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PubMed2003

Itch: scratching more than the surface.

In origin, itch can be cutaneous ("pruritoceptive", e.g. dermatitis), neuropathic (e.g. multiple sclerosis), neurogenic (e.g. cholestasis), mixed (e.g. uraemia) or psychogenic. Although itch of cutaneous origin shares a common neural pathway with pain, the afferent C-fibres subserving this type of itch are a functionally distinct subset: they respond to histamine, acetylcholine and other pruritogens, but are insensitive to mechanical stimuli. Histamine is the main mediator for itch in insect bite reactions and in most forms of urticaria, and in these circumstances the itch responds well to H(1)-antihistamines. However, in most dermatoses and in systemic disease, low-sedative H(1)-antihistamines are ineffective. Opioid antagonists relieve itch caused by spinal opioids, cholestasis and, possibly, uraemia. Ondansetron relieves itch caused by spinal opioids (but not cholestasis and uraemia). Other drug treatments for itch include rifampicin, colestyramine and 17-alpha alkyl androgens (cholestasis), thalidomide (uraemia), cimetidine and corticosteroids (Hodgkin's lymphoma), paroxetine (paraneoplastic itch), aspirin and paroxetine (polycythaemia vera) and indometacin (some HIV+ patients). If the remedies specified fail, paroxetine and mirtazapine should be considered. Ultraviolet B therapy, particularly narrow-band UVB, may be superior to drug treatment for itch in uraemia.

Analgesics, Opioid↗

PubMed2003

A controlled pilot study of the utility of mirror visual feedback in the treatment of complex regional pain syndrome (type 1).

BACKGROUND: We assessed mirror visual feedback (MVF) to test the hypothesis that incongruence between motor output and sensory input produces complex regional pain syndrome (CRPS) (type 1) pain. METHODS: Eight subjects (disease duration > or =3 weeks to < or =3 yr) were studied over 6 weeks with assessments including two controls (no device and viewing a non-reflective surface) and the intervention (MVF). Pain severity and vasomotor changes were recorded. RESULTS: The control stages had no analgesic effect. MVF in early CRPS (< or =8 weeks) had an immediate analgesic effect and in intermediate disease (< or =1 yr) led to a reduction in stiffness. At 6 weeks, normalization of function and thermal differences had occurred (early and intermediate disease). No change was found in chronic CRPS. CONCLUSIONS: In early CRPS (type 1), visual input from a moving, unaffected limb re-establishes the pain-free relationship between sensory feedback and motor execution. Trophic changes and a less plastic neural pathway preclude this in chronic disease.

Adult↗

PubMed1990

Role of set-point theory in regulation of body weight.

In adult individuals body weight is maintained at a relatively stable level for long periods. The set-point theory suggests that body weight is regulated at a predetermined, or preferred, level by a feedback control mechanism. Information from the periphery is carried by an affector to a central controller located in the hypothalamus. The controller integrates and transduces the information into an effector signal that modulates food intake or energy expenditure to correct any deviations in body weight from set-point. Evidence for involvement of various factors and physiological systems in the control of food intake and regulation of body weight and fat are reviewed within the context of a control model. Current working hypotheses include roles for nutrients, dietary composition and organoleptic properties, hormones, neural pathways, various brain nuclei, and many neurotransmitters in the regulation of food intake. It is concluded that regulation of body weight in relation to one specific parameter related to energy balance is unrealistic. It seems appropriate to assume that the level at which body weight and body fat content are maintained represents the equilibria achieved by regulation of many parameters.

Adipose Tissue↗

PubMed2002

Intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension.

UNLABELLED: Sympathetic hyperactivity during sudden intracranial hypertension leads to cardiovascular instability, myocardial dysfunction, and neurogenic pulmonary edema. Because spinal anesthesia is associated with sympatholysis, we investigated the protective effects of intrathecal lidocaine in a rodent model. Halothane-anesthetized rats were given a 10-microL intrathecal injection of saline (n = 10) or lidocaine 1% (n = 6). A subdural balloon catheter was inflated for 60 s to produce intracranial hypertension. Hemodynamics were monitored, and hearts and lungs were harvested for histological examination. In Saline versus Lidocaine-Treated rats, peak mean arterial blood pressure during balloon inflation was 115 +/- 4 mm Hg versus 78 +/- 8 mm Hg (P < 0.05), mean arterial blood pressure 30 min after balloon deflation was 47 +/- 2 mm Hg versus 67 +/- 3 mm Hg (P < 0.05), and lung weight was 1.54 +/- 0.03 g versus 1.41 +/- 0.04 g (P < 0.05), respectively. Cardiac dysrhythmias and electrocardiographic changes were more frequent in the Saline-Treated group (P < 0.05). Saline-Treated rats had extensive, hemorrhagic pulmonary edema, whereas the Lidocaine-Treated rats had only patchy areas of lung abnormality. Histological changes in the myocardium were rare, and no difference was found between the two groups. We conclude that intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension. IMPLICATIONS: In a rat model of intracranial balloon inflation, intrathecal lidocaine prevented cardiovascular collapse and neurogenic pulmonary edema. Descending neural pathways are involved in the development of cardiopulmonary complications associated with acute intracranial hypertension.

