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Unilateral Lesion (unilateral + lesion)
Selected AbstractsUnilateral lesions in a patient with keratosis follicularisJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 5 2001E Erkek [source] Pattern Formation And Rhythm Generation In The Ventral Respiratory GroupCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2000Donald R McCrimmon SUMMARY 1. There is increasing evidence that the kernel of the rhythm-generating circuitry for breathing is located within a discrete subregion of a column of respiratory neurons within the ventrolateral medulla referred to as the ventral respiratory group (VRG). It is less clear how this rhythm is transformed into the precise patterns appearing on the varied motor outflows. 2. Two different approaches were used to test whether subregions of the VRG have distinct roles in rhythm or pattern generation. In one, clusters of VRG neurons were activated or inactivated by pressure injection of small volumes of neuroactive agents to activate or inactivate groups of respiratory neurons and the resulting effects on respiratory rhythm and pattern were determined. The underlying assumption was that if rhythm and pattern are generated by neurons in different VRG subregions, then we should be able to identify regions where activation of neurons predominantly alters rhythm with little effect on pattern and other regions where pattern is altered with little effect on rhythm. 3. Based on the pattern of phrenic nerve responses to injection of an excitatory amino acid (DL -homocysteate), the VRG was divided into four subdivisions arranged along the rostrocaudal axis. Injections into the three rostral regions elicited changes in both respiratory rhythm and pattern. From rostral to caudal the regions included: (i) a rostral bradypnoea region, roughly associated with the Bötzinger complex; (ii) a dysrhythmia/tachypnoea area, roughly associated with the pre-Bötzinger complex (PBC); (iii) a second caudal bradypnoea area; and, most caudally, (iv) a region from which no detectable change in respiratory motor output was elicited. 4. In a second approach, the effect of unilateral lesions of one subregion, the PBC, on the Breuer,Hering reflex changes in rhythm were determined. Activation of this reflex by lung inflation shortens inspiration and lengthens expiration (TE). 5. Unilateral lesions in the PBC attenuated the reflex lengthening of TE, but did not change baseline respiratory rhythm. 6. These findings are consistent with the concept that the VRG is not functionally homogeneous, but consists of rostrocaudally arranged subregions. Neurons within the so-called PBC appear to have a dominant role in rhythm generation. Nevertheless, neurons within other subregions contribute to both rhythm and pattern generation. Thus, at least at an anatomical level resolvable by pressure injection, there appears to be a significant overlap in the circuitry generating respiratory rhythm and pattern. [source] Nigrostriatal denervation does not affect glutamate transporter mRNA expression but subsequent levodopa treatment selectively increases GLT1 mRNA and protein expression in the rat striatumJOURNAL OF NEUROCHEMISTRY, Issue 4 2001J.-C. Liévens There is growing evidence that the loss of the nigrostriatal dopaminergic neurones induces an overactivity of the corticostriatal glutamatergic pathway which seems to be central to the physiopathology of parkinsonism. Moreover, glutamatergic mechanisms involving NMDA receptors have been shown to interfere with the therapeutical action of levodopa. Given the key role played by uptake processes in glutamate neurotransmission, this study examined the effects of nigrostriatal deafferentation and of levodopa treatment on the striatal expression of the glutamate transporters GLT1, GLAST and EAAC1 in the rat. No significant changes in striatal mRNA levels of these transporters were detected after either levodopa treatment (100 mg/kg; i.p., twice a day for 21 days) or unilateral lesion of the nigrostriatal pathway by intranigral 6-hydroxydopamine injection. In contrast, animals with the lesion subsequently treated with levodopa showed a selective increase (36%) in GLT1 mRNA levels in the denervated striatum versus controls. These animals also showed increased GLT1 protein expression, as assessed by immunostaining and western blotting. These data provide the first evidence that levodopa therapy may interfere with striatal glutamate transmission through change in expression of the primarily glial glutamate transporter GLT1. We further suggest that levodopa-induced GLT1 overexpression may represent a compensatory mechanism preventing neurotoxic accumulation of endogenous glutamate. [source] Effect of estradiol on striatal dopamine activity of female hemiparkinsonian monkeysJOURNAL OF NEUROSCIENCE RESEARCH, Issue 7 2009Marc