Visual perceptual learning is similar across the extrafoveal central visual fields.

PURPOSE: Visual perceptual learning occurs with the presentation of novel visual stimuli at retinal sites near the fovea to 20 degrees eccentricities. It was unclear if the magnitude and rate of visual learning were similar across the central visual fields or if visual learning decreased with increasing eccentricity. The robustness of learning across the visual fields may affect the magnitude of computer-aided visual recovery after visual brain injury. Therefore we determined if eccentricity was a factor that influenced perceptual learning. METHODS: Subjects were trained to detect the presence or absence of a single line oriented differently (odd-element) from an array of lines that otherwise had the same orientation. The odd-element line was presented 3 degrees, 9 degrees or 18 degrees from fixation. RESULTS: Perceptual performance improved during training trials with a similar magnitude and similar learning curve slopes at all 3 eccentricities. Pre- and post-training performance improved to a similar magnitude at 3 vs 9 degrees in 4 of 4 subjects tested and at 9 degrees vs 18 degrees in 4 of 5 subjects. In the fifth subject there was no post-training improvement in performance at 18 degrees. CONCLUSION: Visual perceptual learning is similar across the extrafoveal central visual fields in almost all subjects.

Perceptual learning of line orientation modifies the effects of transcranial magnetic stimulation of visual cortex.

Perceptual learning may be accompanied by physiological changes in early visual cortex. We used transcranial magnetic stimulation (TMS) to test the postulate that perceptual learning of a visual task initially performed at 60-65% accuracy strengthens visual processing in early visual cortex. Single pulse TMS was delivered to human occipital cortex at time delays of 70-154 ms after the onset of an odd-element, line orientation discrimination task. When TMS was delivered at a delay of 84 ms or later the accuracy of visual discrimination was transiently degraded in ten subjects. As visual performance in control trials without TMS improved with training, the absolute magnitude of TMS suppression of performance decreased in parallel. This result occurred both when TMS was delivered to broad areas of occipital cortex and when TMS was optimally delivered to early occipital cortex. No change in TMS suppression was observed when three new subjects were given feedback during an odd-element task that did not require substantial perceptual learning. Thus, perceptual learning improved visual performance and reduced TMS suppression of early visual cortex in parallel.

Partial peripheral motor nerve lesions induce changes in the conduction properties of remaining intact motoneurons.

A partial injury or loss of peripheral motor axons is followed by compensatory sprouting of remaining intact motor axons in order to reinnervate muscle. Little is known, however, about the electrophysiologic properties proximally of these intact motoneurons and their axons following injury of neighboring motor axons. We studied the conduction properties of intact cat motor axons and motoneurons proximal to the site of a partial peripheral nerve section. Twelve weeks after the partial transection of the cat medial gastrocnemius motor nerve, there was a significant (7%) reduction in conduction velocity and a 13% prolongation in afterhyperpolarization half-decay time in the remaining intact motoneurons, compared with controls. Partial injury to motor nerves thus induces reactive electrophysiologic changes in the remaining intact motoneurons and their axons, perhaps associated with compensatory sprouting within partially denervated muscle.

The selectivity and timing of motion processing in human temporo-parieto-occipital and occipital cortex: a transcranial magnetic stimulation study.

An extrastriate visual area near the human temporo parieto occipital junction (TPO) may selectively mediate motion processing, while contributing little to the perception of color or form. This TPO area may be the human analogue of the monkey middle temporal (MT or V5) and medial superior temporal (MST) extrastriate visual areas. The selectivity of the effect of transcranial magnetic stimulation (TMS) on motion processing was unknown, as was the timecourse of occipital to TPO motion processing. In the first experiment, unilateral TMS was delivered over TPO 50-250 ms after the onset of a random dot motion discrimination display that was presented in the right or left hemifield. TMS reduced the correct discrimination of motion direction only when it was delivered in a discrete time window 100-175 ms following the onset of the display. TMS did not significantly affect hemifield spatial acuity in the same time window. In the second experiment, bilateral TMS delivered over occipital cortex also degraded the discrimination of motion-defined form (MDF) in a discrete time window following the onset of a display presented foveally. Bilateral focal TMS delivered over TPO disrupted the discrimination of MDF in a time window beginning 20-40 ms later than the effect of TMS delivered over occipital cortex. Bilateral focal TMS delivered over TPO also degraded the discrimination of color-defined form, motion direction and color. TMS can trace the timing of visual processing from occipital to extrastriate visual areas.

