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Biomedical subjects

M C Rowbotham

Publications and source records attributed to M C Rowbotham.

36 records · Page 2Linked to original sources
PubMed1995

Topical lidocaine gel relieves postherpetic neuralgia.

Postherpetic neuralgia (PHN) following herpes zoster is a common and disabling neuropathic pain syndrome. In a double-blind, three-session study, 5% lidocaine gel or vehicle was applied simultaneously to both the area of pain and to the contralateral mirror-image unaffected skin. In the local session, lidocaine gel was applied to the painful skin area. In the remote session, lidocaine gel was applied to mirror-image skin. In the placebo session, vehicle was applied bilaterally. For cranial PHN, gel was applied without occlusion for 8 hours. For limb or torso PHN, gel was applied under occlusion for 24 hours. The 16 subjects with cranial PHN reported pain relief significantly favoring local drug application at 30 minutes, 2, 4, and 8 hours. The 23 subjects with torso or limb PHN reported significantly lower pain intensity with local drug application at 8 hours and both pain relief and reduced pain intensity at 24 hours. Remote lidocaine application to mirror-image skin was no different from placebo. No systemic adverse effects were reported and blood levels did not exceed 0.6 microgram/ml. Topical application of 5% lidocaine gel relieves PHN pain by a direct drug action on painful skin.

Administration, Cutaneous↗
PubMed1995

Chronic pain: from theory to practical management.

The neurologist is an important part of the pain management team. Factors that can alter presentation and complicate establishing a diagnosis are reviewed. A multidisciplinary approach to evaluation is advocated, particularly the inclusion of independent psychiatric or psychological evaluation. Treatment planning consists of addressing potential sources of failure of pain management, setting appropriate goals, and using the diagnostic assessment to plan pharmacologic and nonpharmacologic interventions based on pain mechanisms. Even if pharmacologic interventions do not alter pain, an education-oriented behavioral pain program integrated with physical therapy can improve function and foster self-reliance in controlling pain.

Animals↗
PubMed1994

The interpretation of pain relief and sensory changes following sympathetic blockade.

A comparative study of the effects of sympathetic blockade by stellate ganglion block (SGB) and intravenous phentolamine infusion (PhI) was carried out in 24 patients with presumed sympathetically maintained pain of an upper extremity. A total of 15 SGBs and 16 PhIs were performed, with seven patients undergoing both procedures. All patients developed a Horner's syndrome with SGB and nasal stuffiness and cardiovascular changes with PhI. Similar pain relief was obtained with SGB and PhI in six of the seven who underwent both procedures. Pre-procedure patient characteristics including age, sex, duration of pain, historical and physical examination features suggestive of the reflex sympathetic dystrophy syndrome, and sensory disturbances such as allodynia and hyperpathia did not predict pain relief from either procedure. Changes in skin temperature following the sympatholytic procedure did not correlate with pain relief. For PhI, pain relief correlated with the magnitude of decrease in systolic blood pressure. After SGB, changes in quantitative thermal sensory testing (QST) suggestive of a partial deficit in thermal sensation correlated with pain relief. In 20 normal controls, water bath immersion to cool the hand passively by 7 degrees C and warm the hand passively by 4 degrees C had small and selective effects on thermal QST thresholds, but did not produce a general impairment in thermal sensation. In conclusion, the diagnosis of sympathetically maintained pain based on the history and physical examination alone cannot be made with confidence and therefore a sympatholytic procedure is necessary. When SGB produces pain relief but PhI does not, systemic absorption of local anaesthetic and/or sensory blockade by spread to somatic nerves may be the reason. Thus, PhI appears to be a less sensitive but more specific test than SGB. These two procedures provide complementary information and both may be needed to establish the diagnosis of sympathetically maintained pain.

Adult↗
PubMed1993

Response to intravenous lidocaine infusion differs based on clinical diagnosis and site of nervous system injury.

We analyzed retrospectively pain relief from an intravenous lidocaine infusion (5 mg/kg/hr for 60 to 90 minutes) in 111 patients with chronic nonmalignant pain. Patients with peripheral nervous system (PNS) injury reported substantially more pain relief than those with central nervous system (CNS) injury or with pain of unknown etiology. These findings suggest that (1) the pathophysiology of chronic pain due to PNS injury is different from that due to CNS injury and idiopathic pain, and that (2) pain due to PNS damage may be suppressible by local anesthetic antiarrhythmic agents.

Central Nervous System↗
PubMed1992

Treatment of postherpetic neuralgia.

Postherpetic neuralgia (PHN) is the most common and feared complication of herpes zoster. The more severe and painful the initial zoster outbreak, the more likely that PHN will develop, with elderly patients being at greatest risk. There are no proven treatments that have a large impact in reducing the risk of PHN. Tricyclic antidepressants are the mainstay of treatment for established PHN, aided by transcutaneous electrical nerve stimulation, physical therapy techniques, and cautious use of other medications. Topical agents, such as capsaicin, aspirin, and lidocaine, may soon become one of the mainstays of therapy for PHN.

