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Biomedical subjects

C F Bolton

Publications and source records attributed to C F Bolton.

At least 73 records · Page 4Linked to original sources
PubMed1993

Neuromuscular complications of sepsis.

Sepsis and multiple organ failure are major problems in medical and surgical intensive care units. Critical illness polyneuropathy occurs in 70% of these patients. Difficulty in weaning from the ventilator is an early sign. Electrophysiological studies are necessary to establish the diagnosis; these studies show an axonal degeneration of peripheral nerve fibres. Recovery occurs in weeks or months, depending upon severity. Muscle biopsy reveals denervation atrophy. Sepsis itself does not induce a neuromuscular transmission defect, but neuromuscular blocking agents may increase the severity of critical illness polyneuropathy. If steroids are used in addition to neuromuscular blocking agents, a severe myopathy may result. Other effects on muscle are cachectic myopathy and panfascicular muscle fibre necrosis. A variety of combinations of these conditions may affect the same patient. Only well-designed prospective studies will determine the true effect of these medications on the neuromuscular system in septic patients.

Biopsy↗
PubMed1993

Severe axonal degeneration in acute Guillain-Barré syndrome: evidence of two different mechanisms?

Four cases of severe acute Guillain-Barré syndrome (GBS) characterized by severe axonal degeneration are presented. All had electrically inexcitable motor nerves as early as 4 days after onset. The disease was rapid in onset and the residual disability was severe. Two different types of pathology were seen. Nerve biopsies in 3 cases showed severe axonal degeneration without inflammation or demyelination. Autopsy in one of these cases showed that the dorsal and ventral roots were also significantly affected. These cases illustrate the primary axonal form of GBS. Nerve biopsy in the fourth case at day 15 showed marked inflammation and demyelination with axonal degeneration. Contralateral nerve biopsy at day 75 showed almost complete loss of axons. This case illustrates another type of axonal degeneration, that which occurs secondary to inflammation and demyelination.

Aged↗
PubMed1992

Needle electromyography of the diaphragm.

A method is described for performing needle electromyography of the diaphragm which is safe and causes little discomfort. It provides valuable information concerning neuropathies and myopathies which may affect the diaphragm, and complements information derived from phrenic nerve conduction studies. Firing patterns of motor unit potentials during spontaneous respiration identify upper motor neurone disorders causing respiratory insufficiency.

Action Potentials↗
PubMed1992

The electroencephalogram in sepsis-associated encephalopathy.

To define the EEG and associated clinical features of septic encephalopathy, we studied 62 patients with positive blood cultures. Patients were divided into three clinical groups: nonencephalopathic (NE), mildly encephalopathic (ME), and severely encephalopathic (SE); the latter two groups had diffuse cerebral dysfunction. EEGs were classified into five groups: normal, excessive theta, predominant delta, triphasic waves, and suppression or burst suppression, in ascending order of severity. The EEG (1) was more sensitive than our clinical criteria for encephalopathy, (2) showed features that were, when considered with clinical and laboratory characteristics, compatible with a potentially reversible encephalopathy, and (3) had well-defined categories that correlated with percent mortality, even within a single clinical group. We conclude that the EEG is a sensitive index of brain function in septic encephalopathy and that it is especially useful in the intensive care monitoring of patients with sepsis.

Adult↗
PubMed1992

Detection of hereditary motor sensory neuropathy type I in childhood.

Clinical signs and slowed motor nerve conduction velocities were found in 17 of 36 children under 10 years of age who had one parent with hereditary motor sensory neuropathy type I (HMSN I). Four children had slowed conduction velocities at one year or less. Clinical signs were subtle and included pes planus, distal foot wasting, weakness of ankle eversion and dorsiflexion and areflexia. HMSN I can be detected reliably in children, even before one year of age.

Child↗
PubMed1992

Forearm P-31 nuclear magnetic resonance spectroscopy studies in oculopharyngeal muscular dystrophy.

Five siblings with autosomal dominant oculopharyngeal muscular dystrophy (OPMD) underwent P-31 Nuclear Magnetic Resonance Spectroscopy studies of forearm flexor muscles. Mean values of PCr/(PCr+Pi) in the patients were reduced (p = 0.01) and pH elevated (p = 0.02) in resting muscle when compared to controls. During exercise PCr/PCr+Pi) fell quickly to values less than controls (p less than 0.0001) despite submaximal exercise output and developed exercise-induced acidosis which exceeded that of controls (p = 0.05). Acidosis recovered slowly despite relatively normal recovery of PCr/(PCr+Pi) following exercise. Within the patient group, however, one member had normal resting, exercise and recovery values. The studies suggest that OPMD is a more widespread disorder of striated muscle than clinically appreciated. The pattern of findings observed in OPMD differs from those identified in denervation, disuse and mitochondrial myopathy.

