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Dive into the research topics where Robert L. Harmon is active.

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Featured researches published by Robert L. Harmon.


American Journal of Physical Medicine & Rehabilitation | 2003

Pudendal nerve entrapment as source of intractable perineal pain.

Christopher E. Ramsden; Michael McDaniel; Robert L. Harmon; Kenneth M. Renney; Alexis Faure

Ramsden CE, McDaniel MC, Harmon RL, Renney KM, Faure A: Pudendal nerve entrapment as source of intractable perineal pain. Am J Phys Med Rehabil 2003;82:479–484. Perineal pain caused by pudendal nerve entrapment is a rarely reported entity, with only a handful of cases in the modern literature. A 25-yr-old male medical student had refractory unilateral orchialgia for 32 mo and concomitant proctalgia for 14 mo. Pain was positional in nature, exacerbated by sitting and partially relieved when standing or recumbent. Pudendal nerve entrapment was diagnosed clinically, with computed tomography–guided nerve blocks providing temporary relief. A prolonged left pudendal nerve distal motor latency on electrodiagnostic testing later confirmed the diagnosis. At surgery, the left pudendal nerve was found flattened in the pudendal canal of Alcock and in contact with the sharp inferior border of the sacrospinous ligament. After surgical decompression and rehabilitation, the patient experienced significant relief of pain and returned to medical school. This case suggests pudendal nerve entrapment should be considered in the differential diagnosis of chronic urogenital or anorectal pain, particularly if the pain is aggravated by sitting or if there is a history of bicycle riding.


American Journal of Physical Medicine & Rehabilitation | 1994

Comparative effects of fluoxetine, amitriptyline and serotonin on functional motor recovery after sensorimotor cortex injury

Michael G. Boyeson; Robert L. Harmon; Jennifer L. Jones

ABSTRACT A recent investigation of the effects of the antidepressants desipramine and trazodone on behavioral recovery in brain-injured animals suggested that antidepressants, which act to increase noradrenergic activity in the brain, may facilitate the rate of recovery, whereas those that act to increase serotonergic (5-HT) activity may hinder recovery and reinstate deficits in recovered animals. The present study was designed to evaluate these findings further by assessing the effect of a single intraperitoneal injection of fluoxetine (a relatively pure 5-HT reuptake blocker), amitriptyline (a mixed 5-HT and noradreneregic reuptake blocker with α1-adrenergic receptor blocking activity) or a single intraventricular infusion of 5-HT on recovery of beam-walking ability in animals with a unilateral sensorimotor cortex injury. None of the drugs significantly affected the rate of recovery. Although fluoxetine was ineffective in reinstating the motor deficit in recovered animals, amitriptyline reinstated the deficit in a dose-dependent fashion. Infusion of 5-HT resulted in an extremely transient reinstatement of the deficit, which was largely attributable to its short-term sedative properties. These results suggest that 5-HT may be less involved in functional recovery than previously thought. They also add further support to previous findings that indicate that drugs which act to antagonize α1-adrenergic activity (e.g., phenoxybenzamine) may interfere with motor recovery after sensorimotor cortex injury. An appreciation of the potential impact of certain antidepressants on functional recovery in brain-injured patients appears warranted.


American Journal of Physical Medicine & Rehabilitation | 1996

Low-intensity, alternate-day exercise improves muscle performance without apparent adverse effect in postpolio patients

James C. Agre; Arthur A. Rodriquez; Todd Franke; Eileen R. Swiggum; Robert L. Harmon; Joel T. Curt

