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Biomedical subjects

E Halar

Publications and source records attributed to E Halar.

15 recordsLinked to original sources
PubMed1987

Neurogenic heterotopic ossification.

Neurogenic heterotopic ossification is a potential sequela of neurological disorders, especially spinal cord injury and head injury. The etiology is unknown. Clinical, radiologic, and bone scan findings are typical. Complications may threaten function. The differential diagnosis is crucial in its early stages. Treatment options include diphosphonates, non-steroidal anti-inflammatory drugs, and surgery. This article has reviewed the literature on neurogenic heterotopic ossification (HO), soft tissue ossification of neurologic disease, including pathogenesis, histology, presentation, diagnosis, natural history, complications, and current treatments.

Animals↗
PubMed1985

Temporal course of motor recovery after Brown-Sequard spinal cord injuries.

Recovery of voluntary motor function after incomplete spinal cord injuries is attributed to a variety of physiological mechanisms, such as resolution of conduction block in injured axons, and neuroplasticity mechanisms in spared axons. To better understand these recovery mechanisms, we have examined motor recovery in one type of incomplete cord injury, the Brown-Sequard Syndrome. This syndrome is observed in patients with unilateral injury of the spinal cord and is manifested as asymmetric weakness and pain/temperature sensory loss contralateral to the weakest extremity. We have followed the course of motor recovery in two patients and reviewed the literature in an additional 59. Common features of this motor recovery include: 1) recovery of ipsilateral proximal extensor muscles before ipsilateral distal flexors, 2) recovery of any weakness in the extremity with pain/temperature sensory loss before the opposite extremity, and 3) recovery of voluntary motor strength and a functional gait by 1 to 6 months. We discuss these observations with respect to three hypotheses to explain motor recovery and suggest that neuroplasticity mechanisms functioning in spared descending axons may mediate much of the observed recovery after Brown-Sequard cord lesions.

Adult↗
PubMed1984

Attenuated skin blood flow response to hyperthermia in paraplegic men.

To clarify how skin and internal temperatures interact in control of skin blood flow, five male paraplegic subjects (lesions at the level of thoracic vertebrae 1-11) (29-47 yr old) were heated in water-perfused suits to elevate oral temperature (To) 1-1.5 degrees C. In part I only the insensate skin was heated; sensate skin was kept at 32-34 degrees C. No appreciable elevation of forearm blood flow (FBF) or sweating occurred, even with To at 38 degrees C. In part II the suit was applied to the whole body so that skin temperature was 40 degrees C, except for one arm that remained at 32-34 degrees C for FBF measurement. Sweating was noted above the lesion in all but one subject. FBF increased in all subjects but was far below levels previously reported for hyperthermic normal men; also, thresholds appeared elevated. To the extent that effector connections are intact, attenuated FBF response implies that either 1) some vasoconstrictor bias associated with cardiovascular regulation is active or 2) thermoregulatory effector outflow is diminished. If the latter is true, it follows that the effector outflow reduction relates to diminished afferent input. But the component of the effector outflow contributed by peripheral thermoreception is small; thus these findings may indicate that what is lacking in the afferent input is central thermoreception from below the lesion, possibly from the spinal cord itself.

Adult↗
PubMed1983

Aldose reductase inhibition improves nerve conduction velocity in diabetic patients.

To assess the potential role of polyol-pathway activity in diabetic neuropathy, we measured the effects of sorbinil--a potent inhibitor of the key polyol-pathway enzyme aldose reductase--on nerve conduction velocity in 39 stable diabetics in a randomized, double-blind, cross-over trial. During nine weeks of treatment with sorbinil (250 mg per day), nerve conduction velocity was greater than during a nine-week placebo period for all three nerves tested: the peroneal motor nerve (mean increase [+/- S.E.M.], 0.70 +/- 0.24 m per second, P less than 0.008), the median motor nerve (mean increase, 0.66 +/- 0.27, P less than 0.005), and the median sensory nerve (mean increase, 1.16 +/- 0.50, P less than 0.035). Conduction velocity for all three nerves declined significantly within three weeks after cessation of the drug. These effects of sorbinil were not related to glycemic control, which was constant during the study. Although the effect of sorbinil in improving nerve conduction velocity in diabetics was small, the findings suggest that polyol-pathway activity contributes to slowed nerve conduction in diabetics. The clinical applicability of these observations remains to be determined, but they encourage further exploration of this approach to the treatment or prevention of diabetic neuropathy.

