Supplementary motor area provides an efferent signal for sensory suppression

Voluntary actions produce suppression of neural activity in sensory areas, and reduced levels of conscious sensation. Recent computational models of motor control have linked sensory suppression to motor prediction: an efferent signal from motor areas may cancel the sensory reafferences predicted as a consequence of movement. Direct evidence for the efferent mechanism in sensory suppression has been lacking. We investigated the perceived size of finger-muscle twitches (MEPs) evoked by TMS in eight normal subjects. Subjects freely chose on each trial whether to make or withhold a voluntary flexion of the right index finger, in synchrony with an instructional stimulus. A test MEP occurred at the instructed time of action. The subject then relaxed and a second reference MEP occurred a few seconds later. Subjects judged which of the two MEPs was larger. Subjects perceived the first test MEP to be smaller in trials where they made voluntary actions than on trials where they did not, demonstrating sensory suppression. On randomly selected trials, a conditioning prepulse was delivered over the supplementary motor area (SMA) 10 ms before the pulse producing the test MEP. The SMA prepulse reduced and almost abolished the sensory suppression effect in voluntary action trials. We suggest the SMA may provide an efferent signal which is used by other brain areas to modulate somatosensory activity during self-generated movement.     

Muscle wasting after prolonged hypoglycaemic coma: case report with electrophysiological data.

A case of distal muscle wasting associated with hypoglycaemia is described. Motor and sensory conduction studies are reported that provide little evidence of a hypoglycaemic peripheral neuropathy. Damage to anterior horn cells or motor roots appears to be a more likely explanation for the amyotrophy. Recovery occurred clinically with evidence of reinnervation by axonal collateral sprouting.     

Sensory experiences during treatment of phobias by in vivo exposure

The author describes several patients undergoing in vivo exposure therapy for simple phobias who reported transient sensory distortions without other evidence of psychosis. The experiences occurred mainly in the tactile, kinesthetic, and visual modes. Their nature and significance are undetermined, but they appear to resemble conversion symptoms, hypnotic sensory distortions, and other nonpsychotic sensory experiences stimulated by emotionally charged ideas.     

Methylmercury poisoning, Clinical follow-up and sensory nerve conduction studies.

Methylmercury poisoning occurred in four cases after passage of methylmercury through the food chain. The neurological damage in all four cases was severe. The damage was greater at younger ages with maximum involvement in the case of transplacental poisoning. Significant recovery occurred in two cases, but on six-year follow-up two cases remained severely impaired. Clinical and electrophysiological evidence suggests that damage to peripheral sensory nerves may not be the cause of the late sensory symptomatology.     

Electrophysiological evidence for vestibular activation of the guinea pig hippocampus

Vestibular information modulates hippocampal activity for spatial processing and place cell firing. However, evidence of a purely vestibular stimulus modulating hippocampal activity is confounded as most studies use stimuli containing somatosensory and visual components. In the present study, high-frequency electrical stimulation of specific vestibular sensory regions of the right labyrinth in anaesthetized guinea pigs induced an evoked field potential in the hippocampal formation bilaterally with a latency of about 40 ms following stimulation onset. Field potentials localized in the hippocampal formation occurred with stimulus current parameters that were too small to produce eye movements. This provides direct electrophysiological evidence of vestibular input to the hippocampus.     

Acral mutilation and nociceptive loss in English Pointer dogs

Summary Acral mutilation and analgesia occurred in three of a litter of nine pups produced by a mating of clinically normal English Pointer dogs. Post-mortem studies on one of the affected pups revealed changes at the level of the primary sensory neuron which included: a reduction in spinal ganglia size, a 22–50% deficiency of ganglionic neurons, and a disproportionately large population of small sensory cell bodies. The only change noted in the spinal cord occurred in the dorsolateral fasciculus where reduced fiber density appeared to correlate well with the observed nociceptive defect. Light- and electron-microscopic examination of spinal roots, ganglia, and peripheral nerves provided evidence of myelinated and unmyelinated fiber degeneration. The neuronal degeneration, however, appeared quantitatively inadequate to account for the deficiency of sensory cell bodies. It was concluded that this mutilating acropathy was a manifestation of a sensory neuropathy in which the neuronal deficiency resulted from insufficient development and slowly progressive, postnatal degeneration.The clinical and pathologic findings in this canine disorder were compared with those reported in hereditary sensory neuropathies of man and other animals.This work was supported by NIH grant NS-14242-01, contact RR-9-2102, and Biomedical Research Support Grant funds     