Analgesia↗
PubMed1991

Both intravenous lidocaine and morphine reduce the pain of postherpetic neuralgia.

We studied the analgesic efficacy of an intravenous infusion of lidocaine and morphine in 19 adults with well-established postherpetic neuralgia in a three-session, randomized, double-blind, placebo-controlled trial. Compared with saline placebo, both lidocaine and morphine reduced pain intensity. Reductions in pain did not correlate with side effects produced by the infusions. For morphine, there was a significant correlation between reductions in pain intensity and blood level achieved. In the majority of subjects who reported definite pain relief, allodynia also disappeared. The results show that neuropathic pain can respond to opioids and to systemically administered local anesthetic drugs.

Aged↗
PubMed1990

Neurologic consequences of cocaine use.

Neurologic consequences of cocaine use frequently present as medical emergencies in the form of stroke, repeated seizures, encephalopathy, acute headache, and unusual transient neurological deficits. The often fatal or disabling neurologic syndromes have only recently been recognized but are now well documented. Cocaine use is a significant cause of stroke in young adults, and the full, long-term ramifications of maternal cocaine use on the fetus will not be known for years to come. Unfortunately, there is not effective treatment other than abstinence, and our understanding of the pathophysiology of cocaine-associated neurologic illness remains limited.

Animals↗
PubMed1989

Thalamomesencephalic strokes after cocaine abuse.

Three young patients developed strokes of rostral midbrain and thalamus shortly following cocaine abuse. Two had infarctions and one had a hemorrhage, but none had clear risk factors other than cocaine for this relatively uncommon type of stroke. Toxicologic analysis confirmed isolated cocaine use in each patient. In the two cases of infarction studied angiographically, one had normal findings and the other had focal narrowing of the P1 segments of the posterior cerebral arteries bilaterally. Since the P1 segment has a uniquely sparse perivascular sympathetic supply, we suggest that direct adrenergic-mediated vasoconstriction is not critical to the production of cocaine-associated stroke.

Adult↗
PubMed1988

Neurologic aspects of cocaine abuse.

These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Drs Homer A. Boushey, Professor of Medicine, and David G. Warnock, Associate Professor of Medicine, under the direction of Dr Lloyd H. Smith, Jr, Professor of Medicine and Associate Dean in the School of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA 94143.

Brain↗
PubMed1987

Cocaine-calcium channel antagonist interactions.

Diltiazem, a benzothiazepine calcium channel antagonist, was given to six healthy men as a single 60 mg oral dose 120 min before IV injection of cocaine (0.2 mg/kg) in a double-blind, placebo-controlled, two-session study. Diltiazem alone produced no significant effects. Cocaine increased blood pressure, heart rate, pupil size and subjective "high" ratings, and decreased skin temperature. Diltiazem pretreatment diminished the cocaine effect on skin temperature, but did not otherwise alter the response to cocaine. Calcium channel antagonists diminish the effects of cocaine in vitro and in animals. Dosage considerations may be critical because of the differential sensitivity of various tissues to calcium channel antagonists.

Adult↗
PubMed1987

Acute neurologic and psychiatric complications associated with cocaine abuse.

This report reviewed 996 emergency room visits and 279 hospital admissions of patients with complications of cocaine abuse seen at the San Francisco General Hospital between 1979 and 1986. In 143 cases, acute neurologic or psychiatric symptoms were the primary complaint, and case-notes provided sufficient detail for analysis. The major neurologic complications included one or more seizures (n = 29), focal neurologic symptoms or signs (12), headache (10), and transient loss of consciousness (six). Psychiatric disturbances included agitation, anxiety, or depression (33), psychosis and paranoia (24), and suicidal ideation (18). The most serious consequences were found in patients with prolonged seizures or strokes, those who jumped out of buildings, and those who attempted suicide by overdosing with other drugs. There was no correlation between the appearance of complications and the reported route of administration, the amount of cocaine used, or prior experience with cocaine. The number of patients who are seeking hospital attention for these or related complaints appears to be rising substantially. Cocaine abuse, regardless of the use pattern, is associated with a variety of potentially severe neurologic and psychiatric complications.

Adult↗
PubMed1984

Trazodone-oral cocaine interactions.

Depression and dysphoria can follow the long-term use of cocaine. Little is known about the interaction of antidepressant drugs with cocaine and similar stimulants in humans. The physiologic and subjective effects of an oral 2-mg/kg dose of cocaine hydrochloride were measured in eight healthy cocaine-using men after pretreatment with a single, 100-mg oral dose of the triazolopyridine antidepressant trazodone hydrochloride or placebo in a double-blind study. The cocaine-induced effects of increased BP, increased pupil size, and decreased skin temperature were diminished by trazodone pretreatment. Trazodone alone did not alter plasma epinephrine or norepinephrine levels. An increase in plasma epinephrine levels after cocaine administration was not altered by trazodone pretreatment, but the increase in the norepinephrine level was larger. Trazodone alone produced mild sleepiness. Cocaine-induced euphoria was not altered by trazodone pretreatment, although feelings of tension and shakiness after cocaine administration were diminished.