Acidosis, Lactic↗
PubMed1991

Neuromyotonia in hereditary motor neuropathy.

Two siblings with a distal motor neuropathy experienced cramping and difficulty in relaxing their muscles after voluntary contraction. Electromyographic recordings at rest revealed repetitive high voltage spontaneous electrical discharges that were accentuated after voluntary contraction and during ischaemia. Regional neuromuscular blockage with curare indicated hyperexcitability of peripheral nerve fibres and nerve block suggested that the ectopic activity originated in proximal segments of the nerve. Symptoms were improved with diphenylhydantoin, carbamazepine and tocainide.

Adolescent↗
PubMed1991

Peripheral nerve function in sepsis and multiple organ failure.

Forty-three patients who had sepsis and multiple organ failure (critical illness) were studied prospectively to determine the incidence and severity of peripheral nerve function and to correlate such function with a number of variables. Electrophysiologic studies indicated a primary axonal degeneration of motor and sensory fibers in 30 (70 percent). Fifteen (30 percent) had the clinical signs of difficulty in weaning from assisted ventilation, weakness of limb muscles, and reduced or absent deep tendon reflexes. Full recovery from the polyneuropathy occurred among the 23 (53 percent) who survived, except three who had a very severe polyneuropathy. A peripheral nerve function index, computed from electrophysiologic measurements, showed statistically significant (p less than 0.01) negative correlations with the time in the critical care unit, and the serum glucose value; the serum albumin level showed a positive correlation. Multiple regression analyses indicated all three factors accounted for 47 percent (r2 = 0.4678) of all potential variables. In a separate analysis, the nerve function index correlated with the amplitude of the diaphragm compound muscle action potential (p less than 0.01). The results were consistent with the polyneuropathy being due to the same mechanisms that are currently postulated to cause dysfunction in this syndrome of other organ systems (including the neuromuscular respiratory system).

Bacterial Infections↗
PubMed1990

The encephalopathy associated with septic illness.

Physicians and surgeons have long recognized that septic illness may be accompanied by abnormal brain functions; however, no systematic, comprehensive study has been done to define the clinical and laboratory features of the syndrome of sepsis-associated encephalopathy. We undertook such a prospective study in a tertiary care hospital and found that of 69 patients with fever and microbial cultures, 32 had marked brain dysfunction, 17 showed mild encephalopathy, and 20 were clinically nonencephalopathic. Severe cases showed obtundation and paratonic rigidity while milder cases showed confusion, inappropriate behavior, inattention, disorientation, and writing errors. There were no focal neurological deficits. The following factors correlated with the severity of brain dysfunction: adult respiratory distress syndrome; fatal outcome; certain types of EEG abnormality; axonal peripheral neuropathy; elevated peripheral white blood cell count; elevated serum levels of alkaline phosphatase, bilirubin, creatinine, phosphate, potassium, and urea; reduced blood pressure and reduced serum albumin level. Our data suggest that brain functions fail with dysfunction of other organs in septic illness. Pathogenetic mechanisms are discussed. The brain dysfunction should be regarded as potentially reversible, even in severely encephalopathic cases. Prompt control of the infection is the most important measure in controlling the encephalopathy and in preventing the increased mortality found with severely encephalopathic patients.

Alkaline Phosphatase↗
PubMed1989

Recording sound from human skeletal muscle: technical and physiological aspects.

In order to examine technical factors that influence muscle sound recording, single twitches of muscle were utilized since their waveforms were likely to be reproducible. We observed that satisfactory recordings could be made with either Archer air interface, or Hewlett-Packard direct contact sensor, microphones. Firm contact and stability between the microphone and the skin surface were particularly important. Frequencies below 20 Hz, the lower limit of the human auditory range, must be recorded, since they account for at least 90% of the power of the muscle sound wave. The chief frequencies were below 4 Hz. The sound wave produced by a maximal twitch of human thenar muscle induced by median nerve stimulation at the wrist is maximal in amplitude over the center and recedes to near zero at the margins of the muscle. It is preceded by the muscle compound action potential and is followed by the force curve, recorded with a strain gauge attached to the thumb. The sound resembles force in total time course, and it increases with increasing strengths of nerve stimulation. However, it differs in its latency, phase relationships, and response to nerve stimulation at different frequencies. Some of the features of muscle sound suggest it relates to both the active contractile and the parallel elastic components of muscle during a twitch contraction, but not the series elastic component.

