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Biomedical subjects

W J Triggs

Publications and source records attributed to W J Triggs.

At least 37 records · Page 2Linked to original sources
PubMed1997

Treatment of acute pandysautonomia with intravenous immunoglobulin.

Acute pandysautonomia has been suggested to be an uncommon variant of Guillain-Barre syndrome. Acute pandysautonomia does not seem to have been treated with intravenous immunoglobulin or other therapies proved efficacious in Guillain-Barre syndrome. A patient is reported with severe acute pandysautonomia who responded dramatically to intravenous immunoglobulin. The findings are consistent with a dysimmune pathogenesis for this syndrome and suggest a possible treatment for future cases.

Adult↗
PubMed1997

Stereotactic pallidotomy lengthens the transcranial magnetic cortical stimulation silent period in Parkinson's disease.

We compared the duration of the EMG cortical stimulation silent period (CSSP) elicited in abductor pollicis brevis using transcranial magnetic stimulation (TMS) before and after stereotactic unilateral globus pallidus internus pallidotomy (PAL) in 12 patients with Parkinson's disease. We used TMS stimulus intensities of 200, 150, 120, and 100% of motor evoked potential (MEP) threshold before and after (86 +/- 25 days) PAL. PAL increased CSSP duration at stimulus intensities of 200% of MEP threshold in the hand contralateral to the stereotactic lesion. In a subset of five patients able to remain at rest during pre-PAL testing sessions, PAL decreased the resting MEP/M-wave area ratio in the hand contralateral to the lesion at a stimulus intensity of 120% of MEP threshold. PAL did not significantly modify the effects of TMS in the hand ipsilateral to the globus pallidus lesion. The results suggest that PAL improves the function of cortical motor inhibitory circuits in Parkinson's disease.

Aged↗
PubMed1997

Valproate-associated carnitine deficiency and malignant cerebral edema in the absence of hepatic failure.

We describe a 27-year-old woman who developed encephalopathy and cerebral edema during treatment of refractory complex partial seizures that included acute administration of valproate (VPA) at a dosage of 35 mg/kg per day. Multiple random VPA levels were within therapeutic range, and results of liver function studies did not show evidence of hepatic failure. Cerebral computerized tomography (CT) showed evidence of massive cerebral edema with central herniation. Just prior to death, plasma levels of free and acyl carnitines were markedly decreased. Analysis of urinary organic acids showed increased excretion of lactate, but a normal distribution of VPA metabolites. Carnitine deficiency may predispose patients to the development of coma and life-threatening cerebral edema associated with acute administration of VPA, even in the absence of concomitant hepatic failure. We suggest specific guidelines for the evaluation and management of altered consciousness in patients with seizures receiving VPA.

Adult↗
PubMed1996

Guillain-Barré syndrome: clinical neurophysiologic studies.

Guillain-Barré syndrome is a well-defined clinical entity corresponding to primary inflammatory demyelinating lesions of peripheral nerves and spinal roots in the majority of cases seen in Western Europe and North America. Documentation of conduction abnormalities characteristic of demyelination in the context of rapidly developing weakness confirms the clinical diagnosis of acute inflammatory demyelinating polyradiculoneuropathy. These abnormalities include (1) conduction block, (2) markedly prolonged distal latencies, (3) marked slowing of motor conduction velocities, and (4) absent or impersistent F responses. Other abnormalities are of ambiguous significance: (1) low amplitude compound muscle responses, (2) absent sensory nerve potentials, (3) reduction in the maximum EMG recruitment pattern, which may all (1, 2, and 3) indicate conduction block or axonal degeneration, and (4) fibrillation potentials due to breakdown of motor axons, a frequent non-specific effect of primary inflammatory demyelination. A Guillain-Barré variant due to immune-mediated primary axonal degeneration has also been recently described.

Acute Disease↗
PubMed1995

Facilitation of magnetic motor evoked potentials during the mixed nerve silent period.

We studied motor neuron excitability during the mixed nerve silent period (MNSP) in a hand muscle using magnetic motor evoked potentials (MEPs) and F-waves. MEPs elicited between the V1 and V2 potentials of the MNSP were much larger than control MEPs elicited at rest, and were even comparable in size to control MEPs elicited during voluntary contraction. This facilitation of MEPs occurred without shortening of MEP latency, suggesting a supraspinal mechanism. MEPs were facilitated during the MNSP when elicited with a figure-8-shaped coil in a posterior-anterior orientation, but not when MEPs of the same size were elicited with the coil held in a lateral-medial orientation. F-waves elicited during the MNSP were variable between subjects, and not consistently different from control F-waves elicited at rest. Our findings may reflect increased cortical motor excitability during the MNSP, possibly related to activation of muscle afferents by mixed nerve stimulation.

Adult↗
PubMed1995

Electrophysiological studies in Guillain-Barré syndrome: correlation with antibodies to GM1, GD1B and Campylobacter jejuni.