Adult↗
PubMed1983

Motor and sensory ulnar nerve conduction velocities: effect of elbow position.

Ulnar motor and sensory nerve conduction velocities (NCV) were studied bilaterally in 20 able-bodied subjects for below elbow (BE) and across elbow (AE) segments to assess the effect of 4 different elbow positions on NCV (0 degrees, 45 degrees, 90 degrees, and 135 degrees). Although constant skin stimulation marker points were used, the AE segment length became progressively longer with increased elbow flexion. At 0 degrees flexion the AE segment motor NCV was found to be slower, and at 45 degrees it was found faster than the BE NCV. At each subsequent elbow flexion position (90 degrees and 135 degrees) there was an erroneous increase in motor and sensory NCV for the AE segments (p less than 0.01). This increase in AE NCV with elbow flexion was mostly due to stretching of skin over the flexed elbow. The nerve itself was observed in 4 cadaver specimens to slide distally with respect to the above elbow skin marker. Since 45 degrees elbow flexion was the position of least variation in motor NCV for AE and BE segments, this degree of elbow flexion appears to be optimum. From these measurements and from literature review neither short AE segment length (less than 10 cm) nor long AE segment length (greater than 15 cm) is optimum for measurement of AE NCV in the assessment of compressive neuropathy at the elbow. Short segments are subject to increased NCV variation while long segments may not detect pathological slowing of NCV only occurring over a short portion of the nerve.

Adult↗
PubMed1981

Diabetic neuropathy and plasma glucose control.

Diabetic neuropathy is defined, and theories of its pathogenesis are reviewed. Recent studies designed to investigate the influence of plasma glucose on nerve function in noninsulin-dependent diabetic patients are summarized. Motor nerve conduction velocities in the median and peroneal nerves were measured using a double-stimulus technique, and sensory conduction velocity was measured by conventional methods before and after therapy with oral agents or insulin. The degree of hyperglycemia was assessed by measurement of fasting plasma glucose and glycosylated hemoglobin concentrations. The degree of slowing in motor nerve conduction velocity in untreated patients was found to correlate with the fasting plasma glucose and glycosylated hemoglobin concentrations, but sensory nerve function, although abnormal, did not show such correlation. Reduction of hyperglycemia was associated with improvement in motor nerve conduction velocity in the peroneal and median motor nerves of these patients, but sensory nerve conduction velocity showed no such improvement. Improvement in median motor nerve conduction velocity was directly related to the degree of reduction in fasting plasma glucose concentration. These findings suggest that metabolic factors related to hyperglycemia are important in the impaired motor nerve function seen in noninsulin-dependent patients with maturity-onset diabetes.

Animals↗
PubMed1981

Glycemic control and nerve conduction abnormalities in non-insulin-dependent diabetic subjects.

The influence of therapy of hyperglycemia on the progression of diabetic neuropathy is unclear. We studied variables of glycemia and motor and sensory nerve conduction velocity in a group of 18 non-insulin-dependent diabetic subjects before and after institution of diabetes therapy. Diabetes therapy significantly reduced variables of glycemia after 1, 3, 6, and 12 months. Conduction velocity of the median motor nerve was improved from baseline at each time tested during treatment. In addition, peroneal and tibial motor nerve conduction velocities improved in patients whose levels of hyperglycemia were lowered. Moreover, extent of improvement of conduction velocity of some motor nerves was related to the degree of reduction of hyperglycemia. Sensory nerve conduction velocity was not altered by diabetes therapy. These findings support the hypothesis of a metabolic component to diabetic neuropathy and suggest that optimal glycemic control may be beneficial to patients with this disorder.