Acute Disease↗

PubMed1984

Comparison of changes in the hypoglossal and the phrenic nerve activity in response to increasing depth of anesthesia in cats.

The effects of increasing depths of anesthesia on the activities of the hypoglossal nerve (HN) and the phrenic nerve (PN) were investigated in artificially ventilated, vagotomized cats. An abrupt increase in inspired concentration of halothane from 1% to 4% immediately decreased both HN and PN activities, but HN activity decreased more and disappeared much earlier than did PN activity. Steady-state responses of HN and PN activities to changes in end-tidal concentration of halothane showed that halothane depressed both HN and PN activities in a dose-related manner but at different rates, suggesting that respiratory control of the tongue muscles and the diaphragm are in part mediated by different neural pathways. Differential suppression of PN and HN activities also was observed following an acute increase in anesthetic depth with thiopental and diazepam. In contrast, no such differential suppression was observed following ketamine administration. Thus, differential suppression of PN and HN may be associated not only with depth of anesthesia but also with the type of anesthetic used.

Anesthesia, Inhalation↗

PubMed1996

Intravenous opioids stimulate norepinephrine and acetylcholine release in spinal cord dorsal horn. Systematic studies in sheep and an observation in a human.

BACKGROUND: Opioids produce analgesia by direct effects as well as by activating neural pathways that release nonopioid transmitters. This study tested whether systematically administered opioids activate descending spinal noradrenergic and cholinergic pathways. METHODS: The effect of intravenous morphine on cerebrospinal fluid and dorsal horn microdialysate concentrations of norepinephrine and acetylcholine was examined in 20 sheep. Animals received either intravenous morphine or fentanyl alone, or morphine plus intravenous naloxone or intrathecal idazoxan. RESULTS: Intravenous morphine (0, 0.5, 1 mg/kg, intravenous) produced dose-dependent increases in cerebrospinal fluid norepinephrine and acetylcholine, but not epinephrine or dopamine. Morphine's effect was blocked by intravenous naloxone and by intrathecal idazoxan. In microdialysis experiments, intravenous morphine increased the concentration of norepinephrine and acetylcholine, but not epinephrine or dopamine, in the dorsal horn. In contrast, intravenous morphine exerted no effect on any of these monoamines in the ventral horn. Intravenous naloxone and cervical cord transection each blocked morphine's effect on dorsal horn norepinephrine. CONCLUSIONS: These results support functional studies that indicate that systematically administered opioids cause spinal norepinephrine and acetylcholine release by a naloxone-sensitive mechanism. Idazoxan blockade of morphine's effects on cerebrospinal fluid norepinephrine was unexpected, and suggests that both norepinephrine and acetylcholine release in the spinal cord may be regulated by alpha 2-adrenoceptors. Microdialysis experiments suggest increased norepinephrine and acetylcholine levels in cerebrospinal fluid resulted from intravenous morphine-induced activation of bulbospinal pathways.

Acetylcholine↗

PubMed1996

Divergence of intracranial and central venous pressures in lightly anesthetized, tracheally intubated dogs that move in response to a noxious stimulus.

