The aetiology of flaccid paralysis in West Nile virus infection.
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Biomedical subjects
Publications and source records attributed to A A Leis.
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OBJECTIVES AND METHODS: We studied cutaneous and mixed nerve silent periods (CSP, MNSP) in 4 patients with cervical syringomyelia documented by magnetic resonance imaging who on clinical examination presented with unilateral hypalgesia and hypothermesthesia. In addition, we recorded upper and lower extremity somatosensory and motor evoked potentials (SEP, MEP), and cortical silent periods. RESULTS: In all patients, CSP and the later portion of MNSP were absent or shortened on their affected side, while both were normal on their unaffected side. In all patients, SEP latencies were normal following both median and tibial nerve stimulation. In two patients, the amplitude N13 (median nerve SEP), and in one patient each the amplitudes N20 (median nerve SEP) and P37 (tibial nerve SEP) were reduced. Central motor conduction time was prolonged to abductor digiti minimi muscle in one patient on the affected side, but was normal to tibialis anterior muscle in all patients. Cortical silent periods where present bilaterally in spite of unilateral complete absence of CSP and MNSP in two subjects tested. Loss of CSP and MNSP were a sensitive parameter of spinal cord dysfunction in syringomyelia. The cervical median nerve SEP response N13 reflected gray matter involvement, while corticospinal tract dysfunction was less frequently observed. CONCLUSION: Our data suggest that CSP and later portion of MNSP are generated at the spinal level by the same small myelinated A-delta fibers, and that their central network is distinct from large diameter fiber afferents and efferents.
The excitability of motoneurons controlling upper limb muscles in humans may vary with cutaneous nerve stimulation. We investigated the effect of noxious and non-noxious conditioning stimuli applied to right and left digit II and right digit V on motor evoked potentials (MEPs) recorded from right thenar eminence, abductor digiti minimi, biceps and triceps brachii muscles in twelve healthy subjects. Transcranial magnetic stimulation (TMS) was applied at interstimulus intervals (ISI) ranging from 40 to 160 ms following conditioning distal digital stimulation. TMS and transcranial electrical stimulation (TES) were compared at ISI 80 ms. Painful digital stimulation caused differential MEP amplitude modulation with an early maximum inhibition in hand muscles and triceps brachii followed by a maximum facilitation in arm muscles. Stimulation of different digits elicited a similar pattern of MEP modulation, which largely paralleled the behavior of cutaneous silent periods in the same muscles. Contralateral digital stimulation was less effective. MEPs following TMS and TES did not differ in their response to noxious digital stimulation. MEP latencies were shortened by cutaneous stimuli. The observed effects were stimulus intensity dependent. We conclude that activation of A-alpha and A-delta fibers gives rise to complex modulatory effects on upper limb motoneuron pools. A-delta fibers initiate a spinal reflex resulting in MEP amplitude reduction in muscles involved in reaching and grasping, and MEP amplitude facilitation in muscles involved in withdrawal. These findings suggest a protective reflex mediated by A-delta fibers that protects the hand from harm. A-alpha fibers induce MEP latency shortening possibly via a transcortical excitatory loop.
BACKGROUND: Activation of distinct muscle groups organized in a stereotyped manner ("muscle synergies") is thought to underlie the production of movement by the vertebrate spinal cord. This results in movement with minimum effort and maximum efficiency. The question of how the vertebrate nervous system inhibits ongoing muscle activity is central to the study of the neural control of movement. OBJECTIVE: To investigate the strategy used by the human spinal cord to rapidly inhibit muscle activation in the upper limb. METHODS: The authors performed a series of experiments in 10 healthy subjects to assess the effect of nociceptive cutaneous stimulation on voluntarily contracting upper limb muscles. They recorded the electromyogram (EMG) with surface electrodes placed over various upper limb muscles. RESULTS: The authors found evidence of a simple inhibitory strategy that 1) was dependent on the intensity of the stimulus, 2) was maximally evoked when stimulation was applied to the fingertips, 3) preceded the earliest onset of voluntary muscle relaxation, and 4) produced inhibition of EMG activity in specific upper limb muscle groups. Nociceptive fingertip stimulation preferentially inhibited contraction of synergistic muscles involved in reaching and grasping (intrinsic hand muscles, forearm flexors, triceps) while having little effect on biceps or deltoid. CONCLUSIONS: Neural circuitry within the human spinal cord is organized to inhibit movement by rapidly deactivating muscles that constitute distinct muscle synergies. This strategy of selective and concurrent deactivation of the same basic elements that produce synergistic movement greatly simplifies motor control.
Intestinal pseudo-obstruction occurs rarely in patients with myasthenia gravis (MG) and thymoma. The etiology of the intestinal pseudo-obstruction remains to be elucidated, although an autoimmune mechanism is postulated. We present the first report of neuronal nicotinic acetylcholine receptor (AChR)-specific antibody in a patient with seropositive MG, malignant thymoma, and intestinal pseudo-obstruction. This finding provides evidence that intestinal pseudo-obstruction associated with thymoma and possibly other neoplasms may be related to antibodies against the neuronal nicotinic receptors at autonomic ganglia.
