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Chronic fatigue syndrome (CFS) patients and controls were compared on a variety of mood state, personality, and neuropsychological measures, including memory, word finding, and attentional tasks that required participants to focus, sustain, or divide their attention, or to perform a combination of these functions. CFS patients demonstrated a selective deficit on 3 measures of divided attention. Their performance on the other neuropsychological tests of intelligence, fluency, and memory was no different than that of normal controls despite their reports of generally diminished cognitive capacity. There was an inverse relation between CFS patient fatigue severity and performance on 1 of the divided attention measures. Given these findings, it is probable that CFS patients will report more cognitive difficulties in real-life situations that cause them to divide their effort or rapidly reallocate cognitive resources between 2 response channels (vision and audition).

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OBJECTIVE: To describe ideomotor apraxia in patients with corticobasal degeneration and those with progressive supranuclear palsy, two parkinsonian disorders that are often misdiagnosed due to the overlap in their clinical features, and to determine whether systematic apraxia testing is useful for differential diagnosis. METHODS: Fourteen patients fulfilling National Institute of Neurological Disorders and Stroke-Society for Progressive Supranuclear Palsy clinical criteria for progressive supranuclear palsy, 13 patients fulfilling modified Lang criteria for corticobasal degeneration, and 12 normal healthy control subjects were given the Test of Oral and Limb Apraxia, which was scored according to the Florida Apraxia Battery for occurrence of various types of apraxic errors. RESULTS: Both patients with progressive supranuclear palsy and corticobasal degeneration committed a greater number of apraxic errors than normal healthy control subjects on both transitive and intransitive tasks (p < 0.001 in both cases), but apraxia was much more severe in patients with corticobasal degeneration than progressive supranuclear palsy (p < 0.001). The index of apraxia severity, in combination with the assessment of the two key features of progressive supranuclear palsy (falls and vertical gaze palsy), correctly classified all patients. CONCLUSIONS: Patients with corticobasal degeneration show more severe ideomotor apraxia than patients with progressive supranuclear palsy, and systematic assessment of ideomotor apraxia facilitates the differential diagnosis between patients with progressive supranuclear palsy and those with corticobasal degeneration.

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Children with hydrocephalus have deficits in several neuropsychological domains. The most notable are motor, visuoperceptual, and visuomotor function. These deficits are multiply determined and depend on the etiology and severity of the hydrocephalus to a large extent. Corpus callosum abnormalities resulting from stretching of callosal fibers and other cortical white matter tracts are implicated as contributory to these deficits. Enlarged ventricles and associated compression of posterior cortical areas also correlate with cognitive impairment. Distinguishing which cognitive domain negatively impacts on the child's functioning and which domains influence behavior in isolation or in combination has been the subject of numerous studies. Developmentally, we know little about the emergence of neuropsychological functioning in children with hydrocephalus. Study of the effects of hydrocephalus at different stages of development is useful to clinicians and researchers interested in the impact of diffuse neurophysiological damage on cognition in the developing brain. The medical and neuropsychological literature have begun to inform about these effects. The core deficits in hydrocephalus have yet to be explicated and a focus on investigations that answer these questions is required. This review summarizes the current knowledge about neurocognitive sequelae of hydrocephalus.

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Patients with schizophrenia did not take significantly more trials than normal controls to learn to use a visual warning signal to avoid a non-aversive stimulus on a simple computer-administered avoidance learning task. When the stimulus to be avoided was aversive (i.e., a loud buzzer), however, the schizophrenic group could be divided into two subgroups based upon their performance; almost one half of the schizophrenic group failed to learn how to avoid this task successfully. The other half, like the normal controls and the closed head injury group in our previous studies, benefited from the aversiveness of the stimulus to be avoided, and learned to avoid more quickly than in the non-aversive condition. A post-hoc analysis of the differences between these two subgroups of the patients suggested that the discrepancy in learning was related to the age of onset of illness.

