Objective: To evaluate CSF levels of beta-amyloid((1-42)) (A beta(42)) alone and in combination with CSF tau for distinguishing AD from other conditions Methods: At 10 centers in Europe and the United States, 150 CSF samples from AD patients were analyzed and compared with 100 CSF samples from healthy volunteers or patients with disorders not associated with pathologic conditions of the brain (CON), 84 patients with other neurologic disorders (ND), and 79 patients with non-Alzheimer types of dementia (NAD) Sandwich ELISA techniques were used on site for measuring A beta(42) and tau Results: Median levels of A beta(42) in CSF were significantly lower in AD (487 pg/mL) than in CON (849 pg/mL; p = 0001), ND (643 pg/mL; p = 0001), and NAD (603 pg/mL; p = 0001) Discrimination of AD from CON and ND was significantly improved by the combined assessment of AB,, and tau At 85% sensitivity, specificity of the combined test was 86% (95% CI: 81% to 91%) compared with 55% (95% CI: 47% to 62%) for A beta(42) alone and 65% (95% CI: 58% to 72%) for tau The combined test at 85% sensitivity was 58% (95% CI: 47% to 69%) specific for NAD The APOE e4 gene load was negatively correlated with A beta(42) levels not only in AD but also in NAD Conclusions: The combined measure of CSF A beta(42) and tau meets the requirements for clinical use in discriminating AD from normal aging and specific neurologic disorders

/pdf/improved-discrimination-of-ad-patients-using-beta-amyloid-1-lbru7ce7xs.pdf

Improved discrimination of AD patients using beta-amyloid((1-42)) and tau levels in CSF

This article presents a three-factor anatomical model of human idea generation and creative drive, focusing on interactions between the temporal lobes, frontal lobes, and limbic system. Evidence is drawn from functional imaging, drug studies, and lesion analysis. Temporal lobe changes, as in hypergraphia, often increase idea generation, sometimes at the expense of quality. Frontal lobe deficits may decrease idea generation, in part because of rigid judgments about an idea's worth. These phenomena are clearest in verbal creativity, and roughly parallel the pressured communication of temporal lobe epilepsy, mania, and Wernicke's aphasia-compared to the sparse speech and cognitive inflexibility of depression, Broca's aphasia, and other frontal lobe lesions. The phenomena also shape non-linguistic creativity, as in that of frontotemporal dementia. The appropriate balance between frontal and temporal activity is mediated by mutually inhibitory corticocortical interactions. Mesolimbic dopamine influences novelty seeking and creative drive. Dopamine agonists and antagonists have opposite effects on goal-directed behavior and hallucinations. Creative drive is not identical to skill-the latter depends more on neocortical association areas. However, drive correlates better with successful creative output than skill does. Traditional neuroscientific models of creativity, such as the left brain - right brain hemispheric model, emphasize skills primarily, and stress art and musical skill at the expense of language and mathematics. The three-factor model proposed here predicts findings in a broad range of normal and pathological states and can be tested in many experimental paradigms.

/pdf/frontotemporal-and-dopaminergic-control-of-idea-generation-20p5jpjgly.pdf

Frontotemporal and dopaminergic control of idea generation and creative drive

Since Fisher's detailed observations in the 1960s, the term lacunar infarction has become established in the cerebrovascular literature. To some extent, users of the term implicitly accept the bipartite hypothesis that, among patients with cerebral infarction of diverse cause, there exists, first, a small number of distinct clinical syndromes that are associated with small deep infarcts or lacunes and, second, that these are the result of occlusion of single perforating arteries by characteristic vascular lesions. Several studies have suggested that lacunar infarcts may constitute up to 20% of all cases of cerebral infarction'though less is known about the specificity of the underlying arteriopathy. Despite their relative frequency, there have not been any trials of specific treatments, and furthermore, few treatment trials of cerebral infarction in general have taken this important subgroup into account, perhaps resulting in the inappropriate discarding of therapeutic measures that might benefit other subgroups.To decide whether this is due to some basic flaw in the hypothesis, to inadequate testing, or to poor communication of its clinical implications to other physicians, two questions need to be answered: are the clinically recognizable lacunar syndromes usually caused by lacunes and, if they are, are these lacunes usually caused by a specific disorder of the small perforating arteries at the base of the brain, which differs qualitatively from the more widely studied atheroma of extracranial arteries.

https://www.ahajournals.org/doi/pdf/10.1161/01.STR.19.9.1074

Evolution and testing of the lacunar hypothesis.