The purpose of this study was to examine the effect of a low-intensity, alternate-day, 12 wk quadriceps muscle-strengthening exercise program on muscle strength and muscle and motor unit integrity in 12 postpolio patients. Patients performed six to ten repetitions of a 5-s duration knee extension exercise with ankle weights. After completing six repetitions, patients rated the perceived exertion (RPE) in the exercised muscle. The patient continued repetitions until RPE was >/= 17 or ten repetitions were performed. The weight was increased the next exercise day whenever the RPE was < 17 after ten repetitions. Before and after the training program, median macroamplitude as well as jitter and blocking were determined electromyographically (EMG), serum creatine kinase (CK) was measured, and quadriceps muscle strength was assessed. The ankle weight lifted after 2 wk of training and at the end of the program were also recorded. Although the ankle weight lifted at the end of the program significantly (P < 0.05) increased from a mean +/- SD of 7.1 +/- 2.7 to 11.2 +/- 4.7 kg, the dynametrically determined muscle strength measures did not significantly (P > 0.05) increase. The EMG and the serum CK variables also did not significantly (P >0.05) change as a result of the exercise program. We conclude that performance was improved, as demonstrated by an increase in the amount of weight the patients lifted in the exercise program. No evidence was found to show that this program adversely affected the motor units or the muscle as the EMG and CK did not change.


American Journal of Physical Medicine & Rehabilitation | 1993

Effects of trazodone and desipramine on motor recovery in brain-injured rats.

Michael G. Boyeson; Robert L. Harmon

Rats pretrained to walk a narrow balance beam received unilateral sensorimotor cortex lesions, resulting in a contralateral transient paresis that lasted 14 days. In a dose-dependent manner, a single injection of the antidepressant trazodone given 24 hours after injury transiently slowed motor recovery compared with injured controls. After final recovery level of motor function, a reinjection of trazodone reinstated the hemiparesis for up to 6 hours. In other animals, a single injection of the antidepressant desipramine significantly facilitated motor performance when compared with injured controls. Desipramine had no deleterious motor effect when administered to animals that had recovered on the beam-walking task. These findings would suggest that the predominately noradrenergic neurotransmitter effects of desipramine may facilitate, and those of the predominately serotonergic trazodone may hinder, the recovery of locomotor performance after cortical injury in rats. Further studies appear indicated, including applying these findings to the clinical setting.


American Journal of Physical Medicine & Rehabilitation | 1998

Heterotopic ossification in moyamoya disease: a case report.

Jagmohan Sharma; Karn V. Sehgal; Robert L. Harmon

Moyamoya disease is a rare disorder of cerebrovascular circulation. A review of the literature failed to reveal the association of heterotopic ossification in patients with this disease; such a case is now presented. The patient described had atraumatic intracranial hemorrhage, was in a coma for a period of time, underwent ventriculostomy and shunt placement, and was left with residual spastic hemiparesis. Evidence of heterotopic ossification around the hemiparetic shoulder and hip was subsequently noted on radiographic studies and was managed conservatively. Heterotopic ossification may be a rare complication of the neurological deficits associated with moyamoya disease and needs careful consideration when joint stiffness persists, despite usual conservative measures.


Brain Injury | 1996

Trends in incidence of hospitalization for traumatic brain injury in Wisconsin from 1989 through 1992

Robert L. Harmon; M. J. Hodgson; J. D. Cobb

To aid in determining health care service needs, Wisconsin Department of Health and Social Services (DHSS) data on Wisconsin hospital discharges for traumatic brain injury (TBI), using ICD-9-CM codes for intracranial injury with and without skull fracture, and Wisconsin Department of Transportation data on incapacitating non-fatal head injuries (INHI) from traffic accidents from 1989 through 1992 were reviewed. Yearly TBI hospital discharges in Wisconsin declined 15.0%, and by 23.9% for Milwaukee County residents, over 1989 through 1992, correlating closely with changes in yearly INHI in Wisconsin (r = 0.999; p < 0.01) and in Milwaukee County (r = 0.989; p < 0.05). Using 1990 census data the yearly TBI risk ratio for Milwaukee County residents compared to the rest of Wisconsin increased from 1989 (1.76) to 1990 (1.92) and then decreased in 1991 (1.83) and 1992 (1.51). The results of this pilot study suggest there was a decrease in the incidence of hospitalization of patients with TBI in Wisconsin from 1989 through 1992, paralleling a decline in INHI from motor vehicle accidents. There appeared to be a relatively greater decline in these patients in Milwaukee County from 1991 to 1992 as compared to the rest of the state. The techniques employed in this study may be used to help assess rehabilitation service needs in other areas.