Adult↗
PubMed1979

Nerve conduction abnormalities in untreated maturity-onset diabetes: relation to levels of fasting plasma glucose and glycosylated hemoglobin.

The role of metabolic abnormalities in the development of diabetic neuropathy is controversial. To investigate the influence of hyperglycemia on nerve conduction, we studied 20 untreated maturity-onset diabetic patients and 23 normal control subjects of similar age. Nerve conduction velocity of motor (median, peroneal, and tibial) and sensory (median and sural) nerves in diabetic patients was significantly slowed and H-reflex latency time prolonged. Levels of fasting plasma glucose in diabetic subjects were correlated with slowed motor conduction velocity of the median, peroneal, and tibial nerves but not with sensory nerve conduction velocities. Levels of glycosylated hemoglobin, an index of long-term glycemia, were correlated with slowing of peroneal motor conduction velocity in diabetic patients. These associations could not be explained by patient age or duration of diabetes. These findings suggest that the degree of hyperglycemia of untreated maturity-onset diabetes contributes to the motor nerve conduction abnormalities in this disease.

Adult↗
PubMed1978

Temperatures in human thighs after hot pack treatment followed by ultrasound.

Temperature distributions were measured in the anterior thigh of human volunteers after preheating with a hot pack followed by ultrasound, a frequently used therapeutic procedure. The skin surface temperature is elevated by this procedure but the highest temperature is still produced at the bone-muscle interface at the end of the treatment session.

Adult↗
PubMedDate not supplied

Correlations among autonomic, sensory, and motor neural function tests in untreated non-insulin-dependent diabetic individuals.

A well-defined group of untreated non-insulin-dependent (NIDD) subjects were evaluated to determine whether involvement of neural function measurements is generalized and symmetrical and to compare the autonomic, sensory, and motor neural measurements. After age adjustment, the sensory and motor neural function measurements were significantly slower in the diabetic group than in normal subjects (P less than 0.01). Similarly, the autonomic nervous system function measurements were also abnormal in the NIDD group (P less than 0.01). Further analysis revealed that each of the specific measurements--median motor nerve conduction velocity (NCV,P less than 0.005), peroneal motor NCV (P less than 0.005), median sensory NCV (P less than 0.005), dark-adapted pupil size after muscarinic blockade (P less than 0.02), pupillary latency time (P less than 0.02), and RR-variation after beta adrenergic blockade (P less than 0.001)--was significantly less by analysis of covariance after age adjustment in the NIDD group than in normal subjects. Thus, there was evidence of motor and sensory neural impairment in the upper and lower extremities as well as evidence of impairment of the reflex arcs involving the parasympathetic nerves to the heart and eye and the sympathetic nerves to the iris. Further analysis revealed that right and left NCV were correlated (P less than 0.01), as were the median motor and median sensory NCV (P less than 0.01), the median motor and peroneal motor NCV (P less than 0.001), and the peroneal motor and median sensory NCV (P less than 0.001). Thus, there was evidence of symmetrical upper and lower limb, as well as motor and sensory proportional involvement of large nerve fiber NCV in this group of NIDD subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Monopolar recording of H reflexes at various sites.

Various monopolar recording electrode sites have been used to record H reflexes and M responses. This investigation revealed a decrease in maximum M response amplitude accompanied by an increase in the H/M amplitude ratio as the active recording electrode was positioned more distally, below the gastrocnemii muscle bellies. H and M latencies were also significantly longer at the most distal recording site, but the latency difference is relatively independent of recording site. Serial variation was least at the most proximal recording site for an immobilized ankle. For an unrestrained ankle, serial variation was greater, but was least at the most distal site. The standard recording site, midway between knee and ankle, was not the best site for minimizing serial variation, and it was the least sensitive to vibration-induced reflex excitability changes. For serial testing of H reflex excitability, an immobilized ankle and measured proximal and distal recording sites are recommended.

Adult↗