Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPERESTHESIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1979

Acute hyperesthesia after spinal trauma.

Four cases of acute hyperesthesia after spinal trauma are presented. An attempt is made to characterize the natural history of this syndrome. In the three cases with truncal sensory aberration, hyperesthetic zones developed only anteriorly. All four patients demonstrated spontaneous relief of pain within 2 weeks after injury. The pain was modified by transcutaneous stimulation in one case and by l-dopa in another case. It is suggested that the "lesion" responsible for the hyperesthetic response is partial damage to dorsal root fibers at a point medial to the dorsal root ganglion.

Acute Disease↗
PubMed1986

Hindlimb hyperesthesia associated with rabies in two horses.

Rabies was diagnosed in 2 adult Quarter Horses with hindlimb hyperesthesia and progressive weakness. Microscopic examination of the cord and brain of the first horse revealed nonsuppurative meningomyelitis and ganglioneuritis in the cord extending cranially to the 6th cervical segment. Fluorescent antibody test results of both horses were positive for rabies in hindlimb peripheral nerve specimens, but negative in sections of the upper lip. Salivary gland, cerebrum, cerebellum, hippocampus, musculocutaneous nerve, cornea, and optic nerve specimens were tested for rabies by fluorescent antibody technique to determine viral distribution in the body of the second horse.

Animals↗
PubMed1977

[Chronic hyperesthesia in rats caused by lesions in the dorsal roots of the branchial plexus].

Traumatic avulsions of the brachial plexus in Man is followed by development of hyperesthesia which is known to be reistant to pharmacological medication. We have been able to reproduce this syndrome in the Rat and have used this disturbed animal as a model. This model will give us the possibility of studying nervous mechanisms responsible for these abnormal pains and to look for effective treatments.

Animals↗
PubMed1996

Mechanisms of paresthesiae, dysesthesiae, and hyperesthesiae: role of Na+ channel heterogeneity.

Paresthesiae, dysesthesiae, and hyperesthesiae ('positive symptoms') result from ectopic nerve impulses secondary to inappropriate membrane excitability which develops in the setting of chronic sensory axonal injury. The molecular changes in the membranes of dorsal root ganglion neurons which underlie ectopic impulse generation as a result of chronic axonal injury are unknown. Preliminary evidence has suggested that voltage-dependent Na+ channels are one of the participants in the production of ectopic impulses, but the precise form of their participation remains to be determined. The present paper reviews normal sensory anatomy and Na+ channel physiology, as well as clinical syndromes heralded by positive sensations and what is so far known about the cellular and molecular mechanisms underlying them. Properties of two distinct populations of Na+ channels native to the DRG neurons which give rise to cutaneous afferents are described. The biophysical properties of each population of Na+ channels must be tuned with respect to the other in order to cooperate in the generation of action potential activity underlying normal sensory function. A novel hypothesis is put forth suggesting that chronic axonal injury leads to intraneuronal heterogeneity of the populations of Na+ channels in cutaneous afferents, as revealed by their characteristic properties. This may result in one population of Na+ channels activating the other, leading to membrane instability, and possibly to ectopic impulse generation.

Axons↗
PubMed1992

Spinal pharmacology of thermal hyperesthesia induced by constriction injury of sciatic nerve. Excitatory amino acid antagonists.

This study evaluated the effects of spinally administered excitatory amino acid antagonists on the thermal hyperesthetic state induced by unilateral partial ligation of the sciatic nerve in the rat. The measured response was the latency to paw withdrawal of each hind paw after application of a focused heat lamp on the plantar surface of the paw through a glass plate upon which the animal stood. In this work, antagonists (MK801, DL-2-amino-5-phosphonovalerate, ketamine) of the N-methyl-D-aspartate receptor (NMDA), the glycine potentiation site at the NMDA receptor (5-chloro-indole-2-carboxylic acid) and non-NMDA receptor (kynurenic acid: g-D-glutamylaminomethyl sulphonate) were injected through chronically implanted lumbar intrathecal catheters in normal rats (no lesions) and in rats with unilateral constriction injury. In the normal rat study, NMDA and non-NMDA antagonists had little effect upon paw withdrawal latency at intrathecal doses which did not produce readily detectable motor weakness. In the hyperesthetic rat study, NMDA antagonists would temporarily eliminate the hyperesthetic state at doses below those which altered the response latency of the normal paw or which altered motor function. These results suggested that spinal NMDA receptors play an important role in the hyperesthetic state induced by peripheral nerve injury.

Amino Acids↗
PubMed2004

Corneal epitheliopathy of dry eye induces hyperesthesia to mechanical air jet stimulation.

PURPOSE: To evaluate corneal sensation in different groups: normal subjects, dry eye patients, and patients with and without dry eye after laser in situ keratomileusis (LASIK) using the modified Belmonte gas esthesiometer. DESIGN: A retrospective, clinic-based, case-control study. METHODS: We evaluated 20 normal subjects, 20 dry eye patients, 20 post-LASIK patients without dry eye, and six post-LASIK patients with dry eye. The corneal sensation was measured with the modified Belmonte gas esthesiometer that uses two different stimuli to assess mechanical and polymodal receptors on the corneal surface. Mechanoreceptors were assessed by 2-second pulsed air jets of variable intensity. Polymodal receptors were measured by stimulating the corneal with 2-second pulsed air jets of varying concentrations of CO(2), a gas that is converted to carbonic acid on contact with the corneal surface. The main outcome measure was determining corneal sensation. RESULTS: The mean +/- standard deviation (+/- SD) age was similar in all groups. The mean mechanical threshold was 61.50 +/- 20.07 ml/min in the normal group (n = 20), 34.60 +/- 21.09 ml/min in the dry group (n = 20, P <.05 vs normal), 99.50 +/- 47.40 ml/min in the post-LASIK group (n = 20, P <.01 vs normal), and 50.00 +/- 15.49 ml/min in the post-LASIK patients with keratitis sicca (n = 06, P <.05 vs post-LASIK). The percentage of CO(2) to elicit discomfort was similar in all groups (P >.05). No sex-related differences were noted (P >.05). There was a significant inverse correlation between the threshold of mechanical stimulation and the severity of corneal fluorescein staining. CONCLUSIONS: The Belmonte modified noncontact esthesiometer is a sophisticated instrument that can assess different types of corneal sensory receptors. Patients with dry eye were hypersensitive to the air jet stimulus of this instrument, and this appears to be due to altered corneal epithelial barrier function. Profound hypoesthesia was observed after LASIK and similar to dry eye, post-LASIK patients with dry eye were sensitized. These findings provide new insight into the hypersensitivity to environmental stresses, particularly air drafts experienced by dry eye patients.

Adult↗