Effect of intraoperative mild hyperventilation on the incidence of shoulder pain after laparoscopic sleeve gastrectomy: A randomized, controlled trial.

BACKGROUNDS: To observe the effect of using mild intraoperative hyperventilation on the incidence of postlaparoscopic shoulder pain (PLSP) in patients undergoing laparoscopic sleeve gastrectomy. METHODS: Eighty patients undergoing laparoscopic sleeve gastrectomy, aged 22 to 36 years, with American Society of Anesthesiologists grade I or II, were divided into 2 groups according to method of random number table. A mild hyperventilation was used in group A with controlling pressure of end-tidal carbon dioxide (PETCO2) of 30 to 33 mm Hg, while conventional ventilation was used in group B with PETCO2 35 to 40 mm Hg during the operation. The incidence and severity of PLSP, dosage of remedial analgesia and adverse reactions such as nausea and vomiting at 12, 24, 48, 72 hours and 1 week after surgery were recorded. Arterial blood gas was recorded before anesthesia induction, 20 minutes after pneumoperitoneum, during suture skin, and 24 hours after surgery. RESULTS: Compared with 12, 24, 48, and 72 hours after operation, the incidence of PLSP at 1 week decreased significantly (P < .01). Compared with group B, the incidence of PLSP, pain score, and dosage of remedial analgesic at 12, 24,48, 72 hours, and 1 week after surgery were significantly decreased (P < .01). There was no significant difference between the 2 groups in arterial blood gas analysis before anesthesia induction, 20 minutes after pneumoperitoneum, during suture skin, and 24 hours after surgery (P > .05). There were no significant difference of the occurrence of adverse reactions such as nausea and vomiting between the 2 groups within 1 week after surgery (P > .05). CONCLUSION: Mild hyperventilation can reduce the incidence and severity of PLSP after laparoscopic sleeve gastrectomy without increasing the associated adverse effects.

Spectrum of Disorders associated with Tetany.

INTRODUCTION: Awareness regarding the etiological spectrum of tetany is poor among physicians. Because of poor awareness, tetany is underdiagnosed and undertreated. MATERIALS AND METHODS: Databases like PubMed, PubMed Central, Scopus, and Google Scholar are searched to identify peer-reviewed articles on tetany. Case reports, case series, and original articles are analyzed to identify different causes of tetany prevalent in the community. Different causes found are analyzed and tabulated, and finally, a flowchart is made on the approach for diagnosing different underlying pathologies of tetany. RESULTS: Both metabolic and respiratory alkalosis are important causes of tetany because of reduced ionized calcium levels. Gitelman syndrome (GS) is associated with metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria, and frequently causes normocalcemic tetany. Recurrent vomiting and primary hyperaldosteronism also cause tetany due to metabolic alkalosis. Hyperventilation syndrome (HVS) leads to respiratory alkalosis and is a frequent cause of tetany. Hyperventilation-induced tetany is also seen after spinal anesthesia and in respiratory disorders like asthma. Vitamin D deficiency (VDD), primary hypoparathyroidism, and pseudohypoparathyroidism (PHP) (1a, 1b, and 2) cause hypocalcemic tetany. Hypomagnesemia causes hypocalcemia and tetany due to peripheral parathyroid hormone resistance and impaired parathyroid hormone secretion. Drugs causing tetany include bisphosphonates, denosumab, cisplatin, antiepileptics, aminoglycosides, diuretics, etc. Tetany is also seen in acute pancreatitis, dengue, falciparum malaria, hyperemesis gravidarum, tumor lysis syndrome (TLS), massive blood transfusion, etc. Conclusion: The spectrum of disorders associated with tetany is diverse. Awareness of different causes will help early and proper diagnosis of tetany.

Alcalosis respiratoria grave, la transformación de un cuadro funcional en orgánico. Caso clínico / Severe respiratory alkalosis due to psychogenic hyperventilation. Report of one case

Severe respiratory alkalosis is a life-threatening condition, as it induces hypo- calcaemia and extreme adrenergic sensitivity leading to cerebral and myocardial vasoconstriction. We report a 37-year-old woman with previous consultations for a conversion disorder. While she was infected with SARS-CoV-2 (without pulmonary involvement), she consulted in the emergency room due to panic attacks. On admission, she developed a new conversion crisis with progressive clinical deterioration, hyperventilation, and severe respiratory alkalosis (pH 7.68, Bicarbonate 11.8 mEq/L and PaCO2 10 mmHg). Clinically, she was in a coma, with respiratory and heart rates 55 and 180 per min, a blood pressure of 140/90 mmHg, impaired perfusion (generalized lividity, distal coldness, and severe skin mottling) and tetany. She also had electrocardiographic changes and high troponin levels suggestive of ischemia, and hyperlactatemia. She was managed in the hospital with intravenous benzodiazepines. The clinical and laboratory manifestations resolved quickly, without the need for invasive measures and without systemic repercussions.

