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At least 145 records · Page 8Linked to original sources
PubMed1991

[A study of blink reflex in person with severely handicapped].

1) We evaluated blink reflex from 50 cases of severe handicapped. 7 cases (14%) had normal blink reflex. Abnormality of prolonged latency or no response of blink reflex was much more easily seen on R2 and R2' than R1, and dysfunction of spinal trigeminal complex or bulbar reticular formation might be existed in those cases. 2) We found abnormal blink reflex had some relationship with mental disturbance or bulbar function. Result of ABR and head CT also suggested that some kinds of cerebral factors might influenced to blink reflex of severe handicapped cases. 3) Blink reflex was one of the useful records for severe handicapped patients to evaluated underline pathogenesis of brain stem function.

Adult↗
PubMed1999

The impact of cachexia on cardiorespiratory reflex control in chronic heart failure.

BACKGROUND: The mechanism of persistent neurohormonal and cardiorespiratory reflex abnormalities in chronic heart failure remain unclear. Also, why chronic heart failure patients who develop cachexia demonstrate a particularly abnormal neurohormonal profile and have a high risk of death is not known. Impaired reflex control within the cardiac and respiratory systems, and abnormal heart rate variability have both been linked to a poor outcome. Muscle reflexes may contribute to persistent neurohormonal overactivity in wasted patients. Thus, we hypothesized that patients with cardiac cachexia might exhibit particularly profound abnormalities in cardiorespiratory reflexes and heart ratevariability. METHODS AND RESULTS: We investigated 39 chronic heart failure patients: 13 with cardiac cachexia (non-intentional, non-oedematous, documented weight loss of >7.5% of previous normal weight over more than 6 months), and 26 non-cachectic chronic heart failure patients matched according to the severity of chronic heart failure (all men, mean age: 59 vs 60 years, NYHA functional class: 2.6 vs 2.5, peak O(2)consumption: 16.2 vs 16.8 ml. kg(-1). min(-1), left ventricular ejection fraction: 23 vs 24%, all P>0.2 for cachectic vs non-cachectic). In the assessment of the cardiorespiratory reflex control we investigated: cardiac sympathovagal balance (using spectral analysis of heart rate variability to derive low (LF, 0. 04-0.15Hz) and high frequency (HF, 0.15-0.4Hz) components), baroreflex sensitivity (using the phenylephrine method), and peripheral chemosensitivity (using the transient hypoxic method). There was a severely abnormal pattern of cardiorespiratory reflex control in patients with cachexia compared with non-cachectic patients. The former group exhibited severely impaired autonomic reflex control, characterized by an abnormal profile of heart rate variability (reduced LF component), and depressed baroreflex sensitivity (P=0.0001 and P=0.02, respectively, vs non-cachectics). Patients with cachexia also demonstrated an increased peripheral chemosensitivity (0.91 vs0.46 l. min(-1). %SaO(2)(-1), P<0.001, cachectic vs non-cachectic, respectively). In the correlation analyses the degree of impairment in the reflex control was more closely related to wasting, and to the level of neurohormonal activation (as measured by the levels of epinephrine and norepinephrine) than to conventional markers of the severity of heart failure. CONCLUSIONS: Chronic heart failure patients who developed cardiac cachexia demonstrate an abnormal reflex control within the cardiovascular and respiratory systems. The nature of the link between this phenomenon and hormonal changes and the poor prognosis of cachectic chronic heart failure patients warrants further investigation.

Cachexia↗
PubMed1989

Vestibular abnormalities in encephalopathia pugilistica.

Vestibulological examination of boxers revealed that 80% had vestibular abnormalities. These were obvious, but well compensated, so that they remained hidden in everyday life and appeared only on laboratory examination or under stress. Regarding the origin of vestibulo-ocular reflex, abnormalities in boxing contribute three etiopathogenetic factors: the first is the direct traumatization of the vestibular apparatus by a direct blow. The second is the diffuse damage of the brain-stem white matter and of vestibular nuclei. The third factor is the traumatization of the cervical spine via the traumatization of the proprioceptive systems, cervical sympathetic and the adjacent vascular mechanisms. One-third of the abnormalities are caused by direct labyrinthine traumatization. The findings of simultaneous EEG, OKN and ETT abnormalities in one-half of our subjects suggests that there are probably also supratentorial lesions caused by the above-mentioned mechanisms.

