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Effect of hemiparetic stroke on pulse oximetry readings on the affected side.

BACKGROUND AND PURPOSE: Hypoxia is common after stroke, and monitoring by pulse oximetry is suggested in the acute phase. Physical changes on the affected side or intravenous infusions may affect oximeter readings. This study was designed to test whether pulse oximetry recordings are the same on the affected and nonaffected sides in stroke patients. METHODS: Oxygen saturation (SpO(2)) and heart rate (HR) were assessed simultaneously in the left and right hands in patients with hemiparetic stroke over a 3-hour period with 2 Minolta Pulsox-3i oximeters attached to the index fingers. RESULTS: Fifteen patients (53% men; 67% left hemiparesis; mean age, 73 years [SD, 7.5 years]) were recruited. HR and SpO(2) (12 measurements per minute) were monitored. The maximum difference between simultaneous left and right arm readings was 2% SpO(2). HR fluctuated more, but no affected/nonaffected side pattern was seen. Means for each patient of HR and SpO(2) for the affected and nonaffected sides were compared by t tests. Mean SpO(2) was 96% (SD, 1%) on both sides. Mean HR was 81 bpm (SD, 11 bpm) on the affected side and 80 bpm (SD, 10 bpm) on the nonaffected side. There was no significant difference between the 2 sides for either parameter (n=15; P=0.86 for SpO(2) and P=0.91 for HR). CONCLUSIONS: Oximeters can be attached to either the affected or nonaffected side in hemiparetic stroke.

Aged↗

Superinduction of cyclooxygenase-2 activity in human osteoarthritis-affected cartilage. Influence of nitric oxide.

Cartilage specimens from osteoarthritis (OA)-affected patients spontaneously released PGE2 at 48 h in ex vivo culture at levels at least 50-fold higher than in normal cartilage and 18-fold higher than in normal cartilage + cytokines + endotoxin. The superinduction of PGE2 production coincides with the upregulation of cyclooxygenase-2 (COX-2) in OA-affected cartilage. Production of both nitric oxide (NO) and PGE2 by OA cartilage explants is regulated at the level of transcription and translation. Dexamethasone inhibited only the spontaneously released PGE2 production, and not NO, in OA-affected cartilage. The NO synthase inhibitor HN(G)-monomethyl-L-arginine monoacetate inhibited OA cartilage NO production by > 90%, but augmented significantly (twofold) the spontaneous production of PGE2 in the same explants. Similarly, addition of exogenous NO donors to OA cartilage significantly inhibited PGE2 production. Cytokine + endotoxin stimulation of OA explants increased PGE2 production above the spontaneous release. Addition of L-NMMA further augmented cytokine-induced PGE2 production by at least fourfold. Inhibition of PGE2 by COX-2 inhibitors (dexamethasone or indomethacin) or addition of exogenous PGE2 did not significantly affect the spontaneous NO production. These data indicate that human OA-affected cartilage in ex vivo conditions shows (a) superinduction of PGE2 due to upregulation of COX-2, and (b) spontaneous release of NO that acts as an autacoid to attenuate the production of the COX-2 products such as PGE2. These studies, together with others, also suggest that PGE2 may be differentially regulated in normal and OA-affected chondrocytes.

Adult↗

Fibromyalgia and major affective disorder: a controlled phenomenology and family history study.

Fibromyalgia is a form of nonarticular rheumatism characterized by diffuse musculoskeletal pain. To investigate the relationship between fibromyalgia and major affective disorder, the authors evaluated 31 patients with fibromyalgia and 14 patients with rheumatoid arthritis for rates of current or past major affective disorder and family history of major affective disorder. Both the rate of major affective disorder and the familial prevalence of major affective disorder were significantly higher in the fibromyalgia patients than the rheumatoid arthritis patients. The results suggest that fibromyalgia may be related to major affective disorder.

Adult↗

Are schizophrenia and affective disorder related? A selective literature review.