Exercise hyperventilation and pulmonary gas exchange in chronic thromboembolic pulmonary hypertension: Effects of balloon pulmonary angioplasty.

BACKGROUND: Excessive ventilation (V̇E) and abnormal gas exchange during exercise are features of chronic thromboembolic pulmonary hypertension (CTEPH). In selected CTEPH patients, balloon pulmonary angioplasty (BPA) improves symptoms and exercise capacity. How BPA affects exercise hyperventilation and gas exchange is poorly understood. METHODS: In this longitudinal observational study, symptom-limited cardiopulmonary exercise tests and carbon monoxide lung diffusion (DLCO) were performed before and after BPA (interval, mean (SD): 3.1 (2.4) months) in 36 CTEPH patients without significant cardiac and/or pulmonary comorbidities. RESULTS: Peak work rate improved by 20% after BPA whilst V̇E at peak did not change despite improved ventilatory efficiency (lower V̇E with respect to CO2 output [V̇CO2]). At the highest identical work rate pre- and post-BPA (75 (30) watts), V̇E and alveolar-arterial oxygen gradient (P(Ai-a)O2) decreased by 17% and 19% after BPA, respectively. The physiological dead space fraction of tidal volume (VD/VT), calculated from measurements of arterial and mixed expired CO2, decreased by 20%. In the meantime, DLCO did not change. The best correlates of P(Ai-a)O2 measured at peak exercise were physiological VD/VT before BPA and DLCO after BPA. CONCLUSIONS: Ventilatory efficiency, physiological VD/VT, and pulmonary gas exchange improved after BPA. The fact that DLCO did not change suggests that the pulmonary capillary blood volume and probably the true alveolar dead space were unaffected by BPA. The correlation between DLCO measured before BPA and P(Ai-a)O2 measured after BPA suggests that DLCO may provide an easily accessible marker to predict the response to BPA in terms of pulmonary gas exchange.

Langerhans cell histiocytosis in a young patient with Pitt-Hopkins syndrome.

Pitt-Hopkins syndrome (PTHS, MIM #610954) is a rare neurodevelopmental disease characterized by the association of intellectual disability, characteristic facial gestalt and episodes of abnormal and irregular breathing. PTHS is due to heterozygous loss-of-function variants in the TCF4 gene (transcription factor 4, MIM #602272) encoding for a basic helix-loop-helix transcription factor. TCF4 is highly expressed during early development of the nervous system, and it is involved in cellular differentiation and proliferation. Since the first clinical description in 1978, less than 200 PTHS patients have been described. A comprehensive phenotype, especially regarding cancer predisposition, is not yet well defined. We report the case of a 7-year-old boy affected by PTHS with a 4-week history of progressive swelling of the frontal bones diagnosed with Langerhans cell histiocytosis.

Repeated Spontaneous Intracranial Epidural Hemorrhage After Hysterical Crying.

BACKGROUND: Spontaneous epidural hemorrhage (EDH) is a rare occurrence that may be caused by vascular anomalies, infections, coagulopathies, or tumors. Spontaneous EDH occurring in patients without specific underlying disease has been reported only as intraspinal lesion but has never been demonstrated in the intracranial area. This study presents a 19-year-old patient with repeated spontaneous intracranial EDH caused twice by hysterical crying. CASE DESCRIPTION: The patient had spontaneous left frontal EDH after hysterical crying. Two years later, she had a similar episode after crying and a new spontaneous right frontal EDH was revealed. There was no obvious risk factor revealed by laboratory and radiologic survey. We postulated that hyperventilation during crying resulted in a sudden decrease in intracranial pressure. The intracranial hypotension induced detachment of the dura from the skull and spontaneous EDH occurred. CONCLUSIONS: Crying or hyperventilation may trigger spontaneous EDH and should be suspected when there are signs of persisting headache and increased intracranial pressure. The prognosis is excellent if early diagnosis and surgical decompression are achieved.