Adolescent↗
PubMed1996

The mental nerve blink reflex in the diagnosis of lesions of the inferior alveolar nerve following orthognathic surgery of the mandible.

The purpose of this study was to evaluate the diagnostic value of a new modification of the blink reflex test with stimulation of the distribution of the mental nerve in iatrogenic lesions of the inferior alveolar nerve. The test was performed on 23 patients undergoing orthognathic surgery of the mandible, most of them (20) with bilateral sagittal split osteotomies. The function of the inferior alveolar nerve was studied preoperatively, and 2 weeks, 2 months, 6 months and 1 year postoperatively with both mental nerve blink reflex test and clinical neurosensory testing. The objective electrophysiological test proved to be useful in the diagnosis and follow-up of sensory impairment of the inferior alveolar nerve. The results of the mental nerve blink reflex test and clinical neurosensory testing were closely related. The results of the two tests did not differ statistically significantly in the two first postoperative examinations. The positive predictive value of the mental nerve blink reflex test was better than that of clinical neurosensory testing: an initially abnormal reflex response predicted persistent subjective sensory symptoms after one year more reliably than did altered sensation at the first two examinations. Irrespective of the possible coexistent sensory symptoms and signs, a normal mental nerve blink reflex within 2 months after operation also predicted a reasonably good sensory recovery at 1 year.

Adolescent↗
PubMed1986

Muscle degeneration in the posteclosional development of a Drosophila mutant, abnormal proboscis extension reflex C (aperC).

The aperC (abnormal proboscis extension reflex C) mutation in Drosophila melanogaster causes a defect in the proboscis extension reflex (PER) in aged flies. Young flies of the mutant show an apparently normal PER. When aperCTF36 mutants were reared at 25 degrees C, the flies became unable to extend the proboscis at Day 5 of eclosion, but within a few days, many of them recovered the PER. When reared at 18 degrees C, the mutants showed a defective PER, but did not show the recovery. At 29 degrees C, only a limited number of the mutant flies showed the defective PER. Histological inspection of the mutant revealed that the degeneration occurs in a pair of muscles, the rostral protractors, which are involved in the extension of the rostrum. The degeneration of the muscle was observed in the mutant by polarizing light microscopy. The cross striation disappeared from the central portion of the muscle fibers at Day 3. Birefringence of the fibers also disappeared. At Day 10 the degenerated muscle fibers showed regeneration. The PER was closely correlated with the degree of muscle degeneration and regeneration. Temperature-shift experiments indicated that the temperature-sensitive-period of the aper CTF36 mutation occurs around Days 2-4 after eclosion. Results indicate that the aperC+ gene regulates the posteclosional maintenance of the muscle fibers.

Age Factors↗
PubMed2000

Impaired endothelium-mediated vasodilation is not the principal cause of vasoconstriction in heart failure.