Serum antibodies to Purkinje cells and dorsal root ganglia neurons in sensory neuronopathy without malignancy

Anti-Purkinje cell antibodies (APCA), believed to be markers of paraneoplastic cerebellar degeneration in females, have been identified in the serum of 3 men with subacute sensory neuronopathies and no evidence of tumors 5 years after the onset of the neurological signs. By indirect immunohistochemistry on sections of rat cerebellum and dorsal root ganglia, the patients' IgG bound to the cytoplasms of both Purkinje cells and dorsal root ganglia neurons. By western blot analysis on whole human cerebellum and whole human dorsal root ganglia homogenates, the IgG from 2 patients bound to a 62-kd protein in both homogenates and the IgG from 1 patient bound to a 110-kd protein in the cerebellum homogenate only. Yo autoantibody test was negative in all patients. Our study provides evidence that non-anti-Yo APCA may be associated with subacute sensory neuronoopathies and are not necessarily markers of an underlying tumor. The previously described anti-Yo APCA has only occurred in females with cancer.     

An epidemic of optic neuropathy and painful sensory neuropathy in Cuba: Clinical aspects

An epidemic of bilateral optic neuropathy and painful sensory neuropathy occurred in Cuba in 1991–1993. Over 45 000 individuals were stated to have been affected. We report a clinical study on 25 patients seen in Cuba in 1993–1994. Affected patients showed either bilateral optic neuropathy with caecocentral scotomata or a distal predominantly sensory neuropathy sometimes associated with deafness, or a combination of both optic and peripheral sensory neuropathy. The nature of the epidemic is discussed. The clinical features in patients with confirmed neurological deficits were consistent with a diagnosis of Strachan's syndrome, probably related to nutritional deficiency. Other patients with similar symptoms showed no evidence either of optic or peripheral neuropathy and were considered to represent disease mimicry on a psychoneurotic basis.     

Evidence and Urgency Related EEG Signals during Dynamic Decision-Making in Humans

A successful class of models link decision-making to brain signals by assuming that evidence accumulates to a decision threshold. These evidence accumulation models have identified neuronal activity that appears to reflect sensory evidence and decision variables that drive behavior. More recently, an additional evidence-independent and time-variant signal, called urgency, has been hypothesized to accelerate decisions in the face of insufficient evidence. However, most decision-making paradigms tested with fMRI or EEG in humans have not been designed to disentangle evidence accumulation from urgency. Here we use a face-morphing decision-making task in combination with EEG and a hierarchical Bayesian model to identify neural signals related to sensory and decision variables, and to test the urgency-gating model. Forty females and 34 males took part (mean age, 23.4 years). We find that an evoked potential time locked to the decision, the centroparietal positivity, reflects the decision variable from the computational model. We further show that the unfolding of this signal throughout the decision process best reflects the product of sensory evidence and an evidence-independent urgency signal. Urgency varied across subjects, suggesting that it may represent an individual trait. Our results show that it is possible to use EEG to distinguish neural signals related to sensory evidence accumulation, decision variables, and urgency. These mechanisms expose principles of cognitive function in general and may have applications to the study of pathologic decision-making such as in impulse control and addictive disorders.SIGNIFICANCE STATEMENT Perceptual decisions are often described by a class of models that assumes that sensory evidence accumulates gradually over time until a decision threshold is reached. In the present study, we demonstrate that an additional urgency signal impacts how decisions are formed. This endogenous signal encourages one to respond as time elapses. We found that neural decision signals measured by EEG reflect the product of sensory evidence and an evidence-independent urgency signal. A nuanced understanding of human decisions, and the neural mechanisms that support it, can improve decision-making in many situations and potentially ameliorate dysfunction when it has gone awry.     