Respiratory and hemodynamic contributions to emotion-related pre-syncopal vasovagal symptoms.

Vasovagal reactions are conventionally understood as resulting from systemic changes in cardiovascular activity; however, there exists a complementary perspective focused on specific changes in cerebral vasoconstriction associated with hyperventilation-induced hypocapnia. The present study investigated the role of cardiovascular and respiratory activity in self-reported pre-syncopal vasovagal reactions to a surgery video in a sample of 49 healthy women. Participants who indicated more previous real-life episodes of dizziness reported experiencing significantly more symptoms in the laboratory consistent with a vasovagal response. They also showed lower total peripheral resistance and higher pre-ejection period in general, suggesting lower sympathetic nervous system activity. Significant decreases in end-tidal carbon dioxide (PETCO2) occurred during the surgery video among susceptible participants, without significant increases in respiration rate. Further, participants who experienced reductions from the neutral video in PETCO2, systolic blood pressure, or both, reported vasovagal symptoms during the surgery video. The results suggest that patterns of respiration associated with decreases in PETCO2 may contribute to vasovagal symptoms reported in non-clinical groups as well as those with blood-injection-injury phobia and are associated with susceptibility to dizziness.

A 56-Year-Old, Otherwise Healthy Woman Presenting With Light-headedness and Progressive Shortness of Breath.

A 56-year-old white woman was referred to the pulmonary clinic for evaluation of unexplained shortness of breath. She enjoyed good health until 3 months prior to this visit when she reported experiencing recurrent episodes of shortness of breath and oppressive retrosternal chest discomfort with radiation to the neck. Episodes lasting 5 to 10 min often occurred at rest and were inconsistently related to physical activity. These symptoms became progressively worse and were often associated with light-headedness and presyncope. Her past medical history was uneventful apart from a prior diagnosis of breast cysts and suspected prolactinoma. Her symptoms escalated to such a level that she was forced to seek urgent medical attention at our institutional ED on two separate occasions in the preceding weeks. These visits precipitated a number of investigations and, eventually, a referral to the pulmonary clinic.

Vibration- and hyperventilation-induced nystagmus in patients with Ramsay Hunt syndrome with vertigo.

OBJECTIVES: The aims of this study were to compare vibration-induced nystagmus (VIN) and hyperventilation-induced nystagmus (HVIN) findings in patients with Ramsay Hunt syndrome with vertigo (RHS-V), sudden sensorineural hearing loss with vertigo (SSNHL-V), and vestibular neuritis (VN) during the acute stage and to address the possible lesion sites of vestibular deficit in RHS-V. STUDY DESIGN: Case series with chart review. SETTING: Tertiary referral center. METHODS: We conducted a retrospective case series study in 27 patients with SSNHL-V, 104 patients with VN, and 17 patients with RHS-V and evaluated the findings of VIN and HVIN tests. RESULTS: An abnormal VIN was observed in 91% of the patients with VN, 89% of those with SSNHL-V, and 94% of those with RHS-V, and the prevalence of abnormal VIN was not significantly different (P = .436). An abnormal HVIN was observed in 51% of the patients with VN, 22% of those with SSNHL-V, and 59% of those with RHS-V. While the prevalence of an abnormal HVIN was significantly different between SSNHL-V and VN groups (P = .007) and between SSNHL-V and RHS-V groups (P = .014), that between VN and RHS-V groups did not show a significant difference (P = .547). CONCLUSION: Since the results of HVIN in RHS-V patients were more similar to those in VN patients than those in SSNHL-V patients, a lesioned site may be more likely within the vestibular nerve than the inner ear as a cause for vestibular deficit in patients with RHS-V who show caloric canal paresis of 25% or greater.

Hyperventilation-induced nystagmus in patients with vestibular schwannoma.

