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At least 19 recordsLinked to original sources
PubMed1976

Myocardial infarction without pain. A study of the sensory function of the upper limbs.

The sensory function of the upper limbs was examined in 18 subjects who had a myocardial infarction without a well-defined episode of chest pain. The cutaneous pain threshold was significantly higher than in normals. The ischaemia of the upper limbs induced patterns of sensations different from the normals, with onset of pain and of autonomic and coenaesthesic disturbances. These modifications of the sensory function are the same as observed in subjects with a previous painful infarction, but are quite different from those observed in patients with angina pectoris.

Angina Pectoris↗
PubMedDate not supplied

[Effect of various forms of physical exertion on selected types of sensory function].

The author reports changes in vibration and two-point discrimation sensitivity in groups of healthy young males after several days of intense physical effort and after one short-lasting intense exercise. The vibration sensitivity was a steady type of sensory function showing no significant changes after these workloads. The two-point discrimination sensitivity was, not infrequently, better after several days of effort in relation to preliminary state, and it was regarded as an evidence of adaptation to work. On the other hand, one sort-lasting exercise reduced significantly discrimination of two stimuli, especially on the lower extremities. This significant impairment of two-stimuli discrimination on the lower extremities in relation to the upper ones after intensive effort suggests easier exhaustion of pathways conveying sensation in the thoracic segment of the spinal cord. On the basis of these investigations the author thinks that aesthesiometric investigations carried out under strictly observed conditions may be useful for assessment of fatigue.

Adult↗
PubMed1992

Sensory nerves in adult rats regenerate and restore sensory function to the skin independently of endogenous NGF.

We have investigated the possible roles of NGF, and of impulse activity, in the regeneration of sensory nerves. Unexpectedly, the ability of crushed axons to regrow and to restore functional recovery of three sensory modalities in adult rat skin (A alpha-mediated touch, A delta-mediated mechanonociception, and C-fiber-mediated heat nociception) was totally unaffected by anti-NGF treatment. This finding applied even when the anti-NGF dosage was almost eight times that which entirely blocked collateral sprouting of the undamaged axons of both classes of nociceptive nerves (the A alpha-axons do not sprout in adult animals). In the same anti-NGF-treated animal, regeneration would proceed normally on the one side, while collateral sprouting was prevented on the other. Light microscopic and EM examination revealed that in the denervated skin the regenerating axons utilized the same dermal perineurial pathways followed by collaterally sprouting axons. Regeneration within these antibody-accessible pathways progressed normally during anti-NGF treatment, extending 1-2 cm beyond the former field borders, that is, into territory whose invasion by collaterally sprouting axons was totally blocked. The blood-nerve barrier is absent within the degenerating peripheral nerve trunk, a putative NGF source for regenerating fibers but not for sprouting ones. The NGF-independent regeneration was also found to be unaffected when putative spinal cord sources of NGF were eliminated by dorsal root excision. Anti-NGF treatment also failed to block regeneration across 4 mm excision gaps in the nerve trunk. The daily anti-NGF regime continued to be effective for at least 8 weeks, at which time newly evoked collateral sprouting could still be blocked. Exogenous NGF, in doses that evoke collateral sprouting de novo in normal skin, failed to influence regeneration. Finally, an electrical stimulus regime, which markedly reduces the latency of collateral sprouting, failed to affect the time to arrival of regenerating axons at the skin, or the rate of their arborization in it. We conclude that, in striking contrast to their collateral sprouting, the regeneration of nociceptive axons occurs independently of endogenous NGF and is unaffected by impulse activity. These findings further support the proposal that these two growth behaviors have basically different biological functions in the organism.

Animals↗
PubMed1992

Central pain in the absence of functional sensory thalamus.

Since the pioneering publication by Dejerine and Roussy, the thalamus has been commonly implicated in the pathogenesis of central pain. It is well known that cerebral lesions that spare the thalamus as well as both small and large ones within that structure produce similar pain syndromes, but could such pain develop if the thalamus were completely destroyed? CT scans of our patients suggested that it could. Moreover, exhaustive physiological explorations of the thalamus with macro- and microstimulation and microelectrode recordings in 2 more patients in whom CT scans suggested thalamic preservation despite massive suprathalamic infarcts, for the purpose of carrying out deep brain stimulation (DBS), revealed no evidence of ascending or descending diencephalic function. Their sensory examinations were similar to those of patients with congenital hemiatrophy who had undergone hemispherectomy. In 1 case, microstimulation of periaqueductal grey-periventricular grey (PAG-PVG) on the unaffected side of the brain induced the spectrum of responses correctly associated with these areas and during acute stimulation nearly abolished the patient's allodynia and hyperpathia. These observations suggest that processes occurring at a subdiencephalic level (or possibly ipsilaterally) may be involved in the generation of pain. Stroke-induced central pain remains a therapeutic dilemma for the pain surgeon, and the mechanisms underlying this pain state remain a mystery.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral Arteries↗
PubMed1979

Sensory functions of the liver--a review.