The amygdala's role in human mnemonic processing

The possible role played by the human amygdaloid complex in the processing of mnemonic information is examined. First, evidence is reviewed from case reports in which amygdaloid damage occurred due to surgical intervention or pathological or age-related changes. Then, studies are evaluated in which the amygdala was stimulated or in which electrical potentials were recorded from it. Based on this survey an hypothesis on the possible involvement of the amygdala in mnemonic information processing is proposed. In essence, it is argued that the human amygdala is responsible for activating or reactivating those mnemonic events which are of an emotional significance for the subjects' life history and that this (re-)activation is performed by charging sensory information with appropriate emotional cues. Supportive evidence for this hypothesis is given based on human case reports, on studies in animals in which information processing was determined following amygdaloid lesions, and on evidence of neuroanatomical connections of the primate amygdala.     

Primary and secondary somatosensory cortex responses to anticipation and pain: a magnetoencephalography study

Several brain regions, including the primary and secondary somatosensory cortices (SI and SII, respectively), are functionally active during the pain experience. Both of these regions are thought to be involved in the sensory-discriminative processing of pain and recent evidence suggests that SI in particular may also be involved in more affective processing. In this study we used MEG to investigate the hypothesis that frequency-specific oscillatory activity may be differentially associated with the sensory and affective components of pain. In eight healthy participants (four male), MEG was recorded during a visceral pain experiment comprising baseline, anticipation, pain and post-pain phases. Pain was delivered via intraluminal oesophageal balloon distension (four stimuli at 1 Hz). Significant bilateral but asymmetrical changes in neural activity occurred in the β-band within SI and SII. In SI, a continuous increase in neural activity occurred during the anticipation phase (20-30 Hz), which continued during the pain phase but at a lower frequency (10-15 Hz). In SII, oscillatory changes only occurred during the pain phase, predominantly in the 20-30 Hz β band, and were coincident with the stimulus. These data provide novel evidence of functional diversity within SI, indicating a role in attentional and sensory aspects of pain processing. In SII, oscillatory changes were predominantly stimulus-related, indicating a role in encoding the characteristics of the stimulus. We therefore provide objective evidence of functional heterogeneity within SI and functional segregation between SI and SII, and suggest that the temporal and frequency dynamics within cortical regions may offer valuable insights into pain processing.     

The Ins and Outs of Consciousness

In Enchanted Looms, Rodney Cotterill defends the hypothesisthat conscious sensory experience depends on motor response. Thepositive evidence for this hypothesis is inconclusive, andnegative evidence can be marshaled against it. I present analternative hypothesis according to which consciousness involvesintermediate level sensory processing, attention, and workingmemory. The circuitry of consciousness can be dissociated fromaction systems and may mark an evolutionary advance from a priorphylogenetic stage in which motor outputs and sensory inputswere more intimately bound.     

Large and small fibre type sensory dysfunction in patients with cancer.

Quantitative sensory testing was used to assess the prevalence of sensory dysfunction in patients with cancer, carefully screened for other risk factors for neuropathy. Large fibre type sensory function was evaluated using vibration threshold (VT) determinations while small fibre type sensory function was assessed by thermal threshold (TT) determinations. Mean VT and TT were significantly elevated in the toes but not the fingers of cancer patients. VT elevations in the toes occurred in 31% of cancer patients and in 6% of control subjects. TT elevations in the toes occurred in 43% of cancer patients and 4% of control subjects. Based on these findings it is concluded that large and small fibre type sensory dysfunction is much more common in carefully screened cancer patients than in control subjects. This sensory dysfunction is most likely to represent a neuropathy related directly or indirectly associated with cancer.     

Critically ill polyneuropathy: electrophysiological studies and differentiation from Guillain-Barré syndrome.