MAIN OBJECTIVE: To determine the utility of the hyperventilation test (HVT) in the diagnosis of vestibular schwannoma (VS). STUDY DESIGN: A retrospective analysis of hyperventilation-induced nystagmus (HVIN) in 45 patients with unilateral VS. SETTING: A tertiary referral center. PATIENTS: Forty-five patients with VS; 30 patients with chronic vestibular neuritis; 20 healthy subjects with normal hearing and without symptoms or a history of vertigo, migraine, or neurological diseases (control group). INTERVENTIONS: Audiological and vestibular examination; "side-stream" measurement of end-tidal CO2 pressure (P(EtCO2)) to standardize the procedure; magnetic resonance imaging (MRI) centered on the cerebellopontine angle. MAIN OUTCOME MEASURES: An analysis of HVIN, its patterns, and its appearance threshold via the measurement of P(EtCO2) correlations with the tumor size. RESULTS: HVIN was observed in 40 of 45 cases (88.9%) in the schwannoma group and in 12 of 30 cases (40%) in the chronic vestibular neuritis group; HVIN was not observed in the control group (0/20 cases) (p < 0.001). In the schwannoma group, HVIN was evoked at a mean P(EtCO2) value of 16.5 ± 1.15 mm Hg. The hypofunctional labyrinth was identified with high sensibility and specificity through caloric test, head shaking test, and head thrust test. The excitatory pattern, which included HVIN with slow phases that beat toward the hypofunctional side, and the paretic pattern, which included HVIN with slow phases that beat toward the hypofunctional side, were not significantly associated with VS size (19.04 ± 10.56 mm for the excitatory pattern and 19.06 ± 11.01 mm for the paretic pattern). The difference in the VS size in HVIN+ (19.05 ± 10.60 mm) and HVIN- (8.40 ± 2.19 mm) cases was significant (p = 0.009). CONCLUSIONS: A 60-second hyperventilation event causes metabolic changes in the vestibular system and reveals a latent vestibular asymmetry. The presence of an excitatory pattern is the major criterion that suggests VS in patients with signs of unilateral vestibular deficit.

Impact of hypocapnia and cerebral perfusion on orthostatic tolerance.

We examined two novel hypotheses: (1) that orthostatic tolerance (OT) would be prolonged when hyperventilatory-induced hypocapnia (and hence cerebral hypoperfusion) was prevented; and (2) that pharmacological reductions in cerebral blood flow (CBF) at baseline would lower the 'CBF reserve', and ultimately reduce OT. In study 1 (n = 24; aged 25 ± 4 years) participants underwent progressive lower-body negative pressure (LBNP) until pre-syncope; end-tidal carbon dioxide (P ET , CO 2) was clamped at baseline levels (isocapnic trial) or uncontrolled. In study 2 (n = 10; aged 25 ± 4 years), CBF was pharmacologically reduced by administration of indomethacin (INDO; 1.2 mg kg(-1)) or unaltered (placebo) followed by LBNP to pre-syncope. Beat-by-beat measurements of middle cerebral artery blood flow velocity (MCAv; transcranial Doppler), heart rate (ECG), blood pressure (BP; Finometer) and end-tidal gases were obtained continuously. In a subset of subjects' arterial-to-jugular venous differences were obtained to examine the independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on cerebral oxygen delivery and extraction. In study 1, during the isocapnic trial, P ET , CO 2 was successfully clamped at baseline levels at pre-syncope (38.3 ± 2.7 vs. 38.5 ± 2.5 mmHg respectively; P = 0.50). In the uncontrolled trial, P ET , CO 2 at pre-syncope was reduced by 10.9 ± 3.9 mmHg (P ≤ 0.001). Compared to the isocapnic trial, the decline in mean MCAv was 15 ± 4 cm s(-1) (35%; P ≤ 0.001) greater in the uncontrolled trial, yet the time to pre-syncope was comparable between trials (544 ± 130 vs. 572 ± 180 s; P = 0.30). In study 2, compared to placebo, INDO reduced resting MCAv by 19 ± 4 cm s(-1) (31%; P ≤ 0.001), but time to pre-syncope remained similar between trials (placebo: 1123 ± 138 s vs. INDO: 1175 ± 212 s; P = 0.53). The brain extracted more oxygen in face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% to 57%) to compensate for reductions in delivery. In summary, cerebral hypoperfusion either at rest or induced by hypocapnia at pre-syncope does not impact OT, probably due to a compensatory increase in oxygen extraction.

Obstructive sleep apnea and other sleep-related syndromes.

Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by repetitive episodes of breathing cessation due to complete or partial collapse of the upper airway therefore affecting ventilation. It is quite common, with a prevalence of about 2-4%, has a strong genetic component, and creates a proinflammatory state with elevated TNFα and other cytokines. If untreated, OSA can lead to significant neurological problems that include stroke, cognitive decline, depression, headaches, peripheral neuropathy, and nonarteritic ischemic optic neuropathy (NAION). Treatment reverses some of these neurological problems. Treatment includes continuous positive airway pressure and its variants, oral appliances, weight loss, upper airway surgery, and rarely maxillofacial procedures. Other sleep breathing disorders such as hypoventilation, central sleep apnea, complex sleep apnea, and Cheyne-Stokes respiration are less common and are sometimes associated with neuromuscular disorders causing diaphragmatic paralysis, but can also be seen in opiate exposure and severe obesity.

Cardiovascular activity in blood-injection-injury phobia during exposure: evidence for diphasic response patterns?

Exposure to feared stimuli in blood-injection-injury (BII)-phobia is thought to elicit a diphasic response pattern, with an initial fight-flight-like cardiovascular activation followed by a marked deactivation and possible fainting (vasovagal syncope). However, studies have remained equivocal on the importance of such patterns. We therefore sought to determine the prevalence and clinical relevance of diphasic responses using criteria that require a true diphasic response to exceed cardiovascular activation of an emotional episode of a negative valence and to exceed deactivation of an emotionally neutral episode. Sixty BII-phobia participants and 20 healthy controls were exposed to surgery, anger and neutral films while measuring heart rate, blood pressure, respiratory pattern, and end-tidal partial pressure of carbon dioxide (as indicator of hyperventilation). Diphasic response patterns were observed in up to 20% of BII-phobia participants and 26.6% of healthy controls for individual cardiovascular parameters. BII-phobia participants with diphasic patterns across multiple parameters showed more fear of injections and blood draws, reported the strongest physical symptoms during the surgery film, and showed the strongest tendency to hyperventilate. Thus, although only a minority of individuals with BII phobia shows diphasic responses, their occurrence indicates significant distress. Respiratory training may add to the treatment of BII phobia patients that show diphasic response patterns.

Bronchial responsiveness to dry air hyperventilation in smokers may predict decline in airway status using indirect methods.

BACKGROUND: Disabling respiratory symptoms and rapid decline of lung function may occur in susceptible tobacco smokers. Bronchial hyperresponsiveness (BHR) elicited by direct challenge methods predicts worse lung function outcomes. The aim of this study was to evaluate whether BHR to isocapnic hyperventilation of dry air (IHDA) was associated with rapid deterioration in airway status and respiratory symptoms. METHODS: One hundred twenty-eight smokers and 26 age- and sex-matched healthy individuals with no history of smoking were investigated. All subjects completed a questionnaire. Spirometry and impulse oscillometry (IOS) measurements were recorded before and after 4 min of IHDA. The tests were repeated after 3 years in 102 smokers and 11 controls. RESULTS: Eighty-five smokers (66 %) responded to the challenge with a ≥2.4-Hz increase in resonant frequency (F res), the cutoff limit defining BHR, as recorded by IOS. They had higher F res at baseline compared to nonresponding smokers [12.8 ± 3.2 vs. 11.5 ± 3.4 Hz (p < 0.05)] and lower FEV1 [83 ± 13 vs. 89 ± 13 % predicted (p < 0.05)]. Multivariable logistic regression analysis indicated that wheezing (odds ratio = 3.7, p < 0.01) and coughing (odds ratio = 8.1, p < 0.05) were significantly associated with hyperresponsiveness. An increase in F res was recorded after 3 years in responding smokers but not in nonresponders or controls. The difference remained when subjects with COPD were excluded. CONCLUSIONS: The proportion of hyperresponsive smokers was unexpectedly high and there was a close association between wheezing and coughing and BHR. Only BHR could discriminate smokers with rapid deterioration of airway status from others.

Hyperventilation provokes symptoms of carpal tunnel syndrome.

Hyperventilation causes respiratory alkalosis. The nervous system is more excitable in alkalosis. This phenomenon can be observed as paraesthesia in fingers and toes as well as around the lips in anxious patients breathing rapidly. We wanted to test this phenomenon on already irritable nerves like the median nerve in carpal tunnel syndrome (CTS). We deployed 50 patients who came in to the day case unit for carpal tunnel decompression with electro-physiologically proven diagnosis. We devised a test whereby patients were made to hyperventilate under prescribed conditions and repeated Phalen's test and Tinel's sign for comparison. These were compared with a control group chosen randomly among hospital staff. 86% patients had a positive result which was just behind Phalen's test in sensitivity. It was also 100% specific as there were no false positives. Hyperventilation is a phenomenon which provokes carpal tunnel syndrome. Its clinical value remains to be seen due to cumbersome method and probable patient non-compliance but it is a new discovery. It may be useful in other irritable-nerve-syndromes as a test to add to our available armament. It may be an additional factor or a primary reason for nocturnal paraesthesias in CTS patients.