Morissette Abstract A higher prevalence and incidence of Parkinson's disease is observed in men, and beneficial motor effects of estrogens are observed in parkinsonian women. In rodents, an effect of estradiol on dopamine systems is documented, whereas much less is known in monkeys. Enkephalin was shown to exert a compensatory modulatory effect on the denervated dopamine nigrostriatal pathway in monkeys and in humans. Moreover in rodents, striatal preproenkephalin mRNA is increased by estrogen treatment. Hence, we investigated the responsiveness of striatal dopamine to estradiol in long-term ovariectomized monkeys bearing a unilateral lesion with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to mimic parkinsonian postmenopausal women. Seven ovariectomized female monkeys received a unilateral MPTP lesion; 4 years after ovariectomy, three received 1-month treatment with 17,-estradiol and the others received vehicle. The lesioned striata showed extensive denervation in all monkeys as measured with dopamine and metabolite concentrations assayed by high-performance liquid chromatography and by autoradiography of the dopamine transporter. The lesioned and intact striata of estradiol-treated monkeys had increased 3-methoxytyramine, and lesioned putamen increased dopamine concentrations compared with vehicle-treated monkeys. Estradiol treatment increased the dopamine transporter in subregions of the intact caudate and putamen compared with the intact striata of vehicle-treated monkeys, but not in the lesioned striata. Preproenkephalin mRNA levels measured by in situ hybridization were increased in the lesioned striata of vehicle treated monkeys and were not further enhanced in estradiol-treated monkeys. These results show that long after ovariectomy, modeling postmenopausal hormonal conditions, brain dopamine metabolism, and transporter are still responsive to estradiol. © 2008 Wiley-Liss, Inc. [source] Neural plasticity of neonatal hypoglossal nerve for effective sucklingJOURNAL OF NEUROSCIENCE RESEARCH, Issue 11 2007Nanae Fukushima Abstract The adaptive movement of the tongue after unilateral lesion of the hypoglossal (XII) nerve during the early postnatal days is essential for recovery of milk intake. The present study investigated the basic mechanisms underlying such adaptation, focusing on the neural plasticity that allows effective suckling. After resection of the ipsilateral XII nerve on P1, 1,1,-dioctadecyl-3,3,3,,3,-tetramethylindocarbocyanine perchlolate (DiI), a postmortem neuronal tracer, was applied to the contralateral uninjured XII nerve on P4 and P7. DiI-labeled fibers were traced successfully within the tongue and showed gradually increased extension over the XII nerve-injured side in the central core portion of the denervated tongue between P4 and P7. Systematic neuroanatomic experiments showed that contralateral axonal sprouting occurred as early as 1 day after nerve injury (P2), and that such axonal sprouting occurred exclusively from the medial branch of the XII nerve responsible for tongue protrusion, an essential movement for suckling. These findings provide direct evidence of functional neural plasticity that allows effective suckling in XII nerve-injured newborns with suckling disturbance. © 2007 Wiley-Liss, Inc. [source] Elbow flexion response as another primitive reflexPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 2 2002Kazumasa Sudo MD Abstract In daily clinical practice we noticed that patients with intellectual impairment spontaneously flex the elbow within a few seconds of the forearm being manipulated during routine examination of spasticity of the muscles in the upper extremities. We termed this phenomenon elbow flexion response (EFR), and prospectively studied it in 229 patients who underwent in-hospital rehabilitation following brain damage. Evaluation of each patient included EFR, patient profile, ability to communicate, scores on three parameters from various intelligence tests, scores on seven parameters testing primitive reflexes, and scores on three parameters describing personality. We investigated for relationships among these parameters. Consequently, although EFR rarely have a statistical association with the varied profiles of patients, patients with bilateral lesion or bilateral paresis demonstrated significantly more marked EFR than those with unilateral lesion or unilateral paresis. Patients with involvement of the frontal lobe showed significantly more marked EFR than those without damage in this area. Elbow flexion responses occurred significantly more frequently in relation with lower scores on intelligence and occurred with significantly higher frequency in conjunction with the more marked appearance of conventional primitive reflexes. Therefore, we conclude that EFR have a strong association with intelligence and with the existence of frontal lobe