A polyneuropathy of varying severity has been observed in association with sepsis and critical illness in 15 patients. Since clinical evaluation is often difficult, electrophysiological studies provided definitive evidence for polyneuropathy. These revealed reductions in the amplitudes of compound muscle and sensory nerve action potentials, the most marked abnormality. Near-nerve recordings confirmed such reductions for sensory fibres. Needle electromyography revealed signs of denervation of limb muscles. Phrenic nerve conduction and needle electromyographic studies of chest wall muscles suggested that the polyneuropathy partially explained difficulties in weaning patients from the ventilator, an early clinical sign. No defect in neuromuscular transmission was demonstrated, despite the use of aminoglycoside antibiotics in some patients. In those who survived the critical illness, clinical and electrophysiological improvement occurred. The 15 critically ill polyneuropathy patients were compared with 16 Guillain-Barré syndrome patients observed during the same period. The analysis showed that the two polyneuropathies are likely to be separate entities that can be distinguished in most instances by the predisposing illness, electrophysiological features and cerebrospinal fluid results.     

Implicit Neurofeedback Training of Feature-Based Attention Promotes Biased Sensory Processing during Integrative Decision-Making

Complex perceptual decisions, in which information must be integrated across multiple sources of evidence, are ubiquitous but are not well understood. Such decisions rely on sensory processing of each individual source of evidence, and are therefore vulnerable to bias if sensory processing resources are disproportionately allocated among visual inputs. To investigate this, we developed an implicit neurofeedback protocol embedded within a complex decision-making task to bias sensory processing in favor of one source of evidence over another. Human participants of both sexes (N = 30) were asked to report the average motion direction across two fields of oriented moving bars. Bars of different orientations flickered at different frequencies, thus inducing steady-state visual evoked potentials. Unbeknownst to participants, neurofeedback was implemented to implicitly reward attention to a specific “trained” orientation (rather than any particular motion direction). As attentional selectivity for this orientation increased, the motion coherence of both fields of bars increased, making the task easier without altering the relative reliability of the two sources of evidence. Critically, these neurofeedback trials were alternated with “test” trials in which motion coherence was not contingent on attentional selectivity, allowing us to assess the training efficacy. The protocol successfully biased sensory processing, resulting in earlier and stronger encoding of the trained evidence source. In turn, this evidence was weighted more heavily in behavioral and neural representations of the integrated average, although the two sources of evidence were always matched in reliability. These results demonstrate how biases in sensory processing can impact integrative decision-making processes.SIGNIFICANCE STATEMENT Many everyday decisions require active integration of different sources of sensory information, such as deciding when it is safe to cross a road, yet little is known about how the brain prioritizes sensory sources in the service of adaptive behavior, or whether such decisions can be altered through learning. Here we addressed these questions using a novel behavioral protocol that provided observers with real-time feedback of their own brain activity patterns in which sensory processing was implicitly biased toward a subset of the available information. We show that, while such biases are a normal and adaptive mechanism for humans to process complex visual information, they can also contribute to suboptimal decision-making.     

Identifying specific sensory modalities maintaining the stereotypy of students with multiple profound disabilities

In Experiment 1, analogue functional analyses were conducted to identify the functions of stereotypy for six students with multiple profound disabilities. Results indicated that stereotypy (a) occurred across conditions, (b) occurred primarily when alone, or (c) occurred during all sessions except in the Control condition. Experiment 2 analyzed stereotypy while masking visual, auditory, or tactile sensory consequences. Results showed that stereotypy was maintained by visual stimulation, tactile stimulation, or was undifferentiated across conditions. In Experiment 3, we showed that stereotypy could be reduced by providing competing sensory stimulation. In Experiment 4, stereotypy that was undifferentiated in Experiment 1 was analyzed using a concurrent operants procedure. Results showed that stereotypy was not multiply determined, but occurred to produce visual sensory stimulation. Our findings are discussed in terms of the sensory and social reinforcers that maintain stereotypy, assessment procedures used to identify those reinforcers, and the interpretation of assessment results.     

Why can't you tickle yourself?