Descripción, interpretación, análisis e importancia del nistagmus inducido por la hiperventilación en el estudio de patologías vestibulares periféricas y centrales / Description, interpretation, analysis and importance of hyperventilation -induced nystagmus in the study of the peripheral and central vestibular disorders

Recientes estudios clínicos han revelado la utilidad del test del nistagmus inducido por la hiperventilación aguda, en la investigación de patologías vestibulares retrolaberínticas, neurales y de origen central, con la aparición de nistagmus paréticos o bien excitatorios. El propósito de este estudio ha sido: primero, conocer la sensibilidad de este examen según el análisis de los estudios de diferentes autores; segundo, entender la fisiopatología de este nistagmus inducido por la hiperventilación y tercero, efectuar una interpretación y análisis de este examen que permita obtener conclusiones sólidas del mejor nivel de medicina basada en evidencias. Para efectuar este estudio y análisis se procedió a una investigación exhaustiva de las publicaciones sobre el tema en los últimos 25 años, recurriendo para ello como fuentes de información a las principales bases de datos biomédicos y a la revisión en texto completo de estas publicaciones. Llamó la atención la escasez de trabajos clínicos publicados sobre el tema que no superan los 40, y también la escasez de trabajos sobre la fisiopatología del nistagmus inducido por la hiperventilación aguda. La metódica del test es muy simple por lo que su utilización resulta muy atractiva, con un escaso número de falsos positivos. La mayor parte de los estudios publicados, se focaliza en su utilización en el schwanoma vestibularyen la neuronitis vestibular. Respecto al schwanoma vestibular de un total de 107 pacientes estudiados el test fue positivo en el 80 por ciento de los casos, con aparición de nistagmus ipsilesional o contralesional. En la neuronitis vestibular la positividad del test alcanzó a 60 por ciento de un total de 272 pacientes estudiados y que estaba en relación directa con el tiempo de evolución de la enfermedad. En la esclerosis múltiple, en pacientes con síntomas vestibulares, la positividad del test fue de 75 por ciento, en cambio en aquellos pacientes sin síntomas vestibulares...

Recent clinical studies have revealed the usefulness of the hyperventilation-induced nystagmus in retrolabyrinthine and central vestibular diseases with the appearance either excitatory (ipsilateral) or paretic (contralateral) nystagmus. The objectives of this study have been: 1) to get to know the sensitivity of the exam, according to the best literature available; 2) to get to know the physiopathology of this hyperventilation-induced nystagmus, and 3) to carry out an analysis and interpretation of this exam in order to reach solid conclusions of the highest level in evidence based medicine. An exhaustive research of literature published on this topic in the last 25 years was carried out. The main source of information being the most important medical data-based publications and also a thorough revision of these texts. The scarce number of publications on this topic (not more than 40) is what strikes the attention most, as well as the very few studies of the physiopathology of the hyperventilation-induced nystagmus. The method of the test is a simple one; this fact makes its application an attractive one, with a low number of false positive. Most of the studies published are focused on its application in the vestibular schwannoma and in the vestibular neuritis. As to what the Vestibular schwannoma is concerned, ofa group of 107 patients studied, the test was positive in 80 percent of the cases, with the appearance of ipsilesional or contralesional nystagmus. In vestibular neuritis the test was positive in 68 percent of a number of 272 patients; this amount was in direct correlation with the time of evolution of the disease. In multiple sclerosis, in patients with vestibular symptoms, the test gave positive in 75 percent, whereas in those patients without vestibular symptoms it was positive only in 7 percent. In patients with cerebellar diseases, particularly degenerative ones this test was positive in 78 percent of the cases...

Hyperventilation-induced nystagmus in a large series of vestibular patients.

