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Biomedical subjects

G Cordingley

Publications and source records attributed to G Cordingley.

7 recordsLinked to original sources
PubMed2000

Psychosocial correlates and impact of chronic tension-type headaches.

OBJECTIVES: To examine the psychosocial correlates of chronic tension-type headache and the impact of chronic tension-type headache on work, social functioning, and well-being. METHODS: Two hundred forty-five patients (mean age = 37.0 years) with chronic tension-type headache as a primary presenting problem completed an assessment protocol as part of a larger treatment outcome study. The assessment included a structured diagnostic interview, the Medical Outcomes Study Short Form, Disability Days/Impairment Ratings, Recurrent Illness Impact Profile, Beck Depression Inventory, State-Trait Anxiety Inventory-Trait Form, Primary Care Evaluation for Mental Disorders, and the Hassles Scale Short Form. Comparisons were made with matched controls (N = 89) and, secondarily, with Medical Outcomes Study data for the general population, arthritis, and back problem samples. RESULTS: About two thirds of those with chronic tension-type headache recorded daily or near daily (> or =25 days per month) headaches with few (12%) recording headaches on less than 20 days per month. Despite the fact that patients reported that their headaches had occurred at approximately the present frequency for an average of 7 years, chronic tension-type headache sufferers were largely lapsed consulters (54% of subjects) or current consulters in primary care (81% of consulters). Significant impairments in functioning and well-being were evident in chronic tension-type headache and were captured by each of the assessment devices. Although headache-related disability days were reported by 74% of patients (mean = 7 days in previous 6 months), work or social functioning was severely impaired in only a small minority of patients. Sleep, energy level, and emotional well-being were frequently impaired with about one third of patients recording impairments in these areas on 10 or more days per month. Most patients with chronic tension-type headache continued to carry out daily life responsibilities when in pain, although role performance at times was clearly impaired by headaches and well-being was frequently impaired. Chronic tension-type headache sufferers were 3 to 15 times more likely than matched controls to receive a diagnosis of an anxiety or mood disorder with almost half of the patients exhibiting clinically significant levels of anxiety or depression. Affective distress and severity of headaches (Headache Index) were important determinants of headache impact/impairment. CONCLUSIONS: Chronic tension-type headache has a greater impact on individuals' lives than has generally been realized, with affective distress being an important correlate of impairment. If treatment is to remedy impairment in functioning, affective distress, as well as pain, thus needs to be addressed.

Adolescent↗
PubMed1993

Increases in serum prolactin levels associated with syncopal attacks.

Numerous investigators have found that serum prolactin levels increase after tonic-clonic and partial complex seizures, but the effect of syncope on prolactin levels has been studied little. Serum prolactin levels were measured following unexpected syncopal attacks in patients seeking emergency treatment in a community hospital. Levels sampled 18 to 60 minutes after syncopal episodes were increased in 8 of 11 cases. Follow-up prolactin levels, measured 17 to 222 days later, were normal in all eight cases in which they were initially increased. Most subjects had concurrent illness. Although the current study does not clarify whether it was the syncope, the concurrent illness, or both that caused the prolactin elevations, it implies that measurement of this hormone will not help the clinician in distinguishing between seizures and syncopal attacks.

Adolescent↗
PubMed1981

Sarcoidosis presenting as senile dementia.

Cerebral sarcoidosis was found at autography in a 68-year-old woman with progressive dementia. Of 35 previously reported cases of central nervous system sarcoidosis with dementia, only 1 was over 65 years old, and in only 2 was the presenting clinical syndrome that of a degenerative dementia. Other unusual features of the index case include the restriction of the initial cognitive deficit to memory loss and mild anomia, the scarcity of antemortem evidence for systemic sarcoidosis, a positive tuberculin test, a cerebrospinal fluid (CSF) protein concentration as high as 2028 mg per deciliter. sarcoidosis is a rare but potentially treatable cause of dementia. Consistently normal CSF probably excludes the diagnosis.

Aged↗
PubMed1977

Phenobarbital actions in vivo: effects on extra cellular potassium activity and oxidative metabolism in cat cerebral cortex.