OBJECTIVE: Although most modern investigators accept the Kraepelinian view that schizophrenia and affective disorder are biologically distinct, others have suggested the psychoses are on a continuum of liability. This article is a selective review of evidence for the continuum model. METHOD: The author focuses on family, twin, and adoption data that do not support the Kraepelinian view of psychosis. Evidence characterized to a lesser extent includes the frequency of intermediate forms of illness (i.e., schizoaffective disorder), the inability to separate psychoses by classical symptoms into well-defined clusters, and the inability of laboratory measures to clearly define psychotic subgroups. RESULTS: The data demonstrate that schizophrenia and affective disorder do co-occur in some families. Whether this co-occurrence reflects true overlap is unclear, and significant pathophysiological heterogeneity may underlie clinical continuity. In some recent studies the inclusion of nonmelancholic depressions in the affective illness category may have masked overlap. CONCLUSIONS: The author suggests that the Kraepelinian view of psychoses may need modification. Future research should focus on factors that may reveal overlap between schizophrenia and affective disorder: severity of schizophrenia and affective disorder in probands, severity of depression in relatives, the effect of the unipolar-bipolar disorder relationship on the co-occurrence of affective disorder and schizophrenia, and the relationship of nongenetic factors that might alter the clinical expression of a shared genotype. Also, investigators should not presume a dichotomy or continuum but should examine pure and mixed pedigrees and look for state- and trait-related endophenotypes, the convergence of which would provide the basis for focused molecular genetic study.

Adult↗

Initial findings on preventive intervention for families with parental affective disorders.

OBJECTIVE: The purpose of this study was to develop a clinician-based cognitive, psychoeducational, preventive intervention for families with parental affective disorder that would be suitable to widespread use, test its feasibility and safety, and define the areas affected by the intervention. The intervention was designed to increase understanding of parental illness and resilience in the children. METHOD: The authors studied the first seven families (14 parents) to receive the intervention. Enrollment criteria included affective disorder during the preceding year in at least one parent, presence of at least one child between the ages of 8 and 14 years who was not psychiatrically ill at the time of participation, and willingness to participate in the research study. The intervention consisted of parent, child, and family sessions. Assessment included semistructured interviews with parents about affective disorders, standard ratings of marital satisfaction and therapeutic alliance, and a recently developed semistructured interview to assess response to the intervention. RESULTS: Overall satisfaction with the intervention was rated moderate to high by parents. No harm was reported. Ten of 14 parent subjects reported five or more behavior and attitude changes that they attributed to the intervention. The most frequent behavior and attitudinal changes reported were increased discussion of the illness and related issues and increased understanding of information about affective illness. CONCLUSIONS: The authors conclude that the intervention is safe and feasible in families with parental affective disorder.

Adult↗

Contrasts between patients with affective disorders and patients with schizophrenia on a neuropsychological test battery.

OBJECTIVE: This study was designed to ascertain the degree and specificity of cognitive impairments in patients with schizophrenia and patients with affective disorders. METHOD: Cognitive function was assessed with a neuropsychological test battery in consecutively admitted patients with schizophrenia (N = 57), unipolar depression (N = 29), and bipolar disorder (N = 16). RESULTS: The performance of the schizophrenic group was significantly below that of the groups with affective disorders on measures of attention and psychomotor speed, verbal and visual memory, and problem solving and abstraction. IQ was lower in the schizophrenic group and appeared to have deteriorated from a normal premorbid level that was not different from that of the affective disorder groups, as determined by the Wide Range Achievement Test--Revised reading test, a putative measure of premorbid intelligence. When IQ was controlled, differences between the groups in problem solving and visual memory remained. Psychiatric symptoms had a larger impact on test performance in the affective disorder groups than in the schizophrenic group. CONCLUSIONS: These results suggest that patients with schizophrenia perform systematically worse on cognitive measures than patients with affective disorders, which is consistent with their generally poorer outcome. The results also indicate that schizophrenia and affective disorders are qualitatively distinguishable in neuropsychological terms, given differences in apparent intellectual deterioration, profiles of cognitive impairment, and associations between cognitive performance and psychopathology.