BACKGROUND: Intracranial pressure (ICP) may increase in tracheally intubated subjects during periods of movement (e.g, "bucking" and coughing). Recent research has suggested that factors other than passive congestion of the cerebral vessels, resulting from increases in central venous pressure, may contribute to the ICP response. The current study evaluated this issue in a canine model of intracranial hypertension and additionally evaluated the relationship between ICP and static increases in superior vena caval pressure. METHODS: Six dogs were lightly anesthetized with 0.65% end-expired halothane in oxygen and nitrogen, and ventilation was mechanically controlled. Intracranial pressure was increased to a stable baseline of 15-20 mmHg using a subarachnoid infusion of warm 0.9% saline solution. The following variables were quantified before, and for 6 min after, initiating a 1-min noxious stimulus to the trachea and skin: ICP, central venous pressure, electromyograms (masseter, deltoid, and intercostal muscles), intrathoracic pressure, and cerebral perfusion pressure (defined as mean arterial pressure -- ICP). Later, the protocol was repeated in the presence of neuromuscular block with pancuronium. Finally, in the same dogs, occlusion of the superior vena cava at its junction with the right atrium was used to increase superior vena caval pressure in 5-mmHg increments, from 5 to 30 mmHG, so that the resulting increases in ICP could be quantified. RESULTS: In unparalyzed dogs whose heads were maintained at the level of the right atrium, there was a 22-mmHg increase in ICP at 1 min after initiating the noxious stimulus (P<0.05). The ICP increase was related to electromyogram activation and a 6-mmHg increase in central venous pressure; however, it was not associated with significant increases in intrathoracic pressure or cerebral perfusion pressure. Treatment with pancuronium abolished the electromyographic, ICP, and central venous pressure responses to noxious stimulus. When superior vena caval pressure was statically manipulated, the resulting ICP increase was only one half the magnitude of the superior vena caval pressure increase. After elevating the head 14 cm, the ratio of ICP to superior vena pressure increases was reduced to one third. CONCLUSIONS: If these results apply to humans, it was concluded that increases in ICP that accompany movement in tracheally intubated patients may arise from two complementary factors: (1) cerebrovascular dilation that correlates with electromyographic activity and is mediated by ascending neural pathways that transmit proprioreceptive information, and (2) passive venous congestion that results from any increase in central venous pressure. The influence of the latter factor can be reduced by elevating the head. (Key words: Blood pressure, venous pressure; mean arterial pressure. Muscle: afferent activity; electromyograms, skeletal. Neuromuscular relaxants: pancuronium.)

Anesthesia↗

PubMed2000

Alpha2-adrenergic receptors in human dorsal root ganglia: predominance of alpha2b and alpha2c subtype mRNAs.

BACKGROUND: Nonselective alpha2-adrenergic receptor (alpha2AR) agonists (e.g., clonidine) mediate antinociception in part through alpha2ARs in spinal cord dorsal horn; however, use of these agents for analgesia in humans is limited by unwanted sedation and hypotension. The authors previously demonstrated alpha2a approximately alpha2b > > > alpha2c mRNA in human spinal cord dorsal horn cell bodies. However, because 20% of dorsal horn alpha2ARs derive from cell bodies that reside in the associated dorsal root ganglion (DRG), it is important to evaluate alpha2AR expression in this tissue as well. Therefore, the authors evaluated the hypothesis that alpha2b mRNA, alpha2c mRNA, or both are present in human DRG. METHODS: Molecular approaches were used to determine alpha2AR expression in 28 human DRGs because of low overall receptor mRNA expression and small sample size. After creation of synthetic competitor cDNA and establishment of amplification conditions with parallel efficiencies, competitive reverse transcription polymerase chain reaction was performed using RNA isolated from human DRG. RESULTS: Overall expression of alpha2AR mRNA in DRG is low but reproducible at all spinal levels. alpha2b and alpha2cAR subtype mRNAs predominate (alpha2b approximately alpha2c), accounting for more than 95% of the total alpha2AR mRNA in DRG at all human spinal nerve root levels. CONCLUSIONS: Predominance of alpha2b and alpha2cAR mRNA in human DRG is distinct from alpha2AR mRNA expression in cell bodies originating in human spinal cord dorsal horn, where alpha2a and alpha2b predominate with little or absent alpha2c expression. These findings also highlight species heterogeneity in alpha2AR expression in DRG. If confirmed at a protein level, these findings provide an additional step in unraveling mechanisms involved in complex neural pathways such as those for pain.

Adult↗

PubMed2003

Mechanism of pupillary reflex dilation in awake volunteers and in organ donors.