Tracing the timing of human analysis of motion and chromatic signals from occipital to temporo-parieto-occipital cortex: a transcranial magnetic stimulation study.

In human visual analysis, the initial processing of motion and chromatic signals may be mediated by feed-forward pathways from striate cortex to segregated areas of extrastriate cortex. The time-course of occipital to temporo-parieto-occipital motion processing was unknown, as was the selectivity of the effect of transcranial magnetic stimulation (TMS) on motion processing. TMS delivered over occipital cortex degraded the discrimination of motion-defined form (MDF) in a discrete time window beginning 100-120 ms from the onset of the visual stimulus. Bilateral focal TMS delivered over the temporo-parieto-occipital junction (TPO) disrupted the discrimination of MDF in a time window beginning 20-40 ms later than the effect of TMS delivered over occipital cortex. Bilateral focal TMS delivered over TPO also degraded the discrimination of CDF, motion direction, and color.

Anticipatory smooth eye movements and predictive pursuit after unilateral lesions in human brain.

Anticipatory smooth eye movements precede expected changes in target motion. It has been questioned whether anticipatory smooth eye movements are a component of the smooth pursuit system. Five subjects with unilateral brain lesions and five control subjects were tested with predictable double-ramp stimuli to determine whether these lesions have a similar effect on horizontal, visually guided smooth pursuit, anticipatory smooth eye movements, and the predictive component of smooth pursuit. All four subjects with a brain lesion involving the parietal or parietal-frontal lobe had parallel velocity asymmetries in all three forms of smooth eye movements, with lowest velocities toward the side of the lesion. A similar uniformity and magnitude of smooth eye movement directional asymmetries were not found in control subjects. Unidirectional attenuation of these three forms of smooth eye movements provides evidence that they are part of a unified smooth eye movement system.

Prolonged confusion with nocturnal wandering arising from NREM and REM sleep: a case report.

A 51-year-old man with Machado-Joseph disease had a 3-year history of prolonged confusion following nightly nocturnal wandering. Polysomnography with videotape monitoring revealed 19- to 120-minute sleepwalking episodes emerging from non-rapid eye movement (NREM) sleep and occasionally from rapid eye movement (REM) sleep, followed by 22-47 minutes of prolonged confusion and disorientation. The patient also had a periodic limb movement disorder and obstructive sleep apnea syndrome. Excessive daytime sleepiness was evident by results from the Epworth Sleepiness Scale and Multiple Sleep Latency Test. A sleep-deprived electroencephalogram (EEG) and a polysomnogram with an expanded EEG montage before and during these episodes revealed no epileptiform activity. A contrast-enhanced brain magnetic resonance imaging (MRI) scan demonstrated findings consistent only with Machado-Joseph disease. The patient improved with a combination of temazepam and carbidopa-levodopa.

Predictive smooth pursuit eye movements near abrupt changes in motion direction.

The stimulus-response characteristics of predictive smooth pursuit eye movements near the time of predictable, abrupt changes in target motion direction were studied. Expectations about the speed and direction of target motion both before and after the direction change affected specific components of the predictive pursuit responses. We propose that, when the direction of target motion is expected to change, the cessation of motion in one direction and the initiation of motion in a new direction are separately anticipated and that predictive pursuit movements are summated responses to these two events.

Memory-contingent saccades and the substantia nigra postulate for essential blepharospasm.

Essential blepharospasm and cranial dystonia are related focal dystonias of unknown aetiology. Blepharospasm induced by acute dopamine depletion in parkinsonism restricts saccade initiation possibly via the substantia nigra pars reticulata (SNpr). If essential blepharospasm and cranial dystonia similarly restrict saccades, then a selective, somatotopically arranged pathway such as the SNpr may be involved. To test this possibility memory-contingent and visually-guided saccades were measured in patients with essential blepharospasm and cranial dystonia. The latency of both forms of saccades was either significantly prolonged or excessively variable, while the accuracy and peak velocity of these fast eye movements were similar to age-matched control subjects. Essential blepharospasm and cranial dystonia alter the initiation of saccadic eye movements. Subcortical brain regions or pathways where eyelid, saccade and cranial/cervical motor control are somatotopically approximated, such as the SNpr, may be involved in blepharospasm.

