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Biomedical subjects

W J Becker

Publications and source records attributed to W J Becker.

At least 19 recordsLinked to original sources

Long term treatment of intractable reflex sympathetic dystrophy with intrathecal morphine.

BACKGROUND: Some patients with reflex sympathetic dystrophy (RD) develop intractable symptoms unresponsive to conventional therapy. Recently, intrathecal morphine therapy has been used with some success in such patients. METHODS: The clinical course of two patients with intractable reflex sympathetic dystrophy (RSD) is described. Both patients developed intractable leg pain, swelling and autonomic changes after a leg injury. Numerous medical treatments and surgical sympathectomies failed to provide long term relief. RESULTS: Relatively satisfactory symptom control was achieved only with the use of long term intrathecal morphine therapy delivered by subcutaneously implanted infusion pumps. Exacerbations of the RSD continued to occur, at times in association with further leg trauma, but these could be controlled by a temporary escalation of the intrathecal morphine dose. Complications of morphine therapy were relatively minor. A red rash appearing over the pump site was the first sign that a drug catheter break had occurred, necessitating surgical catheter revision. CONCLUSION: Long term intrathecal morphine therapy is a useful treatment option for patients with intractable severe RSD who have failed other therapies and remain markedly disabled.

Adolescent

Modulation of the soleus H-reflex during pedalling in normal humans and in patients with spinal spasticity.

Soleus H-reflexes were recorded in 10 normal subjects and seven patients with spasticity caused by incomplete spinal cord injury while they pedalled on a stationary bicycle which had been modified to trigger electrical stimuli to the tibial nerve at eight precise points in the pedal cycle. Stimulus strength was adjusted to yield M-waves of constant amplitude at each pedal position. During active pedalling, all normal subjects showed modulation of the H-reflex with the amplitude being increased during the downstroke portion of the pedal cycle and the reflex suppressed or absent during the upstroke. This modulation was not present during passive pedalling, with the experimenter cranking the pedals by hand, or when the pedals were locked at each of the eight positions. In five of the seven patients with spasticity, there was reduced or absent modulation of the H-reflex during active pedalling and the reflex remained large during pedal upstroke. It is concluded that descending motor commands that produce patterned voluntary activity during pedalling normally cause cyclical gating of spinal reflexes by either presynaptic or postsynaptic inhibitory mechanisms. Loss of supraspinal control over these spinal inhibitory systems could result in failure to produce appropriate suppression of reflexes during patterned voluntary movements such as pedalling or walking, and may be an important factor contributing to the functional disability in spasticity.

Adult

Myoclonus and sensorimotor integration in a patient with Ramsay Hunt syndrome.

Clinical and neurophysiologic studies were done on a patient with action myoclonus secondary to Ramsay Hunt syndrome (dyssynergia cerebellaris myoclonica). Myoclonic jerks in the arms were much more common during movements directed to a target than in other movements. They appeared to be triggered primarily by external sensory inputs relevant to the movement rather than by the motor activity itself. Both somatosensory and visual inputs appeared able to trigger the myoclonic jerks. Myoclonic jerks in the deltoid muscle followed finger contact with a target by approximately 100 msec. Electrical stimuli delivered to the fingers during a reaching movement also triggered myoclonic jerks with a similar latency and also evoked giant cortical potentials which preceded the myoclonic jerks in deltoid by 15-20 msec. Our results suggest that during sensory guided movements, sensory inputs relevant to successful completion of the movement may have access to motor systems controlling the muscles involved. In our patient, who likely has lesions involving the cerebellar nuclei and/or cerebellar cortex, these sensory inputs appeared to result in an excessive motor response, possibly through mechanisms involving cerebellar-motor cortex connections.

Adult

Multi-joint reaching movements and eye-hand tracking in cerebellar incoordination: investigation of a patient with complete loss of Purkinje cells.