BACKGROUND: The mechanism of reflex pupillary dilation was investigated in eight patients who were declared brain dead after rupture of intracranial vascular malformations and in eight awake volunteers. The authors hypothesized that the reflex was primarily a spinal sympathetic reflex that would be blocked by topical application of the alpha1-adrenergic blocking agent dapiprazole and that it would be present in organ donors with intact spinal reflexes and no history of hypoxia. METHODS: In volunteers, pupil size was measured with an infrared pupillometer while brief painful electric stimuli were delivered to the finger. Pain was assessed with a visual analog scale and adjusted with each volunteer to equal 3 on a visual analog scale of 0-10. Subjects were studied before and after topical application of the alpha1-adrenergic antagonist dapiprazole. In organ donors, the authors measured pupil size after high-intensity tetanic electric stimulation and in dapiprazole-blocked and -unblocked pupils after surgically induced nociception. RESULTS: In volunteers, the pupil dilated 0.43 +/- 0.23 mm after nociceptive stimuli. Dapiprazole eyedrops blocked this dilation, confirming that the reflex in awake humans is primarily a sympathetic reflex. Baseline diameters were 5.7 +/- 0.5 mm before dapiprazole and 4.1 +/- 0.9 mm after dapiprazole. In organ donors, a tetanic electric current failed to dilate the pupil, whereas the skin incision dilated the pupil 0.4 +/- 0.4 mm, but this dilation was not blocked by dapiprazole. CONCLUSION: The authors conclude that pupillary reflex dilation, as it is clinically performed in awake subjects by stimulating somatic nociceptors, is a sympathetic reflex. Because it is not present in organ donors, the neural pathway must require a supraspinal component for completion.

Adult↗

PubMed1974

Glucose tolerance and insulin response during and after elective skeletal surgery.

Six patients undergoing elective femoral osteotomy were subjected to a series of intravenous glucose tolerance tests and plasma insulin determinations in a study of the way in which a standard operation affects carbohydrate metabolism. The glucose tolerance of all patients assumed a diabetic pattern; this was already observable in the test made on admission to the operating theater and was still evident during the last test on the second postoperative day. The changes were most profound during and four hours after the operation. Insulin secretion was suppressed on the day of operation, but exceeded preoperative values in the postoperative period. Urinary excretion of catecholamines was determined in 4 patients; there was no correlation between the degree of insulin suppression and the catecholamine output. The assumption that the hyperglycemic response and insulin suppression are mediated along splanchnic neural pathways was not confirmed in a quadriplegic patient, who responded to an intravenous glucose tolerance test soon after the injury with hyperglycemia, insulin suppression and a low catecholamine output. It is concluded that the hyperglycemia and insulin suppression observed after trauma represent a complex and purposeful metabolic response, in which several causative factors are involved.

Anesthesia, Inhalation↗

PubMed2003

Neurohumoral control of exocrine pancreatic secretion.

Reports over the past year provide significant advances in our knowledge of the neurohumoral control of exocrine pancreatic secretion, especially related to human physiology. Major findings include those demonstrating that human pancreatic acinar cells do not respond to cholecystokinin stimulation and that a major circulating form of cholecystokinin is CCK-58. These findings establish that in humans, cholecystokinin causes pancreatic secretion via a neural circuit after interacting with neural sensory receptors in the mucosa of the intestine and that CCK-58 is the likely form of cholecystokinin that stimulates the neural pathways. Other findings demonstrate significant differences in the pancreatic secretory response in humans as a function of the type of nutrient delivered to the gut, especially the fact the elemental diets and medium-chain triglycerides cause much less stimulation of pancreatic secretion than do complex diets. Finally, convincing evidence demonstrating that pancreatic proteases cause inhibition of pancreatic secretion in humans has been presented. In addition to new insights into the neurohumoral control of pancreatic secretion, these findings provide information relevant to both the pathogenesis of pancreatic disorders and their treatment.

Journal Article↗

PubMed2004

Neurohumoral control of exocrine pancreatic secretion.

PURPOSE OF REVIEW: Advancing knowledge about normal physiology of the exocrine pancreas is essential for investigations into the mechanisms of disorders of the pancreas. To this end, reports published during the past year give further insights into the complexity of the hormonal and neural interactions and processes involved in exocrine pancreatic physiology. RECENT FINDINGS: Key findings include demonstrations of different biologic effects of cholecystokinin peptides on pancreatic secretion, underlining the importance of measurement techniques to determine specific forms of peptide hormones involved in physiologic processes; investigations of the details of the central neural pathways involved in the vago-vagal reflex in pancreatic secretion; the demonstration of the essential role for intrapancreatic nerves in mediating meal-induced responses; and identification of a modulatory role for leptin in exocrine pancreatic secretion. SUMMARY: These findings should not only spur further investigations into mechanisms of normal physiology but also provide impetus for application of these findings to studies of pancreatic disorders.

Journal Article↗

PubMed1991

Measuring time to awareness.