Differential diagnosis of choreiform tardive dyskinesia.

Orofacial dyskinesias and choreiform movements of limbs occur with moderate frequency among psychiatric patients. Abnormal involuntary movements are symptoms of a wide variety of neurological and medical disorders. For both therapeutic and medicolegal reasons, psychiatric patients should be thoroughly evaluated before being given the diagnosis of tardive dyskinesia. This review presents the differential diagnosis of disorders associated with orofacial and appendicular choreiform involuntary movements. In addition, this paper provides a guide to the clinical and laboratory evaluation of patients with these symptoms.

Motion perception prominence alters anticipatory slow eye movements.

Perceived motion may be a stimulus for anticipatory slow eye movements. To test this possibility, the production of anticipatory slow eye movements in humans was studied using apparent motion stimuli. Short range apparent motion was produced with random dot stimuli and the anticipatory slow eye movements were isolated from the smooth pursuit responses by occasionally including trials in which the random dot stimulus did not appear. Long range apparent motion was produced with subjective contour stimuli. Both short range and long range apparent motion were found to be effective stimuli for anticipatory slow eye movements. The prominence of perceived motion was altered by changing the spatiotemporal displacement intervals in the short range apparent motion stimuli. Changing the subjective contours also changed the motion percepts of the long range apparent motion stimuli. With both stimuli, the peak anticipatory slow eye velocities that were achieved decreased as the prominence of the motion percepts decreased, while the time-course of the anticipatory responses were similar under the different conditions. These findings indicate that the expectation of perceived motion is necessary for anticipatory slow eye movements.

Neurologic complications of cardiac transplantation.

The neurologic evaluation of an individual cardiac transplant recipient often does not lead to a succinct bedside diagnosis. There are few consistent clinical observations. The onset of seizures in the early postoperative period is associated with embolic cerebral infarction. Seizures occur most commonly, however, as a neurotoxic manifestation of cyclosporine. The onset of an acute delirium or psychosis in the first week after cardiac transplantation usually has multiple causative factors and is reversible. A postoperative brachial plexopathy or mononeuropathy can be identified with a neurologic examination, confirmed by appropriate electrophysiologic testing and is usually reversible. The onset of periorbital inflammation, ophthalmoplegia, and nasal turbinate or sinus invasion and necrosis is consistent with phycomycosis. Most patients, however, present with nonspecific findings of impaired mentation with or without focal neurologic signs. These patients require a fairly systematic search for potentially treatable neurologic complications (see Table 3). In a medically stable patient an aggressive diagnostic approach, at times including stereotaxic brain aspirate or biopsy, is indicated. In the severely ill patient with multiple organ failure, empirical therapy for the most probable treatable disorder is justified.

Stimulus conditions that enhance anticipatory slow eye movements.

Anticipatory slow eye movements are predictive responses that occur prior to both ramp and step target motions. These low velocity eye movements are enhanced and can be studied in isolation by transient target disappearance before ramp motion onset. Slow eye velocities also decrease prior to the termination of target motion. In experiments using a bistable apparent motion stimulus, it was found that perceived motion is a stimulus for anticipatory slow eye movements. This relationship between motion perception and anticipatory slow eye movements can explain previously noted differences between these predictive movements and the predictive component of smooth pursuit.

The search for a physiologic marker of Machado-Joseph disease.

Machado-Joseph disease is a dominantly inherited, multisystem, degenerative disorder that lacks a proven genetic marker. Peripheral nerve conduction-refractory period, sensory evoked potentials, and quantified oculomotor recordings were studied in nine patients affected with this disease to look for a potential physiologic marker. Only the oculomotor measurements of saccade and smooth pursuit gain were consistently abnormal in all patients. Identical eye movement recordings in 12 asymptomatic individuals at risk for Machado-Joseph disease revealed findings typical of affected patients in only 1 individual. Quantified oculomotor studies may contribute to the early confirmation of the disease, primarily in individuals at risk with minor or equivocal neurologic signs.

