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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Headaches may occur in as many as 25% of hypertensive patients and generally bears little relationship to level of diastolic blood pressure. Previous observations, in normotensive patients, suggested that abnormalities in both potassium and ammonia metabolism might be related to the pathogenesis of these headaches. The present study was undertaken to see whether these factors also occurred in hypertensive patients with headaches. The present observations were made in thirteen hypertensive patients with vascular headaches. The major findings include potassium levels of 3.45 +/- 0.25 mEq/L; CO2, 29.85 +/- 1.21 mEq/L; blood ammonia, 41 +/- 8.40 U mol/L and an alkaline pH of the urine. The blood ammonia levels, when factored by the BUN, yielded elevated ammonia to BUN ratios (3.81 +/- 1.82). These findings are similar to those previously observed in normotensive patients with vascular headaches. The profile of hypokalemia and/or alkalosis, increased blood ammonia to BUN ratios and a relatively alkaline urine appears to be a commonly observed pattern in patients with vascular headaches. These data suggest that a biochemical basis exists for the genesis of vascular headaches in patients with hypertension.
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PMID:The pathogenesis of vascular headaches in patients with hypertension; the role of the ammonia-potassium axis. 364 6

1. Injection of CO2-saturated saline in a distal direction into either a vertebral artery or an internal maxillary artery in pentobarbitone-anaesthetized cats produced abrupt changes in respiration. Vertebral-artery injections produced a transient inhibition of respiration, followed by a stimulation of it. Internal-maxillary-artery injections produced only the inhibition. 2. Injections during inspiration usually shortened that inspiration, reduced its volume and prolonged the following expiration. In the first 30% of an expiration they prolonged that expiration, but given in the next 50% they shortened it. In the last 20% of expiration internal-maxillary-artery injections again slightly prolonged the expiration. 3. Phenyl diguanide injected into either a vertebral or an internal maxillary artery also produced abrupt effects on respiration. 4. The effects of CO2-saturated saline were abolished by intravenous acetazolamide, suggesting that nociceptors may be affected by a change in local pH. 5. The effects may arise from the excitation of vascular nociceptors, and our observations may suggest a way of studying in animals the receptors responsible for headache.
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PMID:The effects on respiration in the cat of the sudden excitation of cerebral vascular nociceptors by carbon dioxide. 681 15

By providing a non-invasive method for continuous display of mean flow velocity (Vmean) in the cerebral arteries, transcranial Doppler (TCD) ultrasound supplements evaluation of cerebral perfusion. Dynamic exercise increases middle cerebral artery (MCA) Vmean from approximately 55 to 65 cm s-1 dependent on work rate, and even more when corrected for changes of the arterial carbon dioxide tension. Evaluation of Vmean corresponds to that of cerebral blood flow as determined with the 133Xenon clearance technique, and reflects regional cortical regulation of the active muscles with important afferent nervous influence. Concomitant increases of mean arterial pressure (MAP) and heart rate is only of minor importance as illustrated during static exercise and post-exercise muscle ischaemia, where Vmean is not significantly elevated. During sustained head-up tilt, the Vmean remained unchanged at a MAP approximately 83 mmHg. Below this level, it decreased in parallel with MAP until MAP reached 50 mmHg. At an even lower MAP, Vmean seemed to approach a lower limit approximately 25 cm s-1, but at a diastolic pressure of 21 mmHg there was no flow in the MCA. Conversely, during post-exercise muscle ischemia, an increase in MAP to 140 mmHg did not influence Vmean. This is in contrast to patients operated for carotid artery stenosis and who develop ipsilateral headache. In these patients the ipsilateral MCA Vmean changed in parallel with MAP, and autoregulation was re-established only after one to two weeks. In patients with severe carotid stenosis and poor collateral circulation, the CO2-reactivity as expressed by Vmean was the lowest, and could be negative on the ipsilateral side. During carotid endarterectomy, a Vmean clamp/Vmean pre-clamp ratio below 0.6 identified patients with a cerebral blood flow below 20 ml 100 g-1 min-1. Furthermore, when the ratio was below 0.4 pathological electroenchephalographic changes developed. Thus, Vmean of the large basal cerebral arteries reflects cerebral perfusion with respect to regional flow distribution, autoregulatory response, and CO2-reactivity in normal man and patients with limited cerebral flow.
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PMID:Transcranial Doppler ultrasound for cerebral perfusion. 748 67