In this paper we critically review anatomic, electrophysiological, physiological, and behavioral evidence for neural receptors in the liver. Several lines of evidence suggest that the afferent innervation of the liver may be substantial, although few anatomic studies have directly addressed the question of an hepatic sensory supply. On the other hand, there is convincing functional evidence for a variety of hepatic sensory receptors. Hepatic osmo-, ion, and baroreceptors, sensitive to changes in the osmolarity and electrolyte concentrations in blood and to variations in portal venous pressure, modulate diuresis and natriuresis. Metabolic receptors, for which the adequate stimuli have not yet been specified, influence feeding behavior and gastric acid secretion in response to alterations in hepatic metabolism associated with changes in the supply of metabolic fuels. Directions for future research are suggested and general conclusions about the role of hepatic receptors in homeostasis are discussed.

Afferent Pathways↗
PubMed1979

Sensory functions in chronic neuralgia.

Eleven patients with sustained neuralgia, in most cases after traumatic nerve lesion, were subjected to quantitative sensory testing with thermal and non-noxious mechanical stimuli. Measurements were made in the pain area and at a homologous site on the contralateral normal side. All patients were hypoaesthetic with raised thresholds for warm and cold or touch, or both. Thermal pain thresholds were also raised in some patients but lowered in others indicating hypersensitivity of the nociceptor system or dysaesthesia for thermal input. In six patients single mechanical stimuli produced a painful response above the touch detection threshold. Reaction time measurements indicated that this painful response to suprathreshold mechanical pulses was measured by magnitude estimation as a function of stimulus amplitude. The results were fitted by power functions, as in normal skin, but with steeper slopes on the abnormal side. Suprathreshold hyperaesthesia (recruitment) may exist in the presence of normal threshold functioning.

Adult↗
PubMed1979

Cutaneous sensory function in diabetes mellitus.

That disorders of cutaneous sensation are common in diabetes mellitus can be substantiated by quantitative cutaneous sensory testing. Cutaneous sensory disturbances are not clearly related to clinical factors such as the type, treatment, or duration of diabetes, or ocular complications. Diabetics can be distinguished from nondiabetics on quantitative examination of skin sensation. Juvenile diabetics appear to have fewer cutaneous abnormalities than adults who develop the disease, but the juvenile diabetic is not spared. Disorders of cutaneous sensation may represent a fundamental abnormality of the nervous system in diabetes mellitus. While altered peripheral sensory mechanisms are likely, abnormality of central sensory processing is not excluded by the results of this study.

Adolescent↗
PubMed1992

Weighted needle pinprick sensory thresholds: a simple test of sensory function in diabetic peripheral neuropathy.

A simple device is described, consisting of 12 weighted 23 gauge disposable needles (0.2 to 5.2 g), for testing sensation in busy diabetic clinics. The pinprick sensory threshold (PPT) is the lightest weighted needle which consistently elicits a sharp sensation. The subjects were 48 healthy controls (hospital staff), 44 diabetic patients without neuropathic symptoms, and 35 diabetic patients with chronic painful neuropathy. In the controls, the mean PPT from the right hand and foot obtained on two test occasions a week apart did not differ significantly. In diabetic patients without symptomatic neuropathy, the mean PPT in the right hand and right foot were significantly higher than in the controls. The diabetic patients with painful neuropathy had clearly increased mean PPT in the right hand and foot compared with controls. Marstock thermal limen in diabetic patients with painful neuropathy correlated significantly with PPT determinations. PPT and thermal thresholds probably give comparable information on small fibre dysfunction in diabetic patients with symptomatic neuropathy. Compared with thermal threshold determinations however, the weighted needle apparatus is inexpensive, simple, and rapid to use.

Adolescent↗
PubMed1976

Quantitative assessment of cutaneous sensory function in subjects with neurologic disease.