Extracellular potassium activity and changes in the reduction levels of intramitochondrial pyridine nucleotide (NAD) and cytochrome-a,a3 were monitored in the cerebral cortex of cats at rest and during electrical stimulation, before and after administration of sodium phenobarbital. Stimulation of the cortical surface evoked a transient increase in the level of oxidized NAD which was proportional in magnitude to the associated transient elevation of extracellular potassium. Phenobarbital (i.v.) produced, within minutes, a persistent shift in NAD to a more reduced level indicative of decreased oxygen consumption. Electrical excitability of the cortex also decreased within minutes, although there was no concomitant change in the resting extracellular potassium activity. Cortical stimulation produced transient elevations of [K+]0 and NADH oxidation and these responses returned to base lines more slowly following the barbiturate administration. However, the proportionality between NADH oxidation and [K+]0 elevation was not altered by phenobarbital. The kinetics of the cytochrome-a, a3 response to cortical stimulation mirrored those of NADH, implying that phenobarbital was not blocking electron transport in the respiratory chain between NADH and cytochrome-a, a3 even at doses where "resting" tissue oxygen consumption was decreased. The prolongation of recovery metabolism following phenobarbital was interpreted as being the result of protracted elevation of extracellular potassium activity. The slow return to "resting" levels of extracellular potassium is probably caused by interference with passive clearance mechanisms.

Animals↗
PubMed1976

Potassium, neuroglia, and oxidative metabolism in central gray matter.

Reviewed is the author's investigation of potassium in extracellular fluid of cerebral neocortex and spinal cord determined with ion-selective microelectrodes, and of oxidative metabolism monitored by fluorometric determination of intramitochondrial NADH in intact cortex. When gray matter is excited by afferent input, or by direct electrical stimulation, the logarithm of the rise of extracellular potassium concentration ([K+]0), the sustained shift of electrical potential, and the response of oxidative metabolism are linearly correlated. However, during seizures and during spreading depression, the correlation is broken, suggesting that the demand for oxidative energy exceeds that corresponding to the elevation of [K+]0. There exists a critical concentration of [K+]0 at which spreading depression inevitably erupts (12 mM for cat cerveau isole), but no such critical level could be detected for seizures. The rate of clearance of excess potassium from extracellular fluid is slower for high concentrations than for low; this rate is further slowed by the administration of phenobarbital, and possibly also of diphenylhydantoin. Changes of membrane potential of glia cells in the mammalian spinal cord can adequately be described by the Nernst equation.

Animals↗
PubMed1975

Responses of electrical potential, potassium levels, and oxidative metabolic activity of the cerebral neocortex of cats.

We measured simultaneously the oxidative metabolic activity, monitored as the tissue fluorescence attribute to intramitochondrial NADH, the extracellular potassium level with ion-selective microelectrodes, and the focal extracellular electrical potential, of one site in intact cerebral cortex of cats. When the cerebral was stimulated by trains of repeated electric pulses applied either directly to its surface or to an afferent pathway, the corrected cortical fluorescence (F-R) declined indicating oxidation of NADH, the activity of extracellular potassium [K+]o increased, and the extracellular potential (Vec) shifted in the negative direction. When mild to moderate stimuli not exceeding 10-15 sec in duration were used, a 3-fold correlation was found between these three variables. The regression of F-R over either Vec, or over log [K+]o had a positive ordinal intercept. The results are in agreement with earlier suggestions 4,24,25,43,45,46 that (a) much but not all the oxidative metabolic response of cortex to electrical stimulation is expended in restoring disturbed ion balance; and (b) that sustained shifts of potential (SP) in response to repetitive electrical stimulation are generated by glia cells depolarized by excess potassium. The magnitude of SP shifts associated with a given elevation of [k+]o are smaller in cerebral cortex than in spinal cord48,49. The correlation of F-R with [K+]o breaks down when pathologic processes of either seizure activity or spreading depression set in. During paroxysmal activity [K+]o tends to remain confined below 10-12 mM, a level observed in non-convulsing cortex as well, but oxidation of NADH progresses beyond that seen in non-convulsing cortex as well, but oxidation of NADH progresses beyond that seen in non-convulsing tissue. This observation is hard to reconcile with the suggestion that excess potassium is a factor in the generation of seizures, at least of the type observed in this study. When [K+]o levels exceeded 10-12 mM, spreading depression invariably followed at least under the unanesthetized condition in these experiments. During spreading depression [K+]o levels rose to exceed 30 mM, sometimes 80 mM. NADH was oxidized during spreading depression to a level comparable to that seen in seizures. The observations are compatible with the suggestion13 that spreading depression occurs whenever the release of potassium into extracellular fluid is overloading its clearance therefrom.

Animals↗