The timing of two simultaneous responses to one single visual event, namely the sudden subjective expansion of a real object occurring at the onset of a reaching movement, was measured in normal subjects. The motor response was represented by the earliest sign of correction in trajectory of the movement. The subjective report was represented by a vocal utterance that the subjects were instructed to emit when they became aware of the change in appearance of the object. The subjective report lagged the motor response by 150 ms. Control experiments ruled out a possible interference between the two responses. It is concluded that this temporal dissociation reflects a duality of neural pathways involved in processing object-related information.

Awareness↗

PubMed1994

Induction of LTD but not LTP through metabotropic glutamate receptors in visual cortex.

Long-term potentiation (LTP) and long-term depression (LTD), often used as essential components in synaptic models for learning, memory and forgetting, can be produced in cortical tissue by repetitive activation of neural pathways under different stimulus conditions. The involvement of metabotropic glutamate receptors (mGluRs) has been postulated to be necessary for the establishment of either or both forms of synaptic plasticity in hippocampus. The recent introduction of a specific antagonist for mGluRs, (+/-)-alpha-methyl-4-carboxyphenylglycine, prompted the investigation of the respective involvement of this receptor population in the induction of LTP and LTD in visual cortex of the rat in vitro. The results suggest the critical involvement of mGluRs in producing LTD but not LTP.

Animals↗

PubMed1996

Grasping without form discrimination in a hemianopic field.

Although patients with blindsight are usually unable to discriminate forms, recent neuropsychological data have suggested that they could still use some form attributes in object-oriented actions. One patient with a complete right hemianopia due to a medial occipital lesion has been tested for his capacities to process orientation and size of visual objects. He was presented with either a slot of variable orientation or with rectangular objects of the same surface but variable length. His performance was studied in three types of tasks: motor, in which he had to insert a card in the slot or to grasp the rectangle between thumb and indexfinger; verbal, in which forced-choice verbal guesses were required; and matching, which required matching orientation or size with wrist or fingers. Although responses were at chance level in the two latter conditions, motor responses were systematically influenced by both orientation and size of the stimulus. These data provide further evidence for two dissociable modes of visual information processing dealing respectively with 'what"' the object is vs 'how' to grasp it. They also indicate that the neural pathway controlling visuomotor transformation in humans is much less dependent on V1 input than the pathway involved in visual discrimination and identification.

Adult↗

PubMed1998

Investigating form and colour perception in blindsight using an interference task.

Patients with striate cortical damage causing a hemianopic field defect can nevertheless demonstrate residual visual capacities in their blind field. Previous research investigating blindsight required patients to respond explicitly to stimuli appearing in the blind field by making forced choice judgements. We present data from a patient with a left occipital lesion resulting in a homonymous hemianopia, using the flanker task. This patient displayed a significant flanker congruency effect (FCE) for colour and letter stimuli even when they appeared in the blind field. A control patient with a lesion of the right thalamus showed no FCE in the blind field. This suggests that thalamo-extrastriate neural pathways are necessary for residual functioning in blindsight.

Aged↗

PubMed2000

The development of the nociceptive responses in neurokinin-1 receptor knockout mice.

An important yet unanswered question is how neonates respond to painful stimuli, given the immaturity of their neural pathways. We examined the development of the neurokinin system using a novel approach, examining changes of this system by observing the pain responses of mice lacking the NK1 receptor at different stages of development We show that the NK1 receptor is not involved in nociception to heat, mechanical or chemical stimuli, at 3 days. In contrast, the NK1 receptor is involved in nociceptive responses to high intensity heat and mechanical stimuli, and mediates the second phase of the formalin response in 21-day-old mice. This indicates that nociception in neonates does not require the NK1 receptor and that the functional maturation of the NK1 receptor allows diversity in both the type of stimuli that activate the pain system and the types of responses elicited by nociceptive stimuli.

Aging↗

PubMed2000

Serotonin depletion decreases light induced c-fos in the rat suprachiasmatic nucleus.

The suprachiasmatic nucleus (SCN) is the locus of the biological clock in mammals. Daily light cycles entrain the endogenous circadian rhythms in mammals through direct and indirect neural pathways from the retinae to the suprachiasmatic nucleus. We have studied the effect of serotonin depletion on the photic induction of the early response gene c-fas in the SCN of rats. Serotonin depletion, verified by immunohistochemistry, produced a significant decrease (42%) in the number of c-FOS positive cells in the ventrolateral portion of the SCN. These results support the involvement of serotonin as a mediator of photic information to the SCN through the retinal projection to the dorsal raphe nucleus.

Animals↗