The Hyperventilation Test is widely used in the "bed-side examination" of vestibular patients. It can either activate a latent nystagmus in central or peripheral vestibular diseases or it can interact with a spontaneous nystagmus, by reducing it or increasing it. Aims of this study were to determine the incidence, patterns and temporal characteristics of Hyperventilation-induced nystagmus in patients suffering from vestibular diseases, as well as its contribution to the differential diagnosis between vestibular neuritis and neuroma of the 8(th) cranial nerve, and its behaviour in some central vestibular diseases. The present study includes 1202 patients featuring, at vestibular examination, at least one sign of vestibular system disorders or patients diagnosed with a "Migraine-related vertigo" or "Chronic subjective dizziness". The overall incidence of Hyperventilation-induced nystagmus was 21.9%. It was detected more frequently in retrocochlear vestibular diseases rather than in end-organ vestibular diseases: 5.3% in Paroxysmal Positional Vertigo, 37.1% in Menière's disease, 37.6% in compensated vestibular neuritis, 77.2% in acute vestibular neuritis and 91.7% in neuroma of the 8(th) cranial nerve. In acute vestibular neuritis, three HVIN patterns were observed: Paretic pattern: temporary enhancement of the spontaneous nystagmus; Excitatory pattern: temporary inhibition of the spontaneous nystagmus; Strong excitatory pattern: temporary inversion of the spontaneous nystagmus. Excitatory patterns proved to be time-dependent in that they disappeared and were replaced by the paretic pattern over a period of maximum 18 days since the beginning of the disorder. In acoustic neuroma, Hyperventilation-induced nystagmus was frequently observed (91.7%), either in the form of an excitatory pattern (fast phases towards the affected site) or in the form of a paretic pattern (fast phases towards the healthy side). The direction of the nystagmus is only partially related to tumour size, whereas other mechanisms, such as demyelination or a break in nerve fibres, might have an important role in triggering the situation. Hyperventilation-induced nystagmus has frequently been detected in cases of demyelinating diseases and in cerebellar diseases: in multiple sclerosis, hyperventilation inhibits a central type of spontaneous nystagmus or evokes nystagmus in 75% of patients; in cerebellar diseases, hyperventilation evokes or enhances a central spontaneous nystagmus in 72.7% of patients. In conclusion the Hyperventilation Test can provide patterns of oculomotor responses that indicate a diagnostic investigation through cerebral magnetic resonance imaging enhanced by gadolinium, upon suspicion of neuroma of the 8(th) cranial nerve or of a central disease. In our opinion, however, Hyperventilation-induced nystagmus always needs to be viewed within the more general context of a complete examination of the vestibular and acoustic system.

[Sudden infant death syndrome (SIDS) caused by ATP-depletion following hyperventilation, tissue-hypoxia and hypermetabolism--a hypothesis]. / ATP-Depletion durch Hyperventilation, Gewebehypoxie und Hypermetabolismus als Ursache für Plötzlichen Kindstod--eine Hypothese.

INTRODUCTION: Despite a decreasing incidence, sudden infant death syndrome (SIDS) is still the most frequent cause of death in industrial nations during the first year of life. Hypoxia plays a major role in the pathogenesis, but the exact mechanism is not fully understood. METHODS: This study was based on personal considerations and a selective online literature search. HYPOTHESIS: SIDS is the result of a frequently protracted ATP-depletion. DISCUSSION: Especially in combination, all risk factors for SIDS favour an ATP-deficiency by increasing ATP-catabolism and/or by diminishing ATP-synthesis. Prenatal chronic hypoxaemia and an insufficient supply with nutrients lead to low birth-weight, reduced adipose tissue, elevated haemoglobin F, increased sympathetic activity, hypermetabolism, and diminished hypoxia tolerance in the neonates. Because of reduced adipose tissue, more energy for thermogenesis is needed after birth. In reaction to hypoxaemia, infants with risk factors show hyperventilation instead of hypoxic hypometabolism and respiratory depression. Enhanced breathing, however, requires additional ATP and causes increasing oxygen affinity, which is elevated physiologically during the first months of life. Thereby, tissue-hypoxia and diminished ATP-synthesis may arise. Besides, enhanced sympathetic activity leads to hypermetabolism and increased ATP-catabolism. While innate risk factors may reduce ATP-production in burdening situations, like food deprivation, postnatal hyperthermia and stress augment ATP-catabolism by hyperventilation and hypermetabolism and empty energy stores. For term newborns, the peak incidence of SIDS might be explained by the haemoglobin nadir of physiological anaemia and by the therefore reduced capacity for oxygen transport. Thereby, the risk of tissue-hypoxia, which follows increased oxygen affinity and vanishing ability to hypoxic hypometabolism, is further enhanced. The almost identical symptoms of SIDS and ATP-deficiency diseases like hypophosphataemia, heat stroke, and carbon monoxide poisoning support the presented hypothesis.