The extent to which abnormal endothelium-dependent vasodilator mechanisms contribute to abnormal resting vasoconstriction and blunted reflex vasodilation seen in heart failure is unknown. The purpose of this study was to test the hypothesis that the resting and reflex abnormalities in vascular tone that characterize heart failure are mediated by abnormal endothelium-mediated mechanisms. Thirteen advanced heart-failure patients (New York Heart Association III-IV) and 13 age-matched normal controls were studied. Saline, acetylcholine (20 microg/min), or L-arginine (10 mg/min) was infused into the brachial artery, and forearm blood flow was measured by venous plethysmography at rest and during mental stress. At rest, acetylcholine decreased forearm vascular resistance in normal subjects, but this response was blunted in heart failure. During mental stress with intra-arterial acetylcholine or L-arginine, the decrease in forearm vascular resistance was not greater than during saline control in heart failure [saline control vs. acetylcholine (7 +/- 3 vs. 6 +/- 3, P = NS) or vs. L-arginine (9 +/- 2 units, P = NS)]. The increase in forearm blood flow was not greater than during saline control in heart failure [saline control vs. acetylcholine (1. 2 +/- 0.3 vs. 1.3 +/- 0.3, P = NS), or vs. L-arginine (1.2 +/- 0.2 ml x min(-1) x 100 ml(-1), P = NS)]. Furthermore, during mental stress with nitroprusside, the decrease in forearm vascular resistance was not greater than during saline control [saline control vs. nitroprusside (7 +/- 3 vs. 5 +/- 4 ml x min(-1) x 100 g(-1), P = NS)], and the increase in forearm blood flow was not greater than during saline control [saline control vs. nitroprusside (1.2 +/- 0.3 vs. 1.3 +/- 0.5 ml x min(-1) x 100 g(-1), P = NS)]. Because the endothelial-independent agent nitroprusside was unable to restore resting and reflex vasodilation to normal in heart failure, we conclude that impaired endothelium-mediated vasodilation with acetylholine-nitric oxide cannot be the principal cause of the attenuated resting- or reflex-mediated vasodilation in heart failure.

Acetylcholine↗
PubMed2004

Cerebellar ataxia and Purkinje cell dysfunction caused by Ca2+-activated K+ channel deficiency.

Malfunctions of potassium channels are increasingly implicated as causes of neurological disorders. However, the functional roles of the large-conductance voltage- and Ca(2+)-activated K(+) channel (BK channel), a unique calcium, and voltage-activated potassium channel type have remained elusive. Here we report that mice lacking BK channels (BK(-/-)) show cerebellar dysfunction in the form of abnormal conditioned eye-blink reflex, abnormal locomotion and pronounced deficiency in motor coordination, which are likely consequences of cerebellar learning deficiency. At the cellular level, the BK(-/-) mice showed a dramatic reduction in spontaneous activity of the BK(-/-) cerebellar Purkinje neurons, which generate the sole output of the cerebellar cortex and, in addition, enhanced short-term depression at the only output synapses of the cerebellar cortex, in the deep cerebellar nuclei. The impairing cellular effects caused by the lack of postsynaptic BK channels were found to be due to depolarization-induced inactivation of the action potential mechanism. These results identify previously unknown roles of potassium channels in mammalian cerebellar function and motor control. In addition, they provide a previously undescribed animal model of cerebellar ataxia.

Animals↗
PubMed2004

Brainstem reflex circuits revisited.

Our current understanding of brainstem reflex physiology comes chiefly from the classic anatomical-functional correlation studies that traced the central circuits underlying brainstem reflexes and establishing reflex abnormalities as markers for specific areas of lesion. These studies nevertheless had the disadvantage of deriving from post-mortem findings in only a few patients. We developed a voxel-based model of the human brainstem designed to import and normalize MRIs, select groups of patients with or without a given dysfunction, compare their MRIs statistically, and construct three-plane maps showing the statistical probability of lesion. Using this method, we studied 180 patients with focal brainstem infarction. All subjects underwent a dedicated MRI study of the brainstem and the whole series of brainstem tests currently used in clinical neurophysiology: early (R1) and late (R2) blink reflex, early (SP1) and late (SP2) masseter inhibitory reflex, and the jaw jerk to chin tapping. Significance levels were highest for R1, SP1 and R2 afferent abnormalities. Patients with abnormalities in all three reflexes had lesions involving the primary sensory neurons in the ventral pons, before the afferents directed to the respective reflex circuits diverge. Patients with an isolated abnormality of R1 and SP1 responses had lesions that involved the ipsilateral dorsal pons, near the fourth ventricle floor, and lay close to each other. The area with the highest probabilities of lesion for the R2-afferent abnormality was in the ipsilateral dorsal-lateral medulla at the inferior olive level. SP2 abnormalities reached a low level of significance, in the same region as R2. Only few patients had a crossed-type abnormality of SP1, SP2 or R2; that of SP1 reached significance in the median pontine tegmentum rostral to the main trigeminal nucleus. Although abnormal in 38 patients, the jaw jerk appeared to have no cluster location. Because our voxel-based model quantitatively compares lesions in patients with or without a given reflex abnormality, it minimizes the risk that the significant areas depict vascular territories rather than common spots within the territory housing the reflex circuit. By analysing statistical data for a large cohort of patients, it also identifies the most frequent lesion location for each response. The finding of multireflex abnormalities reflects damage of the primary afferent neurons; hence it provides no evidence of an intra-axial lesion. The jaw jerk, perhaps the brainstem reflex most widely used in clinical neurophysiology, had no apparent topodiagnostic value, probably because it depends strongly on peripheral variables, including dental occlusion.