A retrospective study of 50 patients with Guillain-Barré syndrome (GBS) correlated analysis of serial motor nerve conduction studies with the presence of antibodies to Campylobacter jejuni, GM1 and GD1b, determined by ELISA. GBS patients with antibodies to C. jejuni (n = 8), GM1 (n = 4), or GD1b (n = 4) showed electrophysiological features suggestive of demyelination with prolonged distal motor latencies and temporal dispersion/conduction block similar to GBS patients without these specific antibodies. Three of 50 GBS patients had poor recovery with inability to walk at 1 year after onset of symptoms. All three patients had antibodies to C. jejuni, but not to GM1 or GD1b. Although later on in the clinical course distal motor responses were absent in two of these patients, reflecting extensive axonal degeneration, early nerve conduction studies showed findings suggestive of demyelination. We suggest that demyelination of peripheral nerve may be the initial disease mechanism in GBS independent of the presence of antibodies to C. jejuni, GM1 or GD1b.

Adult↗
PubMed1994

Effect of [dl]-alpha-tocopherol on FeCl2-induced lipid peroxidation in rat amygdala.

Peroxidative injury of neural membrane lipids can be initiated by iron-containing blood products, chelated ferrous or ferric ions, and low valence iron in aqueous solution. Lipid peroxidation was measured following focal injection of 3 microliters of 100 mM FeCl2 into rat amygdala. Acute parenteral administration of [dl]-alpha-tocopherol as the alcohol limited the quantity of peroxidation products generated. These data suggest a potential role for alpha-tocopherol administration in limiting brain injury responses.

Amygdala↗
PubMed1994

Physiological motor asymmetry in human handedness: evidence from transcranial magnetic stimulation.

We hypothesized that human handedness might be associated with measurable differences in the excitability of the motor system. We compared the thresholds for electromyographic activation of the left and right abductor pollicis brevis (APB) and biceps muscles in 30 left-handers and 30 right-handers, by varying the direction of a brief monophasic pulse in a circular electromagnetic coil centered over the vertex of the scalp. In right-handers, we found that the threshold for activation of muscles in the right arm was lower than the threshold for activation of corresponding muscles in the left arm. In left-handers, the reverse was true. Threshold asymmetry was influenced significantly by the consistency with which each subject used the writing hand to perform other motor tasks, and was not significant between non-consistent left-handers and right-handers. Our results indicate that human handedness, and in particular, consistency of hand preference, are associated with lateralized differences in the excitability of motor system projections activated by transcranial magnetic stimulation. Our findings might reflect physiological differences in corticospinal tract function or cortical motor representation.

Adult↗
PubMed1994

There are no neurophysiologic features characteristic of "axonal" Guillain-Barré syndrome.

Classical views hold Guillain-Barré syndrome (GBS) as a primary inflammatory-demyelinating neuropathy in which secondary axonal degeneration may occur, particularly when inflammatory lesions are severe. Feasby and colleagues proposed that primary axonal degeneration can also cause GBS characterized by inexcitable motor nerves and poor outcome. This hypothesis rests largely on the results of a single autopsy in which no inflammation or demyelination were found. Using an illustrative case report confirming earlier studies, we point out that inexcitable motor nerves (or low amplitude compound muscle action potentials [CMAPs]) are of ambiguous significance and may reflect distal demyelination, causing conduction block between distal stimulation sites and target muscles, a pattern not uncommon in GBS. Recovery from such lesions may occur within weeks with restoration of CMAP amplitudes. The recognition of a yet unproven axonal variant of GBS cannot be based solely on documentation of inexcitable motor nerves in the context of rapidly developing weakness.

Action Potentials↗
PubMed1994

Dysaesthesiae induced by physiological and electrical activation of posterior column afferents after stroke.

Six of 48 stroke patients had functionally limiting dysaesthesiae induced by repetitive light touch, joint movement, or neuromuscular electrical stimulation (NMS). Only one of these six patients had a thalamic lesion. Quantitative sensory testing showed substantial impairment of pain and temperature sensation in all six patients, whereas light touch, vibration and position sense, and graphaesthesia were normal (three patients) or relatively spared (three patients). By contrast, none of 15 stroke patients in whom NMS did not evoke dysaesthesiae had clinical evidence of dissociated sensory loss. Conscious perception of joint movement and light touch is mediated mainly by the same population of large myelinated fibres activated preferentially by low intensity electrical stimulation. It is suggested that activation of these non-nociceptive, presumably dorsal column, afferents may contribute to dysaesthesiae in some patients with sensory loss after stroke.

Adult↗
PubMed1994

Motor neglect associated with a discrete parietal lesion.

The syndrome of motor neglect may follow brain lesions affecting frontal, subcortical, and parietal structures. However, pure motor neglect has not been previously associated with a lesion confined to the parietal lobe. We observed a 79-year-old right-handed man with right-sided limb akinesia and motor neglect without concomitant sensory or visuospatial neglect. MRI showed a left posterior parietal infarct sparing the primary sensorimotor cortex. Transcranial magnetic stimulation showed comparable thresholds for electromyographic activation of the muscles of the right and left arm and normal central motor conduction times, indicating functional integrity of the motor cortex. This case demonstrates that a discrete parietal lesion can produce a pure intentional disorder, independent of sensory or visuospatial neglect.