Methodology and indications of H2-breath testing in gastrointestinal diseases: the Rome Consensus Conference.

BACKGROUND: Breath tests represent a valid and non-invasive diagnostic tool in many gastroenterological conditions. The rationale of hydrogen-breath tests is based on the concept that part of the gas produced by colonic bacterial fermentation diffuses into the blood and is excreted by breath, where it can be quantified easily. There are many differences in the methodology, and the tests are increasingly popular. AIM: The Rome Consensus Conference was convened to offer recommendations for clinical practice about the indications and methods of H2-breath testing in gastrointestinal diseases. METHODS: Experts were selected on the basis of a proven knowledge/expertise in H2-breath testing and divided into Working Groups (methodology; sugar malabsorption; small intestine bacterial overgrowth; oro-coecal transit time and other gas-related syndromes). They performed a systematic review of the literature, and then formulated statements on the basis of the scientific evidence, which were debated and voted by a multidisciplinary Jury. Recommendations were then modified on the basis of the decisions of the Jury by the members of the Expert Group. RESULTS AND CONCLUSIONS: The final statements, graded according to the level of evidence and strength of recommendation, are presented in this document; they identify the indications for the use of H2-breath testing in the clinical practice and methods to be used for performing the tests.

Avaliação neuropsicológica da atenção visual e do videoeletroencefalograma na condição de hiperventilação, nas epilepsias e em indivíduos normais / Neuropsychological assessment of visual attention and videoelectroencephalogram on condition of hyperventilation in epilepsy and normal individuals

Hiperventilação é um método tradicional de ativação para descargas epileptiformes generalizadas, ou crises em eletroencefalografia. Alterações comportamentais durante crises induzidas pela hiperventilação, são avaliadas por um método clinico no qual o paciente conta, em voz alta, o número de cada incursão respiratória após cada expiração. Comprometimento da consciência é detectado por omissões, repetições ou hesitação na sequência numérica. Baseados no estudo de um caso-controle de adulto com crises de ausência, nas quais as crises só puderam ser diagnosticas, com certeza, através da utilização de um teste computadorizado da atenção visual, organizamos o presente estudo com o objetivo de estudar se a hiperventilação durante 5 minutos provocava alteração na atenção visual de voluntários normais, utilizando o teste computadorizado da atenção visual com monitorização vídeoeletroencefalográfica. Em adição verificamos a contribuição do teste para o diagnóstico sindromico de um paciente com o diagnóstico presuntivo de epilepsia de lobo temporal. Nossos resultados demonstraram que a hiperventilação durante 5 minutos não altera a atenção visual de indivíduos normais, sugerindo que este possa ser útil para uso rotineiro em encefalografia ou em monitorizações videoeletroencefalográficas, com o objetivo de detectar crises, cuja identificação seja difícil apenas pela observação visual do comportamento.

Hyperventilation has been a traditional activation method for generalized epileptiform discharges or seizumes in routine electroencephalography (EEG). Behavioral alterations during hyperventilation-induced seizures are assessed by a clinical method in which patients count aloud the number of their breaths after each expiration. Impairment of consciousness is detected by omissions, repetitions of hesitation of numbers in a counting sequence. Based on an anecdotal case-control study of a patient with epilepsy with absences, in which the absences could only be diagnosed using a continuous performance test, we organized the study aiming to study the effects of hyperventilation on attention, using the CTVA during normal breathing and in the 5 minutes hyperventilation in normal adults. Our goal was to determine if hyperventilation altered the performance of normal subjects on the different parameters of the CTVA. Our data showed that hyperventilation did not significantly change any parameter of CTVA, when normal subjects performed the test in normal breathing condition compared with their performance during HV in addition, in a case with presumptive diagnosis of refractory temporal lobe epilepsy, our neuropsychological battery, which included the computadorized test of visual attention, played a critical role in elucidating the syndromic diagnosis and leading to additional tests for the correct diagnosis. Our results suggest that CTVA may be a useful tool to measure unresponsiveness in routine electroencephalography or during videoelectroencephalography monitoring.