Some controversial issues exist whether regional cerebral blood flow (rCBF) changes are present both in migraine with and without aura during the interictal period. For this reason we have studied rCBF characteristics in migraine patients when headache-free. rCBF examinations were performed by the 133Xe inhalation method on 39 normal subjects (24 aged 45 or less and 15 older than 45), on 10 migraine patients with (A+) and on 10 without (A-) aura. The values of each patient were compared with the age-matched control population mean by a computer-assisted mapping system that allows statistical analysis in real time. To compare inter-individual variability 10 subjects, out of 39 normals, constituted an age-, sex- and CO2-matched control group (C). 8 A+ patients and 7 A- showed significant alterations of CBF in comparison with the age-matched control population. The analysis between the age-, sex- and CO2 matched groups showed significant differences of the inter-hemispheric (F = 6.669, p = 0.004) and of the frontal (F = 7.480 p = 0.0008) asymmetries. These data show that in the headache-free period a derangement of the cerebral perfusion is present in both migraine with and without aura, suggesting they are due to the same disease process. Furthermore they show the usefulness of a computer-assisted mapping system, suitable for clinical use, in discovering small alterations in cerebral perfusion.
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PMID:Interictal abnormalities of regional cerebral blood flow in migraine with and without aura. 756 59

Seven SUNCT patients (six men, one woman) took part in this study. In four patients, respiratory variables were compared during and outside attacks. In five patients, peripheral chemosensitivity was tested and compared with a control group matched with respect to age, sex, and smoking habits. The results indicate that SUNCT patients hyperventilate during attacks. Moreover, they appear to hyperventilate slightly under basal conditions. The tests for peripheral chemoreceptor activity indicated no differences between the SUNCT and the control groups except for one variable, namely the mean ventilatory response to a single breath of 13% CO2. It is possible that this indicates a blunted response of the peripheral chemoreceptors. On the other hand, it may also represent a chance finding, since none of the other results presented suggested such a conclusion, and the size of the test group was very small. The results do not indicate that a reduction in oxygen saturation can trigger SUNCT since low levels of oxygen saturation were only rarely accompanied by SUNCT, whereas many attacks were not associated with any appreciable lowering in arterial oxygen saturation.
Headache 1995 Jun
PMID:Respiratory studies in SUNCT syndrome. 763 20

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

Ten patients with cluster headache in an active period and 6 controls were studied as to heart rate, blood pressure, blood flow in the common carotid arteries (CCA), end-tidal PCO2 and pain before, during and after 6 minutes of breathing 6% CO2 in air. Heart rate increased significantly during CO2 breathing in controls but not in patients. The cluster headache patients had significantly lower baseline end-tidal PCO2 than controls. CCA blood flow increased significantly during CO2 breathing in both groups. Vascular resistance decreased during CO2 provocation and increased above baseline levels 5 minutes after provocation in both groups and related to the end-tidal PCO2. Six of eight cluster headache patients, who had an increase of blood flow at provocation, reported slight to moderate unilateral pain in relation to the CO2 provocation in contrast to controls. One patient treated with 6 mg sumatriptan 2.5 hours before the provocation had an end-tidal PCO2 within the range of the controls, and did not get an increase of CCA blood flow or pain at provocation. Six of the cluster headache patients were restudied when out of the active period. There was still no heart rate increase during CO2 breathing and end-tidal PCO2 was still lower than in the controls. Unilateral headache was not provoked.
Headache 1995 Jan
PMID:Provocation of unilateral pain in cluster headache patients by breathing CO2. 786 33

A single-breath CO2 test was carried out in cluster headache patients both during bout and remission, and in matched healthy individuals (n = 10 for each group) to assess peripheral chemosensitivity. The test subjects inhaled one tidal breath of 13% CO2 in air. The response was expressed as the maximal increase in inspiratory minute ventilation (Vi) within 20 seconds from the exposure to CO2, divided by the increase in end-tidal PCO2 (PETCO2) (the difference in PCO2 between the test breath and the preceding control breaths): delta Vi/delta PETCO2. Under the initial resting condition, cluster headache patients within the bout showed a slight hyperventilation in that there was a significantly reduced PETCO2 (P < 0.05, Student's paired t-test), and during remission, higher Vi, and a lower PETCO2 (P < 0.05, Wilcoxon signed rank test), in comparison with the controls. There was no statistically significant difference as regards the peripheral chemosensitivity between cluster headache and control groups. These results indicate that cluster headache patients have an intact and properly-functioning carotid body.
Headache 1994 Feb
PMID:Cluster headache: the peripheral chemosensitivity as indicated by the single-breath CO2 test. 816 71

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Eighteen cluster headache patients and five controls were studied using ultrasound duplex techniques to measure blood flow in the common carotid arteries after nitroglycerin and placebo administration. Vessel diameter and blood flow tended to be greater before nitroglycerin in patients in the cluster headache period than in patients out of period and controls. Nitroglycerin tended to increase blood flow only in patients not in the cluster period and in controls. There was a significant decrease in common carotid blood flow and increase in vascular resistance related to maximum pain in both nitroglycerin-induced and spontaneous cluster headache attacks. Blood flow did not reach the initial flow values after the attack was over. In one patient a hyperventilation attack only temporarily decreased the pain. We suggest that the decrease in blood flow and increase in vascular resistance may be due to constriction of intracranial arteries by reflex activation of sympathetic efferents, rather than to decrease of arterial CO2 tension.
Cephalalgia 1993 Apr
PMID:Pain induces decrease of blood flow in the common carotid arteries in cluster headache attacks. 849 50


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