It is well known that you cannot tickle yourself. Here, we discuss the proposal that such attenuation of self-produced tactile stimulation is due to the sensory predictions made by an internal forward model of the motor system. A forward model predicts the sensory consequences of a movement based on the motor command. When a movement is self-produced, its sensory consequences can be accurately predicted, and this prediction can be used to attenuate the sensory effects of the movement. Studies are reviewed that demonstrate that as the discrepancy between predicted and actual sensory feedback increases during self-produced tactile stimulation there is a concomitant decrease in the level of sensory attenuation and an increase in tickliness. Functional neuroimaging studies have demonstrated that this sensory attenuation might be mediated by somatosensory cortex and anterior cingulate cortex: these areas are activated less by a self-produced tactile stimulus than by the same stimulus when it is externally produced. Furthermore, evidence suggests that the cerebellum might be involved in generating the prediction of the sensory consequences of movement. Finally, recent evidence suggests that this predictive mechanism is abnormal in patients with auditory hallucinations and/or passivity experiences.     

Symptom duration and clinical features in painful sensory neuropathy with and without nerve conduction abnormalities

BACKGROUND: The term "small fiber sensory neuropathy" (SFSN) refers to an axonal sensory polyneuropathy predominantly affecting cutaneous sensory modalities, often associated with pain and with no evidence of large fiber involvement. We hypothesized that, in most patients, SFSN is the earliest manifestation of a nonspecific axonal neuropathy and will usually progress to involve larger, heavily myelinated sensory and motor fibers. We sought indirect evidence of this through an analysis of the correlation between symptom duration and large fiber involvement in patients with painful sensory neuropathy (PSN). METHODS: A clinical diagnosis of PSN was supported by nerve conduction studies or measurement of epidermal nerve fiber (ENF) density in 43 patients. Symptom duration was correlated with the frequency of large fiber loss as measured by nerve conduction abnormalities. The severity and extent of clinical signs and symptoms were also evaluated in subjects with and without electrodiagnostic abnormalities. RESULTS: Patients with large sensory axon involvement had symptoms of longer duration than patients with SFSN. The frequency of electrodiagnostic abnormalities increased in direct proportion to disease duration. Patients with electrodiagnostic abnormalities also had more extensive pinprick sensory deficits, suggesting that small fiber loss was more advanced in this group as well. CONCLUSIONS: In PSN, the incidence of large fiber involvement appears to increase in proportion to symptom duration. This represents indirect evidence that SFSN usually progresses to involve both large and small fibers within 2-10 years.     

Wartenberg's migrant sensory neuritis

We describe a patient with the sudden onset of a painful, purely sensory, mononeuritis multiplex. Investigations showed no evidence for any underlying systemic condition. A nerve biopsy showed fascicular wallerian degeneration with perineurial thickening, inflammatory cells, and immunoglobulin G (IgG) deposition. His painful sensory deficits persisted, with no improvement after treatment with prednisone. The clinical characteristics in this case were very similar to those originally described by Wartenberg, and subsequently by other investigators. The investigations in our case strongly suggest that there may be an underlying immune pathogenesis for cases of Wartenberg's migrant sensory neuritis.     

Multimodal evoked potentials in progressive external ophthalmoplegia with mitochondrial myopathy

Multimodal evoked potentials were studied in 13 patients affected by progressive external ophthalmoplegia with histologically proven mitochondrial myopathy. Progressive external ophthalmoplegia occurred with craniosomatic spreading in all the patients and with a varying degree of nervous and/or other system involvement in most of them. In all but one of the subjects, at least one evoked potential modality was abnormal; 11 of them demonstrated an abnormal visual evoked potential, but this finding might have been influenced by concurrent retinal dysfunction. Abnormalities in brainstem auditory evoked potentials and/or somatosensory evoked potentials, revealing an impairment of central sensory pathways, were detected in 7 subjects, 5 of whom lacked clinical evidence of central nervous system involvement. Thus, evoked potentials represent an useful tool for the detection of subclinical central nervous system involvement in patients affected by progressive external ophthalmoplegia with mitochondrial myopathy.