American Journal of Physical Medicine & Rehabilitation | 1999

Sensory and mixed nerve action potential temporal dispersion in median neuropathy at the wrist

Robert L. Harmon; Andrea H. Naylor

This retrospective pilot study was undertaken to help determine the usefulness of measuring sensory nerve action potential and mixed nerve action potential temporal dispersion in median neuropathy at the wrist (MNW; i.e., carpal tunnel syndrome). The records were reviewed for 34 patients who were referred to an electrodiagnostic medicine laboratory with normal antidromic median sensory nerve action potential (recording from the index finger), median transcarpal mixed nerve action potential, and ulnar transcarpal mixed nerve action potential peak distal latencies (NO group) and 29 patients with prolongation (>2.2 ms) of the left median transcarpal mixed nerve action potential peak distal latency or relative prolongation of this response (>0.4 ms) compared with the ipsilateral normal ulnar transcarpal mixed nerve action potential peak distal latency (MNW group). By using the time difference between onset and negative peak as a measure of waveform temporal dispersion, mean +/- standard deviation of the median transcarpal mixed nerve action potential time difference for the MNW group (0.57 +/- 0.15 ms) was found to be greater than the NO group (0.44 +/- 0.09 ms; P < 0.01). No statistically significant differences were found for the median sensory nerve action potential time difference between the two groups or between the subgroup of MNW patients with concurrent prolongation of the median sensory nerve action potential peak distal latency and the NO group. These findings suggest that increased median transcarpal mixed nerve action potential temporal dispersion may occur in association with median transcarpal mixed nerve action potential peak distal latency prolongation in MNW. The small magnitude of this increase, however, makes the clinical usefulness of this observation unclear.


Journal of Stroke & Cerebrovascular Diseases | 1995

Beneficial effect of clonidine on spasticity antagonized by baclofen in a stroke patient

Joel T. Dall; Robert L. Harmon; Michael G. Boyeson

Although Clonidine has recently been described as a useful antispasticity agent, to our knowledge there has not been a previous report of clonidines antispasticity effect antagonized by baclofen. Using a 0-5 Modified Ashworth Scale to evaluate the right knee extensor tone in a 74-year-old man 5 months following a left middle cerebral artery stroke, tone improved from 3 to 1 on Clonidine 0.6 mg daily in divided doses. The day after addition of baclofen at 15 mg daily in divided doses, tone increased to 4. Baclofen was withdrawn with a decrease in tone to 2. Baclofen alone at the above dose resulted in tone comparable to the clonidine-free baseline. Treatment with Clonidine alone was resumed, and the expected reduction in hypertonicity was again observed. Possible mechanisms of action for baclofen antagonizing the beneficial effect of Clonidine on spasticity after stroke are presented and discussed.


JAMA Neurology | 1994

Sparing of Motor Function After Cortical Injury: A New Perspective on Underlying Mechanisms

Michael G. Boyeson; Jennifer L. Jones; Robert L. Harmon


Brain Injury | 1996

Use of clonidine for treatment of spasticity arising from various forms of brain injury: a case series.

Dall Jt; Robert L. Harmon; Quinn Cm

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Michael G. Boyeson

University of Wisconsin-Madison

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James C. Agre

University of Wisconsin-Madison

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Joel T. Curt

University of Wisconsin-Madison

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Todd Franke

University of California

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Arthur A. Rodriquez

University of Wisconsin-Madison

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Eileen R. Swiggum

University of Wisconsin-Madison

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Joel T. Dall

University of Wisconsin-Madison

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Arthur A. Rodriguez

University of Wisconsin-Madison

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