Adult↗

Demographics, family history, premorbid functioning, developmental characteristics, and course of patients with deteriorated affective disorder.

OBJECTIVE: This exploratory study examined the characteristics of a group of unusual and previously undescribed patients with major affective disorder who not only had been continuously symptomatic for prolonged periods of time but were also so functionally impaired that they required years of continuous care in psychiatric facilities or by family members. METHOD: Twenty-seven inpatients with major mood disorders and 29 inpatients with schizophrenia were recruited from a large state hospital; 27 outpatients with major mood disorders were recruited from an affiliated outpatient facility. The research battery included the Structured Clinical Interview for DSM-III-R--Patient Version, the Premorbid Adjustment Scale, and a semistructured interview designed to assess demographic, family history, developmental, and course information. RESULTS: Inpatients with deteriorated affective disorder differed from outpatients with nondeteriorated affective disorder along several important dimensions, including family history of mental illness, birth-related problems, physical disorders in infancy, premorbid functioning, presence of mixed episodes and rapid cycling, and medication non-compliance between hospitalizations. Inpatients with deteriorated affective disorder differed from inpatients with schizophrenia on the Premorbid Adjustment Scale. Patients with bipolar affective disorder differed from those with unipolar disorder on many of the variables associated with deterioration of functioning. CONCLUSIONS: Birth-related problems, physical disorders in infancy, and poor premorbid adjustment in childhood and adolescence appear to play an important role in deterioration of functioning among patients with unipolar depression. Disruption in treatment because of medication noncompliance and the appearance of mixed episodes and rapid cycling are associated with functional decline in bipolar affective disorder. Several characteristics previously considered specific to deterioration of functioning in schizophrenia, such as a high rate of birth complications and poor premorbid adjustment, appear to be associated with functional deterioration among patients with major depression as well.

Adolescent↗

Deficits in gain of smooth pursuit eye movements in schizophrenia and affective disorder patients and their unaffected relatives.

OBJECTIVE: Disturbance of smooth pursuit eye movements has been discussed as marking a putative endophenotype closely associated with the genetic basis of schizophrenia. Previous studies are not conclusive in regard to the specificity of this marker. Therefore, oculomotor pursuit was evaluated in unaffected family members of index probands diagnosed as having either schizophrenia or affective disorders. METHOD: A series of eye tracking tasks were performed by 54 patients with schizophrenia or schizoaffective disorder, 46 patients with an affective disorder, 43 unaffected first-degree relatives of the schizophrenia patients, 36 unaffected first-degree relatives of the affective disorder patients, and 84 healthy comparison subjects. The gain, which relates the velocity of the eye movement to the velocity of the target, was determined to index the intactness of the oculomotor pursuit system. RESULTS: Mean pursuit gain was significantly lower in the schizophrenia and affective disorder patients than in the healthy comparison subjects. Moreover, the relatives of both the schizophrenia and affective disorder patients showed significant gain deficits of about one-half the size of those observed in the patients. CONCLUSIONS: Gain deficits are present in psychotic patients and in their unaffected biological relatives. This finding supports a genetic origin of eye tracking disturbances in major psychotic disorders. There is no evidence for diagnostic or familial specificity. The weak sensitivity of the marker suggests that it refers to a nonnecessary genetic factor in schizophrenic and affective disorders.

Adolescent↗

Short day lengths affect perinatal development of the male reproductive system in the Siberian hamster, Phodopus sungorus.