Aged↗
PubMed1993

Cortical and spinal motor excitability during the transcranial magnetic stimulation silent period in humans.

We investigated the electromyographic silent period in abductor pollicis brevis (APB) and flexor carpi radialis muscles following transcranial magnetic stimulation of human motor cortex. In APB, we measured cortical stimulation silent period (CSSP) duration as a function of stimulus intensity, motor-evoked potential (MEP) amplitude and muscle twitch force. We used peri-stimulus-time histograms to study the effect of cortical stimulation on single-motor unit firing patterns. We compared F-waves, H-reflexes and magnetic MEPs elicited during the CSSP to control responses elicited at rest and during voluntary contraction. CSSP duration depended on the intensity of cortical stimulation. However, we found no relationship between CSSP duration and MEP amplitude or muscle twitch force, thus the CSSP is not dependent solely on Renshaw cell inhibition or on changes in Ia and Ib afferent activity following the cortically induced muscle twitch. At low intensities of stimulation, the interval to resumption of motor unit firing following the peak in the peri-stimulus-time histogram corresponding to MEP latency sometimes exceeded that which could be accounted for by the motor unit's firing rate prior to the stimulus, suggesting that synchronization of motor unit firing by cortical stimulation cannot account for the CSSP. We found brief inhibition of F-waves during the CSSP in some subjects, reflecting activation of inhibitory corticospinal projections or segmental effects. In contrast, we observed longer inhibition of H-reflexes during the CSSP in all subjects, perhaps resulting from presynaptic inhibition of Ia afferents. Magnetic MEPs also were inhibited during the CSSP, suggesting inhibition of cortical elements by transcranial magnetic stimulation.

Adult↗
PubMed1993

Giant somatosensory evoked potentials in a patient with the anterior spinal artery syndrome.

We studied a previously healthy 25-year-old woman with the anterior spinal artery syndrome, a rare thoracocervical myelopathy with multiple potential etiologies. Quantitative and clinical sensory examination showed dissociated loss of pin-prick and temperature discrimination below the level of the lesion, with normal light touch, vibratory, and position sense. Magnetic resonance imaging was consistent with cervical spinal cord infarction. Median SEPs showed normal Erb's potential with absent spinal N13- and normal scalp N20- latency. Tibial SEPs showed normal lumbosacral responses and normal scalp P30- latency. Both median and tibial nerve stimulation produced cortical responses of unusually large amplitude (median 38 microV, tibial 17 microV). We hypothesize that large SEP amplitudes in this patient resulted from loss of anterolateral inhibitory influences on the dorsal column-medial lemniscal system.

Adult↗
PubMed1993

Facilitation of magnetic motor evoked potentials during the cortical stimulation silent period.

We investigated the relationship between stimulus intensity and magnetic motor evoked potentials (MEPs) elicited 100 msec after a conditioning stimulus that was 25% of stimulator output above resting motor threshold (RMT) during tonic contraction of abductor pollicis brevis. In five subjects, MEPs elicited with stimuli less than 25% above RMT were inhibited during the EMG cortical stimulation silent period (CSSP) produced by the conditioning stimulus, relative to MEPs elicited with the test stimulus given at rest. However, increasing the intensity of the test stimulus increased the amplitude of MEPs elicited during the CSSP relative to MEPs elicited at rest, such that MEPs elicited with stimuli 30 to 45% above RMT were facilitated during the CSSP. Increasing the intensity of the test stimulus also increased the amplitude of MEPs elicited with paired stimulation at rest, and caused facilitation in one subject. Since facilitation of MEPs was never accompanied by shortening of MEP latency, our observations point to supraspinal facilitory mechanisms. We suggest that facilitation of MEPs during the CSSP reflects temporal and spatial summation of conditioning and test stimuli.

Adult↗
PubMed1992

Motor inhibition and excitation are independent effects of magnetic cortical stimulation.

We administered magnetic cortical stimulation (MCS) during voluntary contraction of intrinsic hand muscles to 8 patients with motor neuron disease (MND), 5 patients with pure lower motor neuron syndromes (LMN), a patient with severe subacute sensory neuropathy (SSN), and 10 healthy volunteers. Patients with MND had clinical evidence of upper MND and elevated thresholds for (3 patients) or absence of (5 patients) motor evoked potentials (MEPs). MCS during sustained contraction inhibited electromyographic activity in 6 of 8 patients with MND, without preceding MEPs. MCS had no effect on the electromyogram (EMG) of the other 2 patients with MND. In normal subjects and patients with LMN, inhibition of EMG was never seen without a preceding MEP, regardless of stimulus intensity. In the patient with SSN, MCS elicited normal MEPs and inhibited the EMG in a pattern similar to normal subjects, whereas supramaximal electrical stimulation of median and ulnar nerves failed to inhibit the EMG despite normal M and F responses. Our findings indicate that the inhibitory effects of MCS on EMG are not dependent solely on changes in afferent feedback caused by the muscle twitch produced by the MEP, or on Renshaw cell inhibition. We suggest that some of the inhibitory and excitatory effects of MCS on the motor system are mediated by distinct cortical elements, which may have different susceptibilities to pathophysiological processes in MND.

Adult↗