Saccade responses to dopamine in human MPTP-induced parkinsonism.

Depletion of dopamine content in the substantia nigra resulting from 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) toxicity produces parkinsonism. Management of 3 patients with MPTP-induced parkinsonism required drug holidays during which there was a state of dopamine depletion followed by dopamine replacement. We used this opportunity to study the effect of the selective loss of pars compacta dopaminergic cells on vertical and horizontal saccade (fast) eye movements. During the drug holidays, visually guided saccades were hypometric and had long latencies but retained a normal saccade velocity-amplitude relationship. Dopamine agonists or precursors improved the accuracy and reaction times of saccades in all directions, but not their velocity. Two of the three patients also had intermittent blepharospasm during dopamine depletion. During the episodes of blepharospasm, saccade responses became slow eye movements. MPTP causes a dopaminergic-responsive disorder of saccade initiation that is similar to idiopathic parkinsonism. The inhibition of voluntary eyelid opening during MPTP-induced blepharospasm further increases this impairment of fast eye movements and altered saccade velocity, presumably via the pars reticulata of the substantia nigra.

Regional cooling of human nerve and slowed Na+ inactivation.

Regional cooling of human sensory nerves increases the amplitude and surface area of an evoked sensory compound action potential (SCAP). It has been proposed that these changes are due to cold-induced slowing of Na+ inactivation. Na+ inactivation is also the main voltage-dependent event that underlies the refractory period in myelinated nerve. Therefore, if slowed Na+ inactivation causes the increased SCAP amplitude and area seen in focal cooling, a parallel temperature-dependent change should also occur in the SCAP refractory period. We compared the duration and magnitude of the relative refractory period to the total surface of a median nerve SCAP at 5 intervals of increasing temperature, from 24 degrees C to 36 degrees C. In 5 control subjects, the SCAP surface area and the relative refractory period increased 4-5-fold in parallel and revealed a non-linear relation to temperature change. Prolongation of the duration of individual nerve fiber potentials from slowed Na+ inactivation is proposed as one explanation of these temperature-related changes.

Clinical detection of acute vestibulocerebellar disorders.

The acute onset of vertigo, nystagmus and postural instability, without brain-stem signs, is commonly attributed to a disorder of the labyrinth, the vestibular, sensory end organ. Identical symptoms can occur, however, with discrete infarctions or hemorrhages involving the central vestibulocerebellum. Whereas acute labyrinthine disorders are usually benign and self-limited, vascular injuries of the cerebellum may produce swelling, compression of the brain stem and acute hydrocephalus one to four days after the onset of symptoms. Therefore it is important to accurately distinguish between labyrinthine and vestibulocerebellar disorders with the neurologic examination. Acute labyrinthine disease causes unidirectional nystagmus with past-pointing and falling in the opposite direction of the nystagmus, environmental vertigo in the same direction and suppression of the nystagmus with visual fixation. Disorders of the vestibulocerebellum do not produce this consistent pattern of findings.

Convergence-initiated voluntary flutter: a normal intrinsic capability in man.

The proposal that there is an inherent capability in humans to produce bursts of fluttering saccades was tested by comparing Purkinje image eye movement recordings in subjects with voluntary nystagmus and control subjects. Voluntary nystagmus is composed of recurrent saccades without an intersaccade interval and has been proposed to be an inherited event. No difference in saccade peak velocity-amplitude curves or microsaccades during visual fixation was found between the two groups. With training control subjects learned to produce runs of saccadic flutter identical to voluntary nystagmus. This learned flutter was composed of recurrent complete saccades rather than saccades interrupted in midflight. Voluntary flutter is thus not a genetic trait but a learned event that is usually undeveloped in man. These observations can be explained by the Robinson model of saccade generation and indicate that similar models must have an inherent ability to produce saccadic flutter.

Hyperviscosity-induced dementia.

Dementia was the presenting symptom in a patient with increased serum viscosity secondary to multiple myeloma. Plasmapheresis led to complete resolution of the neurologic syndrome. Serum hyperviscosity should be added to the growing list of reversible causes of dementia. When hyperviscosity-associated dementia is suspected, both serum and whole blood viscosity determinations are indicated.