The Siberian hamster, Phodopus sungorus, breeds seasonally. In the laboratory, seasonal breeding can be controlled by photoperiod, which affects the duration of nightly melatonin secretion. Winterlike, short day lengths induce gonadal regression in adult animals, and pups born and maintained in short days undergo pubertal gonadal development later than animals born into long days. However, to date there have been no reports of gestational photoperiod affecting fetal development of reproductive systems. The spinal nucleus of the bulbocavernosus (SNB) and its target muscles, the bulbocavernosus (BC) and levator ani (LA), compose a sexually dimorphic, androgen-sensitive neuromuscular system involved in male reproduction. The SNB neuromuscular system was studied in male Siberian hamsters maintained from conception in short-day (8 h light, 16 h dark; 8L:16D) versus long-day (16L:8D) conditions. On the day of birth, and at postnatal (PN) days 2 and 18, the BC/LA muscles of hamsters gestated and raised in the short photoperiod were significantly reduced relative to those of their long-day counterparts. Testes weights were not significantly different between groups until day 18. Thus, photoperiod exposure during gestation and after birth affects perinatal development of the SNB system in this species, and these effects can be seen as early as the day of birth. Because photoperiod did not significantly affect testes weights until PN18, these results suggest that either perinatal photoperiod affects fetal androgen production without affecting testes weight or it influences BC/LA development independently from androgen.

Aging↗

Age-related impairments in comprehending affective prosody with comparison to brain-damaged subjects.

This study evaluated the ability to produce and comprehend affective prosody across age groups and compared patterns of impaired performance to deficits observed after focal brain damage. Sixty-nine healthy subjects, ages 22 to 83 years, were given the Aprosodia Battery, a test that distinguishes between affective prosodic processing deficits following right- versus left-brain damage through the use of stimuli with progressively reduced verbal articulatory content. Production of affective prosody, measured by variation in fundamental frequency, was unimpaired in older subjects, whereas comprehension of affective prosody was impaired, particularly for tasks with reduced verbal articulatory content. The pattern of performance across affective comprehension tasks in the older subjects resembled the pattern found after right-brain damage. The results demonstrate age-related loss in comprehension of affective prosody that is most likely due to a processing deficit involving the right hemisphere.

Adult↗

Affective disorder and epilepsy comorbidity: implications for development of treatments, preventions and diagnostic approaches.

Concepts pertaining to affective disorder and epilepsy comorbidity are contributing appreciably to improvements in patient care. Several antiepileptic treatments have become important components of the management of bipolar affective disorder. In contrast, little progress has emerged in developing clinical applications of the anticonvulsant properties of the antidepressants in the treatment of the epilepsies. The slow onset of action of the antidepressants remains a major impediment to fully effective treatment of depressive episodes. Nevertheless, studies from experimental epileptology demonstrate that the anticonvulsant effects of the antidepressants occur rapidly and as a consequence of noradrenergic and/or serotonergic activation. These studies also demonstrate that adequate initial doses of the antidepressants are essential to rapid onset of anticonvulsant action. Pharmacokinetically valid loading dose paradigms are seemingly avoided with antidepressant drugs in humans because of potential toxicities and/or patient unacceptability. However, substantial progress has been made in reducing the adverse effect liability of the antidepressants. No longer is convulsive liability considered to stem from the therapeutic mechanisms of the anti-depressants. Rather, noradrenergic and serotonergic influences have demonstrable anticonvulsant properties. Other side effects may also be separable from the anticonvulsant and antidepressive effects of antidepressive treatments. The concept that the protracted process of antidepressant-induced beta-noradrenergic down-regulation is an essential prelude to the onset of mood benefit is no longer a sustainable premise. Nevertheless, increasing evidence underlies the possibility that knowledge of serotonergic and noradrenergic regulatory processes can be used to design strategies that will hasten the onset of antidepressive action. Similar optimism pervades efforts to determine the possibility that dual inhibition of serotonin and norepinephrine transporters will hasten onset of antidepressive action. Moreover, because noradrenergic and serotonergic systems are determinants of predisposition to seizures and to dysfunctional affective episodes, augmentation strategies may also be applicable to the use of antidepressant drugs in epilepsy and to the use of antiepileptic drugs such as carbamazepine in mood disorders. Recent studies have demonstrated that, in part, the therapeutic effectiveness of carbamazepine may stem from its marked capacity to elevate serotonin concentrations in the extracellular fluid of the brain via mechanisms that differ from those of the membrane reuptake inhibitors. Evidence suggests that the epilepsies and affective disorders may arise from a multiplicity of neurobiological abnormalities. A disorder in one individual may arise via different mechanisms than a phenomenologically similar disorder in another individual. Thus, diagnostic tools are needed to make mechanistic distinctions among individuals so that treatments can be appropriately developed and selected. In terms of epileptogenesis and affective disorder progression, neuroprotective paradigms for one individual may differ from those needed for another. Moreover, diagnostic technologies that are adequate to detect genetically and/or experientially determined vulnerability before the onset of a seizure or dysfunctional affective episode may be valuable steps toward achieving goals of prevention.