Adult↗
PubMed1988

Metabolic changes in human muscle denervation: topical 31P NMR spectroscopy studies.

Metabolic changes in human forearm flexor muscle following partial or complete denervation were studied using 31P nuclear magnetic resonance spectroscopy. In resting muscle, patients with electromyographically verified forearm flexor denervation had a lower ratio of PCr/Pi than healthy controls [4.76 +/- 2.50 (SD) versus 6.50 +/- 1.55 (SD); P less than 0.01] and a higher intracellular pH [7.09 +/- 0.06 versus 7.05 +/- 0.04 (SD); P less than 0.01]. These changes were more apparent when the diseased arm was compared to the contralateral healthy arm in patients with strictly unilateral denervation. Five patients with severe denervation had the lowest PCr/Pi ratio (1.94 +/- 0.70) and the highest pH (7.15 +/- 0.04). Four patients with intact innervation and disuse atrophy as a result of a forearm fracture did not exhibit these changes immediately following removal of the forearm cast. The findings show that denervation leads to a reduction in PCr/Pi within muscle and a rise in intracellular pH, and that these changes correlate with the degree of denervation and improve with recovery. 31P MRS may be useful to follow the course of denervation atrophy.

Adult↗
PubMed1988

Neuromuscular disorders and thymoma.

We describe a patient who had asymmetrical atrophy of limb muscles and myasthenic weakness of neck, facial, and bulbar muscles. Electrophysiological tests indicated myasthenia gravis of facial muscles and changes consistent with an asymmetrical motor neuropathy as a cause of the muscle atrophy. Both conditions occurred as complications of a locally invasive thymoma, and both failed to improve after surgery and radiation but substantially improved with subsequent treatment by corticosteroids, azathioprine, and plasmapheresis. Review of the literature disclosed that several neuromuscular conditions may be associated with thymoma, the commonest being myasthenia gravis. Muscle atrophy may occur in 10% of patients who have myasthenia gravis, whether associated with or without thymoma. Its mechanism is debated, and further studies are needed, but observations in our patient suggest the atrophy is due to a motor neuropathy. Primary treatment of the thymoma by surgery, irradiation if the tumor is invasive, and immunosuppressive therapy for neuromuscular complications offers a relatively good prognosis for this group of patients.

Action Potentials↗
PubMed1987

Electrophysiologic studies of critically ill patients.

Sepsis and critical illness occur as complications of illness, injury, or surgery in approximately 5% of patients in our critical care unit. Clinical evaluation of the nervous system is difficult in this clinical setting, and electrophysiologic studies are therefore quite valuable. Electroencephalography detects encephalopathy and electromyography (EMG) and nerve conduction studies detect neuromuscular disorders at early stages of their development. Thus, septic encephalopathy occurs in almost all patients and critically ill polyneuropathy in at least 50% of such patients. The polyneuropathy is a predominantly distal axonal degeneration of motor and sensory fibers. A catabolic myopathy is also present, but is difficult to detect electrophysiologically. No defect in neuromuscular transmission has so far been demonstrated. Both the encephalopathy and polyneuropathy may be quite severe, but with vigorous management of the sepsis and critical illness complete recovery may occur in the 40% of patients who survive.

Critical Care↗
PubMed1987

Critical illness polyneuropathy. A complication of sepsis and multiple organ failure.

Nineteen patients developed polyneuropathy complicating critical illness. They had been admitted to a critical care unit following intubation for cardiac or pulmonary disease and had developed sepsis and multiple organ failure. Approximately one month following intubation, failure to wean from the ventilator and limb weakness prompted neurological referral. Examination disclosed weakness and wasting of muscles and impaired tendon reflexes in most, but not all, patients. Electrophysiological studies in 17 patients revealed attenuated compound muscle and sensory nerve action potential amplitudes and widespread denervation on needle electromyography. Autopsy in 9 patients who died of their critical illness revealed widespread primary axonal degeneration of motor and sensory fibres, with extensive denervation atrophy of limb and respiratory muscles. Survivors recovered from the polyneuropathy three to six months following discharge. Seventeen of the patients were segregated by electrophysiological criteria into mild (8) and severe (9) polyneuropathy categories. An analysis of these two groups failed to reveal putative metabolic, drug, nutritional or toxic factors that might be responsible for the polyneuropathy. Our studies suggest that the mechanism may be a fundamental defect, still unknown, which causes dysfunction of all organ systems in this syndrome.

Adult↗