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Twenty-three children with autism and two control groups completed an attention battery comprising three versions of the continuous performance test (CPT), a digit cancellation task, the Wisconsin Card Sorting Test (WCST), and two novel, computerized tests of shifting attention (i.e., the Same-Different Computerized Task and the Computerized Matching Task). Children with autism could focus on a particular stimulus and sustain this focus as indicated by their performance on the digit cancellation task and the CPT. Their performance on the WCST suggested problems in some aspects of shifting attention (i.e., disengaging attention). The autism group performed as well as controls on the Same-Different Computerized Task, however, that required successive comparisons between stimuli. This implies that they could, in fact, shift their attention continuously. In addition, they did not differ from controls on the Computerized Matching Task, an analog of the WCST, suggesting that they do not have a general deficit in shifting attention.

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Many Chronic Fatigue Syndrome (CFS) patients complain of memory impairments which have been difficult to document empirically. Subjective complaints of memory impairment may be due to a deficit in metamemory judgment. CFS patients and matched controls were tested with a computerized Trivia Information Quiz that required them to rate their confidence about correctly recognizing an answer in a multiple choice format that they had been unable to remember in a fact-recall format. Even though CFS patients reported significantly greater amounts of fatigue, cognitive, and physical symptoms, the accuracy of their confidence levels and recognition responses were similar to controls. This finding suggests that a metamemory deficit is not the cause of the memory problems reported by CFS patients.

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Like controls, a Closed-Head Injury (CHI) group learned quickly to press a button during a 3-s warning stimulus in order to avoid a noxious buzzer. In a similar task, however, the CHI group had greater difficulty achieving the learning criterion compared to controls when required to prevent an innocuous visual display (i.e., a circle). The difficulty levels of these two avoidance tasks were identical. The major differences concerned the temporal contiguity of the warning cue with the stimulus to be avoided and the intrinsic aversiveness of the buzzer compared to the appearance of a circle on a computer screen. We hypothesize that, although both tasks were operant in essential character, the buzzer may have produced a degree of classical conditioning. These results suggest that CHI survivors may have some difficulty forming connections between arbitrary stimuli when performance depends almost entirely upon conscious, effortful processing. When a stimulus is sufficiently noxious to be capable of producing an affective or autonomic response, however, automatic processes may aid in the formation of associations.

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BACKGROUND: Abnormal cerebral anatomical lateralisation has been reported in schizophrenia and may implicate anomalous neurodevelopment in the aetiology of this disease. A popular recent hypothesis has predicted that such disturbances in normal lateralisation should be especially apparent in the morphology of the temporal lobes. METHOD: A temporal cortical region lying in the plane of the Sylvian fissure--known as the planum temporale--exhibits pronounced leftward asymmetry in normal right-handed males. We compared lateralisation of the planum temporale in schizophrenic and control males using MRI surface-rendering morphometry of the supratemporal cortex. RESULTS: Contrary to the lateralisation hypothesis, normal patterns of leftward planum asymmetry were detected in both the schizophrenic and control groups. Schizophrenics and controls also exhibited a predicted symmetry in the bilateral areas of Heschl's gyrus, a supratemporal cortical structure immediately anterior to the planum. CONCLUSION: These data do not support the notion that neurodevelopmental mechanisms of cerebral asymmetry are abnormal in schizophrenia.

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The spatial learning of rats with medial prefrontal lesions was compared to that of animals with cortical transplants of frontal tissue from donors of embryonic age 17, 19, 21, or 23 days. The age of the donor tissue significantly affected the extent that the transplanted tissue developed as the E17 and E19 grafts were markedly larger than those from E21 or E23 animals. Nonetheless, transplants were viable at all ages. Rats with E19 grafts, but not rats with grafts at other ages, showed significant reduction of the expected deficit on the Morris water task. In contrast, only rats with E21 grafts showed enhanced performance on a T-maze alternation task. The contrasting effects of the grafts of different aged tissue suggests that there may be some specific contributions of cortical grafts of different ages that leads to partial restoration of function.