Animals↗

SDH mutations in patients affected by paraganglioma syndromes: a personal experience.

Mutations in genes encoding mitochondrial succinate dehydrogenase (SDH) are frequently involved in the development of neural crest-derived (NCD) tumors, such as pheochromocytomas (PHEOs) or paragangliomas (PGLs). In this study we report the results of sequencing analysis in leukocyte DNA of patients affected by PHEO/PGL who turned out to be SDH mutation carriers. A nonsense germline heterozygous mutation (Q109X) was found in the exon 4 of the SDHD gene in the index cases of six unrelated families affected by PHEO/PGL. Haplotype analysis showed the presence of a founder effect. Affected patients showed high clinical variability, ranging from monolateral to bilateral glomus tumors, variably associated or not with PGLs or PHEOs. A novel missense SDHD variant, T112I, was also found in one of our families. A new missense G106D mutation, involving a highly conserved amino acid, was found in two sisters affected by bilateral glomus tumors. A P81L mutation associated with abdominal and head and neck PGL was detected in three families. A G12S variant of the SDHD gene was found in one patient affected by a PHEO. The finding of this variant in 3 of 100 control subjects suggests that it is a polymorphism and not a mutation. A novel IVS2-1G>T variant was found at intron 2 of SDHD gene in one patient affected by a glomus tumor. All the tumors associated with SDHD mutations were benign. Conversely, the only mutation we found in SDHB gene (IVS3+1G>A) was associated with a malignant PHEO.

Amino Acid Sequence↗

Abnormal pituitary-adrenal responses to corticotropin-releasing hormone in patients with seasonal affective disorder: clinical and pathophysiological implications.

CRH has been shown to produce increased locomotion, arousal, and anorexia in experimental animals. A deficiency of CRH in patients with seasonal affective disorder could contribute to the characteristic lethargy, hypersomnia, and hyperphagia characteristic of this illness. To test this hypothesis, we studied basal plasma ACTH and cortisol levels and their responses to ovine CRH in controls and depressed patients with seasonal affective disorder before and after light treatment. Untreated seasonal affective disorder patients showed normal basal plasma cortisol and ACTH levels, but their responses to CRH tended to be delayed and were significantly reduced. When patients were studied after 9 days of light treatment, a significant increase in plasma ACTH and cortisol responses to CRH was observed. Our findings in untreated patients with seasonal affective disorder are similar to those in patients with Cushing's disease 2 weeks after transsphenoidal hypophysectomy, who uniformly show sustained suppression of their CRH neuron because of long-standing hypercortisolism. This findings suggest that the CRH neuron of patients with seasonal affective disorder is hypofunctional. We postulate that the clinical symptomatology in patients with seasonal affective disorder could reflect deficient activity of this important arousal-producing system.