Administration, Oral↗
PubMed1983

Failure of naloxone to reverse apomorphine effects in humans.

Twelve male volunteers given apomorphine (20 micrograms/kg/hr) for 40 min by i.v. infusion had significant changes in growth hormone, prolactin, vasopressin, pulse rate, sedation and nausea. Naloxone, (20 mg i.v.) or placebo given in a double-blind manner 10 min before the end of the apomorphine infusion as a concealed bolus did not alter the effects of apomorphine. Vasopressin rise correlated significantly with nausea intensity. We conclude that acute opiate receptor blockade does not reverse most apomorphine effects.

Adolescent↗
PubMedDate not supplied

Effect of systemic adenosine on pain and secondary hyperalgesia associated with the heat/capsaicin sensitization model in healthy volunteers.

BACKGROUND AND OBJECTIVES: Adenosine is an endogenous compound that may have analgesic effects. Results from clinical trials are not consistent, however, and there is a need for large-scale, randomized, placebo-controlled studies to clarify the role of adenosine in the treatment of pain states, including acute nociceptive pain and pain involving central sensitization. METHODS: The analgesic and antihyperalgesic effect of systemic adenosine on the heat/capsaicin sensitization model of experimental pain was investigated in 25 healthy human volunteers. Sensitization was produced by heating the skin to 45 degrees C for 5 minutes, followed by a 30-minute application of 0.075% capsaicin cream, and maintained by periodically reheating the sensitized skin to 40 degrees C for 5 minutes at 40-minute intervals. Subjects received intravenous adenosine 60 microg/kg/min or saline for 85 minutes. Areas of secondary hyperalgesia to von Frey hair and brush stimulation, heat-pain detection thresholds (HPDTs) in normal and sensitized skin, and painfulness of stimulation with 45 degrees C for 1 minute (LTS) in normal skin were quantified before, during, and after study drug infusion. RESULTS: Systemic adenosine had no effect on the area of secondary hyperalgesia to von Frey hair or brush stimulation, HPDT in normal or sensitized skin, or painfulness of LTS in normal skin. CONCLUSION: We conclude that adenosine has no effect on acute nociceptive pain induced by heat stimulation or on secondary hyperalgesia induced by heat/capsaicin sensitization in healthy volunteers.

Adenosine↗
PubMedDate not supplied

Cocaine, nicotine, caffeine, and metabolite plasma concentrations in neonates.

The objective of this study was to measure the umbilical cord plasma levels of cocaine, nicotine, caffeine, and their metabolites. Thirty-six neonates at risk for prenatal cocaine exposure were prospectively enrolled. Umbilical cord plasma was analyzed by gas chromatography-mass spectroscopy for cocaine, cocaethylene, benzoylecgonine (BZE), nicotine, cotinine, and caffeine. Eighteen neonates were plasma positive for BZE, and 50% of these were also positive for cocaine. Cocaethylene was not found. The maximum plasma cocaine concentration was 88 ng/mL (mean, 39 ng/mL). The maximum plasma BZE concentration was 3880 ng/mL (mean, 844 ng/mL). Among BZE-positive babies, the mean plasma drug levels were as follows: nicotine, 1.8 ng/mL; cotinine, 94 ng/mL; and caffeine, 1205 ng/mL. Among the BZE-negative babies, the mean plasma drug levels were as follows: nicotine, 5.2 ng/mL; cotinine, 97 ng/mL; and caffeine, 1440 ng/mL. These cocaine levels raise the possibility of pharmacological effects of cocaine in the early neonatal period.

Caffeine↗
PubMedDate not supplied

Cocaine metabolite kinetics in the newborn.

The study goal was to determine the half-life elimination of cocaine and benzoylecgonine (BZE) in the newborn. Three 0.3-mL blood samples were collected during the first day of life. Urine was collected once daily. Cocaine and BZE concentrations were determined by gas chromatography-mass spectrometry. An extraction method was developed for measuring low concentrations of cocaine and BZE in small (0.1 mL) blood samples. Cocaine had a half-life of 11.6 h in one subject. The half-life of BZE during the first day of life, based on blood data in 13 subjects, was 16 h (95% confidence interval [CI], 12.8 to 21.4 h). The half-life of BZE during the first week of life, based on urine data in 16 subjects, was 11.2 h (95% CI, 10.1 to 11.8 h). The novel extraction method for small blood sample volumes should be applicable to other basic drugs.

Chemistry Techniques, Analytical↗