Based upon techniques devised for the behavioral study of cutaneous sensation in monkeys, a method has been developed which studies quantitatively cutaneous sensation in man. The techniques is analogous to the von Békésy method of audiometry and employs a subject-operated stimulus and signalling divice. In tests utilizing electrical stimulation of the skin surfaces the subject serves as his own control for comparison of one cutaneous zone with another and from one trial session to another. A permanent, written record of stimulus and nonverbal perceptual response is produced in this instrumental method which permits statistical analysis of responses. The analysis includes determination of cutaneous sensory thresholds, limits of stimulus intensity during detection, duration of perception, detection cycle rates, and persistence indices. This instrumental method of cutaneous sensory assessment is quantifiable, free of verbal bias, and repeatable in terms of defined stimulus strengths. In applied clinical studies, patients with peripheral nerve lesions show elevations of perceptual thresholds, reduced numbers of detection-disappearance cycles per unit time, prolonged, contorted decay slopes, and occasionally persistence of perception in the absence of stimulation. Patients with central lesions have variable threshold abnormalities, but little slowing of cycle rate or perceptual persistence. These quantitative sensation parameters can be evaluated longitudinally during the course of an illness and its treatment. The method has potential use in the investigation of basic aspects of sensation and its interactions with behavior.

Adolescent↗
PubMed2026

Hyperbaric oxygen for the treatment of traumatic incomplete spinal cord injury: a systematic review and meta-analysis of randomized controlled trials.

The therapeutic efficacy of hyperbaric oxygen therapy for traumatic incomplete spinal cord injury remains a subject of debate. To comprehensively evaluate the impact of hyperbaric oxygen on motor function, sensory function, and activities of daily living in patients with traumatic incomplete spinal cord injury, we conducted a systematic review and meta-analysis. We performed a comprehensive search across PubMed, Embase, the Cochrane Library, Web of Science, and major Chinese databases for randomized controlled trials published through June 2025. A total of 15 randomized controlled trials were included. The pooled results indicated that hyperbaric oxygen therapy significantly improved the American Spinal Injury Association motor score (mean difference = 10.30, 95% confidence interval: 7.70-12.90), the total American Spinal Injury Association sensory score (mean difference = 29.29, 95% confidence interval: 18.82-39.75), the American Spinal Injury Association light touch score (mean difference = 9.84, 95% confidence interval: 6.15-13.53), and the American Spinal Injury Association pinprick score (mean difference = 8.75, 95% confidence interval: 4.40-13.11). Furthermore, hyperbaric oxygen therapy was associated with significant enhancements in the Barthel Index (mean difference = 16.60, 95% confidence interval: 10.51-22.68) and the Functional Independence Measure (mean difference = 17.41, 95% confidence interval: 10.83-23.98). In conclusion, adjunctive hyperbaric oxygen therapy appears to improve motor function, sensory function, and activities of daily living in patients with traumatic incomplete spinal cord injury compared to conventional treatments alone. However, due to methodological limitations and potential publication bias in the included studies, these findings should be interpreted with caution, and further high-quality, multi-center randomized controlled trials are warranted.

Humans↗
PubMed1979

Sensory neglect after lesions of substantia nigra or lateral hypothalamus: differential severity and recovery of function.

Sensory neglect was studied in cats after unilateral lesions of: lateral hypothalamus (LH); internal capsule (IC) adjacent to the LH; substantia nigra (SN) or the ventromedial hypothalamus (VMH). Special behavioral tests were employed to yield quantifiable data and also to exclude any confounding due to simple movement deficits. Lesions of SN or IC produced severe and enduring contralateral visual and somesthetic deficits and a facilitation of ipsilateral visual responsiveness. In contrast, LH lesions sparing the adjacent IC produced only weak and transient deficits and VMH lesions had no effects on sensory function. This suggests that lesions of the SN or its forebrain connections are important for producing sensory neglect and that sensory deficits after LH lesions are due to infringement on fibers of passage to or from the SN. Lesions which produced neglect often suppressed the amplitude of flash evoked responses in the ipsilateral caudate nucleus and visual and association cortex. However, these evoked potential effects were transient. There was no effect on the spontaneous EEG and this fails to support the hypothesis of a lack of hemispheric arousal in sensory neglect. The results are discussed in relation to nigrotectal projections and the process of attention. This lesion-behavior model is suggested for studies of recovery of function.

Animals↗