Adrenocorticotropic Hormone↗

Are the interpersonal and identity disturbances in the borderline personality disorder criteria linked to the traits of affective instability and impulsivity?

This study examines the degree to which two putative biologically influenced personality traits, affective instability and impulsive aggression, are associated with some of the interpersonal and intrapsychic disturbances of borderline personality disorder (BPD) and with choice of defense mechanism. In a sample of 152 personality disorder patients, affective instability and impulsive aggression were measured. Defense mechanisms were assessed in 140 of these patients using the Defensive Style Questionnaire (DSQ). The correlations between the traits of affective instability and impulsive aggression and the eight DSM-III-R criteria for borderline personality disorder and 20 DSQ defenses were examined. Affective instability was significantly correlated with the DSM-III-R criteria of identity disturbance, chronic emptiness or boredom, inappropriate anger, suicidality, and the affective instability criteria. It also was associated with the defenses of splitting, projection, acting out, passive aggression, undoing, and autistic fantasy. Impulsive aggression was related to unstable interpersonal relationships, inappropriate anger and impulsiveness and with the defense of acting out. It was negatively correlated with the defenses of suppression and reaction formation. A number of the interpersonal and experiential disturbances and defense mechanisms that are features of BPD are associated with the traits of affective instability and impulsive aggression among patients with personality disorders.

Adult↗

The stress and negative affect model of adolescent alcohol use and the moderating effects of behavioral undercontrol.

Empirical evidence for the stress and negative affect model of adolescent alcohol use has been inconsistent. We hypothesized that this inconsistent support was partially due to a third variable that moderates the model's effects. The current study assessed behavioral undercontrol as a moderator of the stress and negative affect model of adolescent alcohol use. Using a community-based sample of adolescent children of alcoholics (COAs) and a demographically matched comparison group (non-COAs), life stress, negative affect, behavioral undercontrol and alcohol use were assessed. Results showed that the stress and negative affect model predicted alcohol use. Consistent with theoretical predictions and previous research, negative affect partially mediated the relation between stress and alcohol use. However, behavioral undercontrol did not moderate the effects of stress and negative affect for COAs and non-COAs. Theoretical and methodological implications of the findings are discussed.

Adolescent↗

Stress, alcohol use and alcohol-related problems: the influence of negative and positive affect in two cohorts of young adults.

OBJECTIVE: Past research has suggested that trait-based positive and negative affect mediate the relationships between self-report measures of stress and health. We extended these assumptions to the study of health-related behaviors, specifically the much studied stress-alcohol relationship. In addition, we sought to replicate previous findings showing that stress is more strongly associated with alcohol problems and not alcohol use as many theories (e.g., tension-reduction hypothesis) have assumed. METHOD: Structural equation modeling was used to test a mediating variable model in two cohorts (574 and 239 subjects) of randomly selected young adults between 18 and 35 years of age. Participants were from the 1996 data wave of the Niagara Young Adult Health Study, a community-based study incorporating a modified cohort-sequential design. The larger (older) cohort consisted of subjects initially contacted in 1990. RESULTS: For both cohorts, the measurement model proved to be very reliable. The final structural models did not match the predicted model. The correlations between the Stress and Alcohol Use latent variables (necessary to test a mediational model) were not significant in either cohort. However, in the older cohort, trait-based positive affect and hostility acted as intervening variables, allowing for an indirect relationship between stress and alcohol use. In the younger cohort, this indirect pattern was not present because none of the latent affect variables led to alcohol use. In both cohorts, stress predicted alcohol problems, even after controlling for the relationships between stress, affect and alcohol use. Significant cohort differences in the structural models were observed. CONCLUSIONS: The assumptions regarding the mediation of affect on the relationship between stress and health cannot be extended completely to the stress-alcohol relationship. Two reasons for this are: (1) the differences between the two age cohorts in the relationships between stress, affect and alcohol use and (2) the finding that stress is more predictive of alcohol-related problems than it is of alcohol use.