lesion, and their mode of clinical presentation parallels that of primitive reflexes particularly that of the grasp reflex. We propose that EFR could be referred as a variation of the grasp reflex occurring in the more proximal or axial part of the body. [source] Selective lesion of retrotrapezoid Phox2b-expressing neurons raises the apnoeic threshold in ratsTHE JOURNAL OF PHYSIOLOGY, Issue 12 2008Ana C. Takakura Injection of the neurotoxin saporin,substance P (SSP-SAP) into the retrotrapezoid nucleus (RTN) attenuates the central chemoreflex in rats. Here we ask whether these deficits are caused by the destruction of a specific type of interneuron that expresses the transcription factor Phox2b and is non-catecholaminergic (Phox2b+TH,). We show that RTN contains around 2100 Phox2b+TH, cells. Injections of SSP-SAP into RTN destroyed Phox2b+TH, neurons but spared facial motoneurons, catecholaminergic and serotonergic neurons and the ventral respiratory column caudal to the facial motor nucleus. Two weeks after SSP-SAP, the apnoeic threshold measured under anaesthesia was unchanged when fewer than 57% of the Phox2b+TH, neurons were destroyed. However, destruction of 70 ± 3.5% of these cells was associated with a dramatic rise of the apnoeic threshold (from 5.6 to 7.9% end-expiratory P). In anaesthetized rats with unilateral lesions of around 70% of the Phox2b+TH, neurons, acute inhibition of the contralateral intact RTN with muscimol instantly eliminated phrenic nerve discharge (PND) but normal PND could usually be elicited by strong peripheral chemoreceptor stimulation (8/12 rats). Muscimol had no effect in rats with an intact contralateral RTN. In conclusion, the destruction of the Phox2b+TH, neurons is a plausible cause of the respiratory deficits caused by injection of SSP-SAP into RTN. Two weeks after toxin injection, 70% of these cells must be killed to cause a severe attenuation of the central chemoreflex under anaesthesia. The loss of an even greater percentage of these cells would presumably be required to produce significant breathing deficits in the awake state. [source] Pattern Formation And Rhythm Generation In The Ventral Respiratory GroupCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2000Donald R McCrimmon SUMMARY 1. There is increasing evidence that the kernel of the rhythm-generating circuitry for breathing is located within a discrete subregion of a column of respiratory neurons within the ventrolateral medulla referred to as the ventral respiratory group (VRG). It is less clear how this rhythm is transformed into the precise patterns appearing on the varied motor outflows. 2. Two different approaches were used to test whether subregions of the VRG have distinct roles in rhythm or pattern generation. In one, clusters of VRG neurons were activated or inactivated by pressure injection of small volumes of neuroactive agents to activate or inactivate groups of respiratory neurons and the resulting effects on respiratory rhythm and pattern were determined. The underlying assumption was that if rhythm and pattern are generated by neurons in different VRG subregions, then we should be able to identify regions where activation of neurons predominantly alters rhythm with little effect on pattern and other regions where pattern is altered with little effect on rhythm. 3. Based on the pattern of phrenic nerve responses to injection of an excitatory amino acid (DL -homocysteate), the VRG was divided into four subdivisions arranged along the rostrocaudal axis. Injections into the three rostral regions elicited changes in both respiratory rhythm and pattern. From rostral to caudal the regions included: (i) a rostral bradypnoea region, roughly associated with the Bötzinger complex; (ii) a dysrhythmia/tachypnoea area, roughly associated with the pre-Bötzinger complex (PBC); (iii) a second caudal bradypnoea area; and, most caudally, (iv) a region from which no detectable change in respiratory motor output was elicited. 4. In a second approach, the effect of unilateral lesions of one subregion, the PBC, on the Breuer,Hering reflex changes in rhythm were determined. Activation of this reflex by lung inflation shortens inspiration and lengthens expiration (TE). 5. Unilateral lesions in the PBC attenuated the reflex lengthening of TE, but did not change baseline respiratory rhythm. 6. These findings are consistent with the concept that the VRG is not functionally homogeneous, but consists of rostrocaudally arranged subregions. Neurons within the so-called PBC appear to have a dominant role in rhythm generation. Nevertheless, neurons within other subregions contribute to both rhythm and pattern generation. Thus, at least at an anatomical level resolvable by pressure injection, there appears to be a significant overlap in the circuitry generating respiratory rhythm and pattern. [source] | |||||||||||||