Performance on an eye-hand tracking task and a multi-joint reaching movement to a visual target was studied in a patient with stable cerebellar ataxia and in control subjects. The patient subsequently died and a full neuropathological examination was performed. The neuropathological findings were similar to those seen in patients with paraneoplastic cerebellar degeneration, but no tumor was found at autopsy eight years after onset of the patient's cerebellar syndrome. A severe cerebellar cortical degeneration with complete Purkinje cell loss was demonstrated, whereas cerebellar nuclei and brainstem structures showed no neuronal loss. Tracking performance by the patient was characterized by abnormally large numbers of high velocity movements and hand direction reversals, and by excessive lagging of the hand behind the target in time. In the multi-joint reaching movement, the patient showed a delay in movement onset at the elbow joint compared to movement onset at the shoulder joint. The velocity profile of the movement at the shoulder joint was abnormal. The duration of the acceleration phase was poorly correlated with both peak angular velocity and the duration of the deceleration phase. One of the most striking findings was the inability of the patient to consistently produce the same movement direction from trial to trial while reaching to the same target. Our data suggests that the cerebellar cortex is involved in multiple aspects of motor control including visuomotor integration mechanisms.

Adult

Effects of unexpected perturbations on trajectories and EMG patterns of rapid wrist flexion movements in humans.

To investigate how motor programs can be modified by sensory inputs we recorded kinematic and EMG patterns from normal human subjects performing well-practised wrist flexion movements in response to an auditory tone. On random trials unexpected wrist perturbations were introduced at varying times after the signal to move had been given. Extension perturbations delivered before agonist EMG onset resulted in an increased maximum velocity (MV) during the wrist flexion movement and in an increased target overshoot even though the wrist was further from the target than expected by the subject at the onset of the movement. The first agonist EMG burst and the antagonist burst were both increased in magnitude in these perturbed trials. Flexion perturbations delivered before the agonist EMG onset moved the hand nearer to the target just prior to movement onset. These resulted in a reduced MV, but the expected increased target overshoot did not occur. The first agonist burst was reduced in magnitude, and the antagonist burst was increased in magnitude. Perturbations delivered after agonist EMG onset produced less change in the first agonist and antagonist EMG burst, and less compensation for the perturbation was evident in wrist position and velocity recordings. These results indicate that, at least in some situations, motor programs for rapid voluntary movements can be modified by afferent inputs. This interaction between central motor commands and sensory feedback might occur at the cortical or spinal level, depending on when perturbations occur relative to onset of EMG and movement. The timing of the EMG changes suggest that both reflex mechanisms and longer latency 'voluntary' adjustments contribute to the compensatory changes in movement trajectory.

Adult

Coordination of a multi-joint movement in normal humans and in patients with cerebellar dysfunction.

The contribution of the cerebellar cortex to coordination of a multi-joint throwing movement was studied by measuring various movement and EMG parameters while normal control subjects and patients with cerebellar cortical atrophy threw a ball at a target. Although patients did not throw as accurately as controls, several coordination measurements were normal in the patients. These included parameters used by us to assess elbow-wrist coordination and the coordination of hand opening with activation of more proximal arm muscles. Postural support for the movement at the shoulder was also normal in that the shoulder was not pushed backwards by the reaction forces resulting from the rapid forward acceleration of the forearm and hand. In contrast, however, patients were unable to coordinate the muscles so as to produce the same hand direction from trial to trial when throwing at the same target. In addition, EMG onset times were abnormal in the antagonist muscles relative to agonist EMG bursts and kinematic parameters of the movement. In conclusion, our patients with cerebellar cortical atrophy showed abnormalities in visual-motor coordination, in that they were unable to consistently produce the appropriate hand direction in response to a visual target. Agonist-antagonist relationships were also impaired. Other aspects of coordination, such as the relative timing of EMG onsets of agonist muscles, even when these were active at different joints, were normal.

Adult

Manual tracking performance in patients with cerebellar incoordination: effects of mechanical loading.

Manual tracking performance was studied in five patients with cerebellar incoordination due to unilateral cerebellar hemisphere lesions. The subjects were required to track a target on an oscilloscope screen by moving a cursor controlled by flexion-extension movements of the wrist. In comparison to normal subjects, the cerebellar patients, using their clinically affected arm, demonstrated irregular tracking patterns with inappropriate accelerations and decelerations, numerous high velocity peaks of movement, and an increased time lag between the cursor and the target. The addition of a viscous load provided by feeding back wrist velocity to a torque motor coupled to the apparatus resulted in significant improvement in tracking performance and suppression of the high velocity peaks. Increasing elastic stiffness by feeding back wrist position or inertial load by adding weights to the hand did not improve performance on this task. It is proposed that a hypotonic cerebellar limb behaves like an underdamped mechanical system. The addition of viscous loads helps restore more normal damping during voluntary movements of the arm.