Adult↗
PubMed1975

Area specific reflexes from normal and supernumerary hindlimbs of Xenopus laevis.

Two area specific reflexes elicited by natural stimulation of different regions of the hindlimbs of Xenopus laevis have been identified. Light or intense mechanical stimulation of the foot evokes reflex activity in the ipsilateral knee flexor nerve; moderate pressure applied to the calf evokes reflex activity predominantly in the ipsilateral knee extensor nerve. The reflex responses have been recorded electrophysiologically to overcome the limitations of behavioral observations for determining the presence of activity in particular muscles. Normal area specific reflexes are elicited in the normal ipsilateral hindlimb by stimulation of grafted supernumerary hindlimbs innervated either by hindlimb (lumbar) or by non-limb (thoracic) spinal cord segments. The area specific reflexes can be elicited only if the limb is grafted to a host younger than stage 54-55 of Nieuwkoop and Faber ('56), the stage at which reflex movements are first observed behaviorally. Abnormal reflex responses are evoked by stimulation of supernumerary limbs innervated by either thoracic or lumbar segments when the limb buds are grafted to older larvae. Supernumerary forelimbs grafted at early stages and innervated by either thoracic or lumbar spinal cord segments generally fail to elicit area specific reflex responses in the normal hindlimb. Single-unit recordings of afferent fibers supplying the normal and supernumerary hindlimbs show that each limb receives a separate nerve supply. No evidence for branched afferent fibers has been found. The implications of these results for theories of neuronal specification are discussed, particularly the hypothesis that peripheral tissues are able to specify the central actions of afferent fibers that innervate them.

Animals↗
PubMed1999

Increased risk of sensory neuropathy in workers with chloracne after exposure to 2,3,7,8-polychlorinated dioxins and furans.

OBJECTIVE: The existence of a peripheral neuropathy after exposure to polychlorinated dioxins (PCDD) is still discussed, as studies concerning dioxin effects on the peripheral nervous system are rare and contradictory. MATERIAL AND METHODS: Clinical and neurophysiological examinations (motor conduction velocity of the peroneal nerve, sensory conduction velocities of the sural and ulnar nerves) were made in 156 dioxin exposed workers (42 with, 114 without cloracne) from one pesticide producing plant. Because of known risk factors for peripheral neuropathy, 7 workers with and 28 without cloracne were excluded from further analysis. RESULTS: Workers with chloracne had a significantly higher exposure against PCDD as documented by back calculated lipid levels. They complained significantly more often of sexual impotence (28.6% compared to 5.8% of workers without chloracne, P<0.001), had significantly more frequent clinical signs of a sensory neuropathy (= abnormal sensory findings plus deep tendon reflex abnormalities) restricted to the legs (17.1% compared to 1.2%, P<0.001), had significantly more frequent > or =2 neurophysiologic abnormalities (34.3% compared to 14.0%, P<0.025), and had significantly lower mean amplitudes of the motor compound muscle potential of the peroneal nerve. CONCLUSION: PCDD has a mild toxic effect on the peripheral nervous system manifesting as mild sensory neuropathy of the legs in a minority of the most severely exposed persons.

Acne Vulgaris↗