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Biomedical subjects

Jeffrey Moak

Publications and source records attributed to Jeffrey Moak.

4 recordsLinked to original sources
PubMed2005

Neurocirculatory abnormalities in Parkinson disease with orthostatic hypotension: independence from levodopa treatment.

Patients with Parkinson disease often have orthostatic hypotension. Neurocirculatory abnormalities underlying orthostatic hypotension might reflect levodopa treatment. Sixty-six Parkinson disease patients (36 with orthostatic hypotension, 15 off and 21 on levodopa; 30 without orthostatic hypotension) had tests of reflexive cardiovagal gain (decrease in interbeat interval per unit decrease in systolic pressure during the Valsalva maneuver; orthostatic increase in heart rate per unit decrease in pressure); reflexive sympathoneural function (decrease in pressure during the Valsalva maneuver; orthostatic increment in plasma norepinephrine); and cardiac and extracardiac noradrenergic innervation (septal myocardial 6-[18F]fluorodopamine-derived radioactivity; supine plasma norepinephrine). Severity of orthostatic hypotension did not differ between the levodopa-untreated and levodopa-treated groups with Parkinson disease and orthostatic hypotension (-52+/-6 [SEM] versus -49+/-5 mm Hg systolic). The 2 groups had similarly low reflexive cardiovagal gain (0.84+/-0.23 versus 1.33+/-0.35 ms/mm Hg during Valsalva; 0.43+/-0.09 versus 0.27+/-0.06 bpm/mm Hg during orthostasis); and had similarly attenuated reflexive sympathoneural responses (97+/-29 versus 71+/-23 pg/mL during orthostasis; -82+/-10 versus -73+/-8 mm Hg during Valsalva). In patients off levodopa, plasma norepinephrine was lower in those with (193+/-19 pg/mL) than without (348+/-46 pg/mL) orthostatic hypotension. Low values for reflexive cardiovagal gain, sympathoneural responses, and noradrenergic innervation were strongly related to orthostatic hypotension. Parkinson disease with orthostatic hypotension features reflexive cardiovagal and sympathoneural failure and cardiac and partial extracardiac sympathetic denervation, independent of levodopa treatment.

Adult↗
PubMed2005

Neurocirculatory abnormalities in chronic orthostatic intolerance.

BACKGROUND: Chronic orthostatic intolerance (COI) occurs in postural tachycardia syndrome (POTS) and in some individuals with repeated neurocardiogenic syncope/presyncope (NCS), without POTS. This study addressed whether patients with COI and POTS or NCS have neurocirculatory abnormalities during supine rest. METHODS AND RESULTS: Adult patients referred for COI who had POTS (n=90, mean+/-SEM age 40+/-1 years, 86% women) or NCS (n=36, 41+/-2 years old, 78% women) underwent measurements of plasma levels of catecholamines and forearm hemodynamics. Comparison data were obtained from 32 age- and gender-matched normal volunteers (39+/-2 years old, 81% women). The POTS group had a relatively fast mean heart rate (79+/-2 bpm) during supine rest compared with the NCS group (69+/-1.6 bpm, P=0.03) and normal volunteers (66+/-3 bpm, P=0.0004). The POTS group also had higher mean arterial norepinephrine (1.61+/-0.11 nmol/L, n=37) and epinephrine (0.39+/-0.03 nmol/L, n=37) concentrations than the NCS group (1.03+/-0.12 nmol/L, n=20, P=0.0012; 0.21+/-0.03 nmol/L, n=20, P=0.0005) and normal volunteers (1.13+/-0.11 nmol/L, n=20, P=0.006; 0.17+/-0.03 nmol/L, n=15, P=0.0001). The NCS group had higher mean forearm vascular resistance (52+/-6 U) than the POTS group (36+/-2 U, P=0.003). CONCLUSIONS: Overall, POTS features increased heart rate and sympathetic nervous and adrenomedullary hormonal system outflows during supine rest. Increased sympathetic outflow may contribute to the relative tachycardia in POTS. NCS features forearm vasoconstriction during supine rest but not sympathoneural or adrenomedullary activation.

Adolescent↗
PubMed2004

Painful sweating.

OBJECTIVE: The authors report a case of spontaneous and gustatory facial pain and sweating. METHODS: The patient had frequent episodes of pain, sweating, and flushing bilaterally in the hairless skin of the ophthalmic and maxillary distributions of the trigeminal nerve. Gustatory stimuli (e.g., orange juice, pickled onions) reliably evoked episodes, but episodes also frequently came on spontaneously. The problem had begun during adolescence, about the time of topical treatment and then electrocauteries for facial warts. The patient reported benefit from tricyclic antidepressants, guanethidine, and trospium chloride (an anti-cholinergic quaternary amine used in Europe for urinary urgency). There was no pain or excessive sweating in other body areas, nor pain with exercise. RESULTS: Administration of edrophonium IV evoked pain and sweating, and ganglion blockade by IV trimethaphan eliminated pain and sweating and markedly attenuated responses to edrophonium. Trospium chloride also prevented edrophonium-induced pain and sweating. Bicycle exercise produced the same increment in forehead humidity as in a spontaneous episode but did not evoke pain. Tyramine infusion did not bring on pain or sweating, whereas iontophoretic acetylcholine administration to one cheek evoked pain and sweating bilaterally. Topical glycopyrrolate cream eliminated spontaneous, gustatory, and edrophonium-induced episodes. CONCLUSIONS: The findings indicate that facial pain and sweating can result from occupation of muscarinic cholinergic receptors after acetylcholine release from local nerves. The authors propose that after destruction of cutaneous nerves, aberrant regenerant sprouting innervates sweat glands, producing gustatory sweating as in auriculotemporal syndrome (Frey syndrome), and innervates nociceptors, producing pain.

Acetylcholine↗