Adolescent

Methanol poisoning: factors associated with neurologic complications.

Hospital records of thirty patients with methanol poisoning were studied. Neurologic manifestations at presentation including coma, seizures and decreased visual acuity were seen in nineteen patients. The mean blood pH at presentation was significantly lower in the patients with these neurologic signs and symptoms than in the eleven patients without them (p less than 0.05). Methanol levels at presentation tended to be higher in patients with neurologic manifestations at presentation and these patients tended to present later after methanol ingestion than those patients without neurologic manifestations. Fifteen patients with methanol poisoning developed serious neurologic sequelae or died. The mean blood pH was significantly lower in this patient group than in those who survived without neurologic sequelae (p less than 0.05). Methanol levels at presentation were not different in the patients who developed neurologic sequelae or died as compared to those who did not. The time from ingestion of methanol to presentation at the hospital was however significantly longer in those patients who developed neurologic sequelae or died (p less than 0.05). Initiation of treatment within eight hours of ingestion of methanol was associated with a better clinical outcome.

Adolescent

Effects of ischemic nerve block on the early and late components of the stretch reflex in the human forearm.

To investigate the peripheral afferent mechanisms which mediate the short latency (M1) and long latency (M2) components of the stretch reflex, we have recorded EMG responses to extension perturbations at the wrist before and following inflation of a blood pressure cuff around the upper arm. After approximately 30 min of ischemia, the reflexes had almost completely disappeared, although subjects were still able to activate the forearm muscles voluntarily. As the ischemic block developed, the M2 component began to decrease in amplitude sooner than M1, and up to the time of complete loss of reflex activity, the suppression of M2 was relatively greater than that of M1. These results suggest that M2 may be mediated by a population of afferent fibers different from the Ia afferents which are believed to generate the M1 response.

Adult

Modulation of reflex and voluntary EMG activity in wrist flexors by stimulation of digital nerves in hemiplegic humans.

Changes in EMG activity in the wrist flexor muscles were studied in response to electrical stimulation of digital nerves and to sudden extension perturbations at the wrist produced by a torque motor in human subjects with unilateral cerebral hemisphere lesions. With the subjects maintaining a steady voluntary contraction against a constant load, digital nerve stimulation produced a series of excitatory and inhibitory changes in tonic EMG activity from the wrist flexors in both the normal and paretic arm. The most consistent response was a period of EMG inhibition beginning approximately 38 msec after the stimulus and lasting approximately 35 msec. With relatively weak electrical stimuli, there was less EMG inhibition in the paretic arm than in the normal arm; with stronger stimuli, the inhibitory response was similar in the two arms. The electrical stimuli and mechanical perturbations were then delivered together, with the interval between them adjusted so that the expected period of inhibition following electrical stimulation coincided with either the early (M1) or the long latency (M2) components of the stretch reflex. In the normal arm electrical stimulation produced more inhibition of the M2 component than of the M1 component. In the paretic arm, inhibition during the M2 component was less marked and similar in degree to that which occurred during M1. These results are compatible with the view that M1 and M2 are normally mediated by separate neural pathways. The long latency EMG activity evoked by muscle stretch in the paretic arm of hemiplegic patients may be generated by pathways or mechanisms different from those in the intact arm.

Electric Stimulation

Colour vision abnormalities in multiple sclerosis.

A battery of colour vision tests was employed to evaluate visual function in patients with multiple sclerosis (M.S.). Colour deficits were found in 45% of patients tested with the Ishihara plates and 42.5% of patients tested with the FM 100-Hue test. 65% of M.S. patients failed at least one of the tests. The colour vision deficits were not restricted to patients with optic neuritis or with visual evoked potential (VEP) abnormalities and there was no significant correlation between an abnormal VEP latency and a colour vision deficit. Colour vision testing may be a useful option to consider in the investigation of M.S. patients, even if there is no other evidence of visual system involvement.

Adult

Effect of cutaneous nerve stimulation on voluntary and stretch reflex electromyographic activity in wrist flexors in humans.

