchematia is a rare variant of aschematia in which patients underestimate the size of part or all of their body. The term also describes an abnormality in drawing tasks, in which patients underestimate the size of 1 side of an image and draw it too small. Little is known about the neuroanatomy of the syndrome.: We report 2 patients who developed contralateral hyposchematia without spatial neglect after suffering an ischemic lesion involving the right insula. Both patients felt that the left side of their face and their left arm and leg were disproportionately smaller than their right. On a drawing task, both patients drew the left sides of objects smaller than the right; they perseverated on the left sides of the images, for example, adding extra left-sided petals to a daisy.: In 2 reported patients, the cause of hyposchematia may be a lesion involving multiple insular circuits that affect the perception of extrapersonal space and self-related systems.

We report a longstanding selective memory deficit in a euthyroid 45-year-old woman who was being treated with levothyroxine for Hashimoto thyroiditis. The patient had complained of memory problems and deterioration of her concentration skills for about 2 years. Her endocrinologist thought that she was depressed. The patient's physical examination was normal. She scored a full 30 points on the Mini-Mental State Examination, but neuropsychological evaluation showed a significant deficit in her verbal memory. Routine blood tests and cerebrospinal fluid analysis showed only antithyroid peroxidase antibodies. Brain magnetic resonance imaging was normal. Electroencephalogram showed scarce intermittent bilateral multifocal theta waves. We increased the patient's daily dose of levothyroxine and started her on dexamethasone therapy. Five months later, we repeated the entire evaluation and found both her cognitive function and her electroencephalogram to be normal. Autoimmune encephalopathy associated with Hashimoto thyroiditis is already known to present with either stroke-like episodes or diffuse progressive deterioration. Our patient shows that the encephalopathy can present as a chronic selective memory deficit that can spare executive functions and short-term memory. This presentation can be missed or mistaken for depression, but can be diagnosed with a detailed neuropsychological evaluation.

The Coin-in-the-Hand Test was developed to help clinicians distinguish patients who are neurocognitively impaired from patients who are exaggerating or feigning memory complaints. Previous findings have shown that participants asked to feign memory problems and patients suspected of malingering performed worse on the test than patients with genuine neurocognitive dysfunction.We reviewed the literature on the Coin-in-the-Hand Test and evaluated test performance by 45 hospitalized patients who had dementia with moderately to severely impaired cognition.We analyzed Coin-in-the-Hand Test scores, neuropsychological findings, and other data to determine whether demographic or neurocognitive variables affected Coin-in-the-Hand Test scores. We also calculated base rates of these scores and provided cutoff ranges for clinical use.Coin-in-the-Hand Test scores were independent of neurocognitive functioning, age, education level, and type of dementia. Base rates of scores suggest that a low cutoff can help differentiate between patients with true neurocognitive impairments and those exaggerating or feigning memory complaints.Both the literature and our findings show the Coin-in-the-Hand Test to have potential as a quick and easy screening tool to detect neurocognitive symptom exaggeration. This test could effectively supplement commonly used neurocognitive screens such as the Mini-Mental State Examination, the Saint Louis University Mental Status Examination, and the Montreal Cognitive Assessment.

Ecstasy/polydrug users have exhibited deficits in executive functioning in laboratory tests. We sought to extend these findings by investigating the extent to which ecstasy/polydrug users manifest executive deficits in everyday life.Forty-two current ecstasy/polydrug users, 18 previous (abstinent for at least 6 months) ecstasy/polydrug users, and 50 non-users of ecstasy (including both non-users of any illicit drug and some cannabis-only users) completed the self-report Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A) measure.Current ecstasy/polydrug users performed significantly worse than previous users and non-users on subscales measuring inhibition, self-monitoring, initiating action, working memory, planning, monitoring ongoing task performance, and organizational ability. Previous ecstasy/polydrug users did not differ significantly from non-users. In regression analyses, although the current frequency of ecstasy use accounted for statistically significant unique variance on 3 of the 9 BRIEF-A subscales, daily cigarette consumption was the main predictor in 6 of the subscales.Current ecstasy/polydrug users report more executive dysfunction than do previous users and non-users. This finding appears to relate to some aspect of ongoing ecstasy use and seems largely unrelated to the use of other illicit drugs. An unexpected finding was the association of current nicotine consumption with executive dysfunction.

To determine whether treatment with memantine plus vitamin D is more effective than memantine or vitamin D alone in improving cognition among patients with Alzheimer disease (AD).We studied 43 white outpatients (mean 84.7 ± 6.3 years; 65.1% women) with a new diagnosis of AD, who had not taken anti-dementia drugs or vitamin D supplements. We prescribed memantine alone (n = 18), vitamin D alone (n = 17), or memantine plus vitamin D (n = 8) for an average of 6 months. We assessed cognitive change with the Mini-Mental State Examination (MMSE). We used age, sex, pre-treatment MMSE score, and duration of treatment as covariables.Before treatment, the 3 groups had comparable MMSE scores. At 6 months, participants taking memantine plus vitamin D increased their MMSE score by 4.0 ± 3.7 points (P = 0.034), while participants taking memantine alone remained stable (change of 0.0 ± 1.8 points; P = 0.891), as did those taking vitamin D alone (-0.6 ± 3.1 points; P = 0.504). Treatment with memantine plus vitamin D was associated with improvement in the MMSE score compared to memantine or vitamin D alone after adjustment for covariables (P < 0.01). Mixed regression analysis showed that the visit by combined treatments (memantine plus vitamin D) interaction was significant (P = 0.001), while memantine or vitamin D alone showed no effect.Patients with AD who took memantine plus vitamin D for 6 months had a statistically and clinically relevant gain in cognition, underlining possible synergistic and potentiating benefits of the combination.

To determine whether side and type of initial motor symptoms in Parkinson disease (PD) predict risk for later development of cognitive impairment or depressive symptoms.We recruited 124 non-demented patients with PD to participate in a cohort study of cognitive function and depressive symptoms that used validated neuropsychological tests and a depressive symptom inventory. We first reviewed the patients' charts to determine their initial motor symptom and side of onset, and then classified the patients into 4 groups: right-sided onset tremor, right-sided onset bradykinesia/rigidity, left-sided onset tremor, and left-sided onset bradykinesia/rigidity. We excluded patients with bilateral symptom onset. We used analysis of variance on neuropsychological test performance and depressive symptoms to determine whether group classification affected risk of cognitive impairment or depressive symptoms. We controlled our analyses for disease duration and motor severity as measured by the Unified Parkinson Disease Rating Scale Part III motor score.There were no differences in any cognitive measure by side and type of initial motor symptoms. The right-sided onset tremor group had the lowest depressive symptom scores, and no patient in any group reported severe depressive symptoms.Our findings suggest that patterns of nigral cell loss correlating to the initial side and type of motor symptoms in PD are not related to the risk of later cognitive impairment. By contrast, patients with right-sided onset of tremor seem to have a lower risk of depressive symptoms than patients with other presentations.