Objectives: To study the behavioral and neuroanatomic characteristics of perseverative behavior encountered on a target cancellation task in patients with neglect. Methods: Motor perseverative behavior during line cancellation task was evaluated retrospectively in 60 patients with left hemispatial neglect from right hemispheric stroke. Results: More than 30% of the patients (21 of 60) showed perseveration, manifested as either repetitive cancellation of the same target (18/21) or cancelling extra lines created by the patients themselves (3/21). Neglect severity correlated positively with the frequency of perseverative errors. Perseveration was most prominent in the rightmost portion of the array. Anterior lesions or massive lesions involving anterior and posterior regions were more likely to be associated with motor perseveration than were lesions restricted to posterior areas. Conclusions: Although the mechanism of motor perseveration remains to be elucidated, our findings suggest that the combination of aberrant approach behaviors associated with frontal lobe injury and an attentional or intentional bias toward the rightsided targets might explain the behavior.

Motor perseverative behavior on a line cancellation task.

Neurinoma of the third, fourth, and sixth cranial nerves: a survey and report of a new fourth nerve case.

A new right hemisphere symptom is reported. Five stroke patients with lesions in the perisylvian cortico-subcortical or thalamic region of the right hemisphere produced linguistically correct but semantically loose writing. The behaviour was initiated by subtle prompting and continued semiautomatically. A possible mechanism underlying this hypergraphia is discussed.

https://jnnp.bmj.com/content/jnnp/49/10/1160.full.pdf

Hypergraphia: a right hemisphere syndrome.

• We studied three cases that fit the clinical syndrome of ataxic hemiparesis. Computed tomography revealed small hemorrhages of the posterior limb of the internal capsule in all the cases, and somatosensory evoked potential studies predicted a disturbance of the lemniscal pathway from the thalamus to the parietal sensory cortex without demonstrable sensory loss. These results suggested that ataxia of the contralateral limbs following capsular lesion might result from a disruption of the thalamocortical sensory projection. The site of the lesion, the pathologic cause, and the underlying mechanism of ataxia are not necessarily homogeneous within the syndrome.

Ataxic Hemiparesis From Small Capsular Hemorrhage: Computed Tomography and Somatosensory Evoked Potentials

Disappearance of sleep apnea by traccheal intubation in creutzfeldt-jakob disease

軽症型視床出血24例 (男18例, 女6例, 平均年齢63歳) について, 臨床症状, CTスキャン, 体性感覚誘発電位 (SEPと略) の経時的変化を検討した.平均3ヵ月のfollow upでは, 瞳孔異常や共同偏視などの眼症状, 及び, 触覚, 温痛覚, 振動覚, 関節位置覚などの感覚障害は, 著明な改善を示したが, 測定障害や振戦などの失調症, 及び, 自発痛などの異常感覚は, むしろ発症時にはみられず, 後になって出現するものが多い.SEPは, CTスキャン上, 高吸収域が消失してからも改善しつづけ, P15, N20, P23の順に出現する.患側の回復SEPに関して, P15及びN20成分の潜時は, 健側コントロール群のSEP成分に比べて変らないが, P23成分の潜時は延長している (N20/P23解離), このような視床出血でピーク間潜時の選択的延長を認めた報告はこれまでにはない.

https://www.jstage.jst.go.jp/article/jstroke1979/6/2/6_2_195/_pdf

Yutaka Kudo

Papers

Hypergraphia: a right hemisphere syndrome.

Ataxic Hemiparesis From Small Capsular Hemorrhage: Computed Tomography and Somatosensory Evoked Potentials

Disappearance of sleep apnea by traccheal intubation in creutzfeldt-jakob disease

Recovery of SEP components in thalamic hemorrhages