1. Changes in electromyographic (e.m.g.) activity in the wrist flexors of normal human subjects were studied in response to electrical stimulation of digital nerves and to sudden extension perturbations at the wrist produced by a torque motor. 2. With the subjects maintaining a steady voluntary contraction, stimulation of the digital nerves produced a series of excitatory and inhibitory changes in the tonic e.m.g. activity from the wrist flexors. The most prominent and consistent response was a period of e.m.g. inhibition beginning 39 ms after the stimulus and lasting for approximately 36 ms. 3. The stretch reflex evoked by extension perturbations of the wrist consisted of an early response (M1) with an onset latency of approximately 30 ms, and a late response (M2) with an onset latency of approximately 60 ms. 4. The electrical stimuli and the mechanical perturbations were then delivered together, varying the interval between them so that the period of inhibition resulting from the electrical stimuli occurred at the same time as the M1 or M2 components of the stretch reflex, or during the later voluntary response. 5. The amount of e.m.g. inhibition during the M2 component was significantly greater than that during M1 (P less than 0.02). This result is compatible with the view that M1 and M2 are mediated by separate neural pathways.

Adult

Variants of Guillain-Barré syndrome: Miller Fisher syndrome, facial diplegia and multiple cranial nerve palsies.

We report the experience at a large teaching hospital over a 10 year period with Miller Fisher Syndrome, facial diplegia, and multiple cranial nerve palsies. In these patients, absence of drowsiness on examination, normal cranial CT scans, albumino-cytological dissociation on CSF examination and slowing of nerve conduction, all suggest that a peripheral nerve dysfunction is the underlying mechanism. Pertinent literature is reviewed, in an attempt to separate these probable variants of Guillain-Barré Syndrome from brainstem encephalitis, with which they may be confused.

Cerebellar Ataxia

Hypoparathyroidism and pseudotumor cerebri: an infrequent clinical association.

We report a patient with chronic, untreated idiopathic hypoparathyroidism who presented with papilledema and progressive deterioration of visual function. The papilledema resolved with treatment of the hypocalcemia. Visual acuity progressively improved as the serum calcium rose during treatment with vitamin D and calcium supplements. Lumbar puncture may also have contributed to the normalization of cerebrospinal fluid pressure and recovery of vision in this patient. The association of hypoparathyroidism and pseudotumor cerebri is rare, and a retrospective review of 41 patients with hypoparathyroidism admitted to two local general hospitals revealed no other cases.

Adult

Serial pattern shift visual evoked potentials in multiple sclerosis.

Forty patients with MS initially tested in our laboratory were recalled for repeat PSVEP testing approximately two years later. Twelve normal controls were tested in a similar manner approximately two years apart. The PSVEP positive peak latency changed little in the 24 control eyes (mean 1.4 msec, range 0-6) over the study interval. Most MS patient eyes also showed little change in PSVEP latency over the two year study interval. Fifty-eight eyes changed 8 msec or less. Eighteen eyes showed a PSVEP latency increase of 10 msec or more. Six of these eighteen eyes were symptomatic (attack of clinical optic neuritis), twelve asymptomatic during the study interval. Symptomatic eyes tended to have greater latency increases during the study interval than asymptomatic eyes. Significant latency increases occurred with equal frequency in previously normal eyes (normal PSVEP on first test) and abnormal eyes (abnormal PSVEP on first test or previous clinical optic neuritis). Significant latency increases occurred with greater frequency in patients with a mixed or progressive course than in patients with a remitting-relapsing course, and in patients with greater disability rating (Kurtzke 3-7) than in patients with lower disability ratings (Kurtzke 0-2). Bilateral latency increases occurred during the study interval more frequently than expected by chance. Patient age and disease duration did not significantly influence the number of PSVEP latency increases seen during the study interval. Four eyes decreased in latency by 10 msec or more during the study interval. All these eyes had had an episode of acute optic neuritis which began in the 5 weeks immediately preceding the 1st PSVEP test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Recurrent aseptic meningitis secondary to intracranial epidermoids.

Two patients with recurrent aseptic meningitis are reported. Intracranial epidermoid tumors were eventually found in both patients. CSF changes in our first case with an epidermoid tumor were similar to those reported in Mollaret's meningitis, with an initial polymorphonuclear pleocytosis early in each attack, followed by a lymphocytic predominance several days later. Large cells which proved to be macrophages were also seen in the CSF of this patient. Both patients had meningitis attacks for several years before the underlying epidermoid tumor was found. Mollaret's meningitis remains a diagnosis of exclusion. These patients should remain tumor suspects for many years and deserve careful and repeated investigation.

Brain Neoplasms