Adult↗

Characterization of carrier females and affected males with X-linked recessive nephrolithiasis.

X-linked recessive nephrolithiasis (XRN) was described in a large kindred in which nephrolithiasis; proximal tubular dysfunction, proteinuria, nephrocalcinosis, and renal failure occur only in males. Carrier females are asymptomatic, but formal studies of them have not been done. The gene for XRN has been mapped to the pericentromeric region of the X chromosome, close to the loci for several eye disease genes. We studied six affected males, 13 carrier females, and 25 normal members of this family including 7 females whose genetic haplotype predicted them to be carriers. Studies were done in the Clinical Research Unit on a diet containing 400 mg of calcium and 2 g of sodium, and by an additional outpatient urine collection was obtained on a 1-g calcium intake. Hypercalciuria occurred in five of six affected males, 4 of 12 carrier females, and three of seven predicted carriers. Significant proteinuria was present in all affected males and in no other subjects. Low-molecular-weight proteinuria was present in all affected males: the excretion of alpha 1-microglobulin exceeded normal by 3- to 14-fold, of beta 2-microglobulin exceeded normal by 100- to 400-fold, and of retinol-binding protein exceeded normal by 1,000- to 3,000-fold. The excretion of these proteins was less strikingly elevated in carrier females, but the excretion of alpha 1-microglobulin was abnormal in 9 of 15 carriers, beta 2-microglobulin was abnormal in 12 of 15, and retinolbinding protein in was abnormal 12 of 13, and this pattern was similar in predicted carriers. The urinary concentrating ability was abnormal in four affected males with renal insufficiency but normal in all other subjects. Urinary wasting of potassium, phosphorous, and glucose occurred infrequently, and no subject was hypouricemic. Formal ophthalmologic studies were normal in five affected males. Thus, the most consistent urinary abnormalities in XRN are hypercalciuria and low-molecular-weight proteinuria, the latter of which appears to be a marker for the carrier state.

Adolescent↗

Coughing, mucus accumulation, airway obstruction, and airway inflammation in control horses and horses affected with recurrent airway obstruction.

OBJECTIVE: To investigate relationships between cough frequency and mucus accumulation, airway obstruction, and airway inflammation and to determine effects of dexamethasone on coughing and mucus score. ANIMALS: 13 horses with recurrent airway obstruction (RAO) and 6 control horses. PROCEDURE: 6 RAO-affected and 6 control horses were stabled for 3 days. Coughing was counted for 4 hours before and on each day horses were stabled. Before and on day 3 of stabling, tracheal mucus accumulation was scored, airway obstruction was assessed via maximal change in pleural pressure (deltaPpl(max)), and airway inflammation was evaluated by use of cytologic examination of bronchoalveolar lavage fluid (BALF). Effects of dexamethasone (0.1 mg/kg, IV, q 24 h for 7 days) were determined in 12 RAO-affected horses. RESULTS: To assess frequency, coughing had to be counted for 1 hour. In RAO-affected horses, stabling was associated with increases in cough frequency, mucus score, and deltaPpl(max). Control horses coughed transiently when first stabled. In RAO-affected horses, coughing was correlated with deltaPpl(max), mucus score, and airway inflammation and was a sensitive and specific indicator of deltaPpl(max) > 6 cm H2O, mucus score > 1.0, and > 100 neutrophils/microL and > 20% neutrophils in BALF Dexamethasone reduced cough frequency, mucus score, and deltaPpl(max), but BALF neutrophil count remained increased. CONCLUSIONS AND CLINICAL RELEVANCE: Because of its sporadic nature, coughing cannot be assessed accurately by counting during brief periods. In RAO-affected horses, coughing is an indicator of airway inflammation and obstruction. Corticosteroid treatment reduces cough frequency concurrently with reductions in deltaPpl(max) and mucus accumulation in RAO-affected horses.

Airway Obstruction↗