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Ramesh K Khurana

Publications and source records attributed to Ramesh K Khurana.

5 recordsLinked to original sources

Experimental induction of panic-like symptoms in patients with postural tachycardia syndrome.

Patients with postural tachycardia syndrome (POTS) might be misdiagnosed with panic disorder due to shared clinical features. The first aim of our study was to investigate the relationship between symptoms of POTS and panic disorder. The second aim was to delineate clinical features distinguishing symptoms of POTS from panic disorder. A total of 11 patients with POTS and 11 control subjects participated in an IRB-approved, prospective, placebo-controlled study. The experimentally induced panic-like symptoms of POTS were systematically studied using the Acute Panic Inventory (API) questionnaire. The participants answered the questionnaire after each placebo infusion and after each of the three provoking stimuli: head-up tilt test (HUT), isoproterenol infusion (ISI), and sodium lactate infusion (SLI). API responses were summed for each subject at each time point of administration. Individual API symptoms and summed responses were analyzed for statistical significance. All patients with POTS developed symptoms of orthostatic intolerance during HUT. Pharmacologically induced symptoms subjectively mimicked spontaneous symptoms in 5 of 11 patients during ISI and in none of 11 patients during SLI. In contrast, API scores in these patients reached panic threshold in 0 of 11 following HUT, in 4 of 11 following ISI and in 4 of 11 following SLI. Individual symptoms analysis revealed that significant increase in scores was limited to the somatic symptoms of palpitations, dyspnea, and twitching or trembling. In conclusion, the symptoms of POTS are phenomenologically different and clinically distinguishable from panic disorder symptoms.

Adult↗

The cold face test: a non-baroreflex mediated test of cardiac vagal function.

Application of cold to the face evokes potent bradycardia and a pressor response, similar to the diving reflex. However, the role of the baroreceptors in this response is unclear. Ten healthy controls and two patients with baroreflex impairment were recruited. A cold face test (CFT) was induced by the application of three cold packs (0.5 degrees C) to the face. Heart rate (ECG), blood pressure (Finapres) and skin temperature (forehead electrode) were recorded continuously. All data were analyzed using unpaired Students t-tests, and expressed as mean +/- SD. In all controls, CFT induced bradycardia. The mean onset latency was 5.6 +/- 4.6 s, and the maximal bradycardia was seen at 35.8 +/- 15.8 s. Systolic blood pressure increased in eight controls, with a mean onset latency of 18.8 +/- 16.6 s and a peak rise at 38.7 +/- 22.7 s. In the controls, bradycardia preceded the pressor response. The heart rate and blood pressure changes during CFT had a longer latency than baroreflex evoked responses. Moreover, one subject had bradycardia despite a fall in blood pressure. The two patients had abnormal Valsalva ratios and no change in heart rate during tilt, indicating impairment of the baroreflex. However, both their heart rate and blood pressure responses to CFT were normal. These data are further evidence of the limited role of the baroreflex in the autonomic responses to CFT. They suggest that the CFT may be of use in assessing the integrity of the efferent cardiovascular autonomic pathways in patients with suspected baroreflex impairment.

Adult↗

Enzyme replacement therapy improves peripheral nerve and sweat function in Fabry disease.

Fabry disease is an X-linked disorder caused by a deficiency of lysosomal alpha-galactosidase A resulting in accumulation of alpha-D-galatosyl conjugated glycosphingolipids. Clinical manifestations include a small-fiber neuropathy associated with debilitating pain and hypohidrosis. We report the effect of a 3-year open-label extension of a previously reported 6-month placebo-controlled enzyme replacement therapy (ERT) trial in which 26 hemizygous patients with Fabry disease received 0.2 mg/kg of alpha-galactosidase A every 2 weeks. The effect of ERT on neuropathic pain scores while off pain medications, quantitative sensory testing, quantitative sudomotor axon reflex test (QSART), and thermoregulatory sweat test (TST) is reported. In the patients who crossed-over from placebo to ERT (n = 10), mean pain-at-its-worst scores on a 0-10 scale decreased (from 6.9 to 4.5). There was a significant reduction in the threshold for cold and warm sensation in the foot. At the 3-year time-point, pre-ERT sweat excretion in 17 Fabry patients was 0.24 +/- 0.33 microl/mm(2) vs. 1.05 +/- 0.81 in concurrent controls (n = 38). Sweat function improved 24-72 h post-enzyme infusion (0.57 +/- 0.71 microl/mm(2)) and normalized in four anhidrotic patients. TST confirmed the QSART results. We conclude that prolonged ERT in Fabry disease leads to a modest but significant improvement in the clinical manifestations of the small-fiber neuropathy associated with this disorder. QSART may be useful to further optimize the dose and frequency of ERT.

Adult↗

Eye examination-induced syncope Role of trigeminal afferents.

The role of trigeminal afferents in a patient with eye examination - induced syncope was investigated. A head-up tilt test precipitated presyncope with a reduced blood pressure. On a separate day, the application of Schirmer's lacrimation test strips in each conjunctival sac caused vasodepression and cardioinhibition. Topical administration of 0.5 % proparacaine hydrochloride produced ocular anesthesia and loss of corneal reflexes. Schirmer's test following anesthesia again caused presyncope with reductions in blood pressure and heart rate. The supramaximal stimulus to a supraorbital nerve before and after topical anesthesia did not affect blood pressure or heart rate. It is concluded that trigeminal afferents did not induce vasodepressive syncope in this patient. Instead, corticohypothalamic centers may have played an important role.

Female↗

Headache in patients with baroreflex failure.

Two cases of baroreflex failure presented with tension-type/exertional headache. The usefulness of noninvasive physiological tests in diagnosing baroreflex failure and the role of baroreceptors in trigeminal nociception are discussed.

Aged↗