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We studied the effect of different postoperative times on the behavioral recovery following brain implants. Adult male rats received cortical tissue grafts 2 weeks after aspiration of the medial frontal cortex. Either 2 (Immediate Group) or 28 (Delay Group) days after grafting, the performance of these rats on a behavioral battery, comprising the Morris water maze task, forepaw use, and grooming, was compared to that of rats with similar lesions and postoperative recovery times but no grafts. Rats tested immediately after receiving implants performed better on the spatial navigation task than rats with similar lesions but no grafts. This improvement, however, was less than that shown by rats with lesions but no grafts permitted to recover for 28 days before testing. In contrast, in the Delay Group, rats with grafts were more greatly impaired than were their operated controls. Neither lesions nor grafts affected grooming although the Immediate Group with grafts were significantly more impaired in using their forepaws during feeding than were any of the other groups. These results lead us to conclude that differing postoperative recovery times and task requirements may account for some of the inconsistent results of the influence of brain grafts on behavioral recovery reported in the literature. We also conclude that cortical tissue implants can have two effects with different time courses and opposite net behavioral effects.

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Dopaminergic blocking agents have been known to suppress intracranial self-stimulation, but whether the suppression results from a reduction in the rewarding value of stimulation or from motor deficits has remained controversial. We have resolved this controversy by developing an operant technique minimally dependent on motor activity: Rats were trained to perform a bar-holding response for 3s or to produce hippocampal theta waves for 3s when the bar was retracted. Decamethonium bromide (a muscle relaxant) reduced bar holding without affecting theta production for brain stimulation. Pimozide (a dopaminergic blocking-agent) reduced both bar holding and theta production for stimulation, though rats were still capable of making the theta response at a rate comparable to the preinjection rate. Dopaminergic blocking at low doses reduces the rewarding value of brain stimulation at the level of the lateral hypothalamus. The method described in this report has wide applicability.

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Adult male Long-Evans rats (90 days of age) were housed in 12 h light: 12 h dark (Group LD), constant white light (Group LL), or constant dark (dim red light) (Group DD) for 60-90 days. The first of two sexual behaviour tests revealed that more (P less than 0.05) rats in Group LD achieved intromission than did those in Groups LL and DD. Only 33% of Group LL and 32% of Group DD rats ejaculated. In contrast, all Group LD rats that mounted eventually ejaculated. Males in Group LD achieved more (P less than 0.05) ejaculations (mean of both tests combined, 3.4) than did males in Groups LL (1.5) or DD (1.2). Although there were no notable differences amongst the groups in the weights of the accessory sex organs, males in Group DD had higher (P less than 0.05) serum androgen levels than did those in Groups LL and LD while Group LL males had higher (P less than 0.05) serum prolactin levels than did those in Groups LD and DD. There were no differences in LH or FSH levels. In addition, more rats in Group LL had disrupted activity rhythms than did Group DD rats. These results indicate that housing in constant white or dim red light disrupts sexual behaviour in male rats and may do so through different neuroendocrine mechanisms.

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Electrical stimulation of the perforant path, which originates in the entorhinal cortex, produces a characteristic excitatory postsynaptic field potential (extracellular EPSP) which can be recorded in the fascia dentata. This evoked response may include a population spike, if stimulation is sufficient. In the anaesthetized rat, stimulation of the medial septum, when paired with perforant path stimulation, was found to augment the population spike component of the evoked field potential. Stimulation of the septum alone produced no apparent field potential. The augmentation effect was found to have a rapid onset (4 ms), which is sufficient for the participation of interneurons, and a relatively long time course (150 ms). Presynaptic mechanisms of facilitation were ruled out as there was no concurrent alteration of the extracellular EPSP. A change in population spike threshold, compatible with a postsynaptic mechanism, was observed and some possible models of action discussed. Augmentation survived depletion of hippocampal norepinephrine caused by injections of 6-hydroxydopamine into the dorsal noradrenergic bundle, indicating that the facilitation was not due to an activation of the ascending noradrenergic fibres of passage originating from the locus coeruleus. The cholinergic septo-hippocampal pathway was ruled out as a likely candidate for the modulation as the augmentation survived injections of the muscarinic antagonists atropine and scopolamine and the nicotinic antagonists tubocurarine and dihydro-beta-erythroidine. A relationship between the septal modulation and hippocampal theta was suggested.

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