Little is known about nociceptive reflex mechanisms in the upper limb in humans. To investigate nociceptive effects on spinal motoneurone excitability, a conditioning noxious stimulus was applied to the index finger of five healthy subjects. Motor evoked potentials (MEPs) following contralateral transcranial magnetic stimulation (TMS) were recorded from thenar eminence (TE) and biceps brachii (BB) muscles ipsilateral to finger stimulation. TMS was randomly applied alone or combined with preceding finger stimulation at an interstimulus interval of 100 ms. MEP amplitudes were profoundly suppressed in TE and augmented in BB. We conclude that nociception produces a differential effect on different spinal motoneurone pools, which may be part of a complex protective reflex mechanism in the upper limb of humans.
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BACKGROUND: Recent evidence suggests that the spinal cord is an important site of anesthesia that is necessary for surgical immobility, but the specific effect of anesthetics within the spinal cord is unclear. This study assessed the effect of isoflurane and nitrous oxide on spinal motoneuron excitability by monitoring the H-reflex and the F wave. METHODS: Eight adult patients, categorized as American Society of Anesthesiologists physical status 1 or 2, who were undergoing elective orthopaedic surgery were anesthetized with 0.6, 0.8, 1.0, and 1.2 times the estimated minimum alveolar concentration (MAC) of isoflurane. Nitrous oxide was added in graded concentrations of 30%, 50%, and 70%, whereas the isoflurane concentration was decreased to maintain a total MAC of 1. The H-reflex of the soleus muscle and the F wave of the abductor hallucis muscle were measured before anesthesia and 15 min after each change of anesthetic concentration. Four or more trials of the H-reflex and 18 trials of the F wave were recorded at each concentration of anesthesia. The effect of the anesthetics on the H-reflex and F wave was analyzed using. Dunnett's test. RESULTS: H-reflex amplitude was decreased to 48.4 +/- 18.6% of preanesthesia level at 0.6 MAC isoflurane and to 33.8 +/- 19.1% when isoflurane concentration increased from 0.6 MAC to 1.2 MAC. F wave amplitude and persistence decreased to 52.2 +/- 33.6% and 44.4 +/- 26% of baseline at 0.6 MAC isoflurane, and to 33.8 +/- 26% and 21.7 +/- 22.8% at 1.2 MAC isoflurane. Isoflurane plus nitrous oxide (total 1 MAC) decreased H-reflex amplitude to 30.4-33.3% and decreased F wave persistence to 42.8-56.3% of baseline. CONCLUSIONS: Both isoflurane alone and isoflurane plus nitrous oxide decrease H-reflex and F-wave amplitude and F-wave persistence. These effects suggest that isoflurane and nitrous oxide decrease motoneuronal excitability in the human spinal cord. This may play an important role in producing surgical immobility.
Second malignant neoplasms are an infrequent but well-documented sequelae of radiation therapy for childhood cancer. We report a 34-year-old man with chondrosarcoma of the spine and thyroid carcinoma diagnosed 24 years after radiation therapy for Hodgkin's lymphoma. Both tumors arose in the previously irradiated field and were not detected until the patient presented with paraplegia. The propensity of these neoplasms to arise in the previously irradiated field warrants physicians to be alert to any manifestations arising in this anatomic area.
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In humans H-reflexes are suppressed during early spinal shock. In animals rostral cord injury results in loss of segmental reflexes within seconds. If H-reflexes persist under general anesthesia, can they be used to monitor the integrity of the rostral cord? In part I of this study, we recorded H-reflexes intraoperatively in 25 patients to elucidate general anesthesia effect. In 23 subjects, H-reflexes were consistently elicited, and within +/- 13% of the normalized group mean amplitude. In part II, we recorded H-reflexes in 31 patients during spinal cord surgery to elucidate H-reflex behavior immediately following rostral spinal cord injury. In 6, abrupt suppression of the H-reflex coincided with cord injury. In 4 of 6, suppression was transient and less than 50% of baseline; none of these patients developed neurological deficits. In 2, suppression exceeded 90% and persisted throughout surgery; both patients developed profound deficits. We conclude that (1) the H-reflex can be consistently elicited under general anesthesia in most patients, (2) rostral cord injury rapidly suppresses the H-reflex, and (3) the degree and duration of H-reflex suppression reflects the severity of the injury.
BACKGROUND: Few studies in humans have assessed the ability of Ia afferent and antidromic motor volleys to activate motoneurons during spinal shock. Hence, little is known about the excitability state of the spinal motoneuron pool after acute spinal cord injury (SCI) in humans. METHODS: In 14 patients with acute SCI involving anatomic levels T10 and above, we performed clinical and electrophysiologic studies early after injury (within 24 hours in seven subjects) and on day 10, 20, and 30 postinjury. Maximal H:M ratios, F-wave persistence, and tendon tap T-reflexes were recorded. Sixteen normal subjects and eight chronic SCI patients served as control subjects. RESULTS: Ten of 14 patients had spinal shock (complete paralysis, loss of sensation, absent reflexes, and muscle hypotonia below the injury) at the time of initial evaluation. F-waves were absent in patients with spinal shock, reduced in persistence in patients with acute SCI without spinal shock, and normal in persistence in patients with chronic SCI. H-reflexes were absent or markedly suppressed in patients with spinal shock within 24 hours of injury but recovered to normal amplitudes within several days postinjury. This recovery occurred despite absence of F-waves that persisted for several weeks postinjury. Deep tendon reflexes were proportionally more depressed in spinal shock than were H-reflexes. All patients had elicitable H-reflexes for days or weeks before the development of clinical reflexes. CONCLUSIONS: Rostral cord injury causes postsynaptic changes (hyperpolarization) in caudal motoneurons. This hyperpolarization is a major physiologic derangement in spinal shock. The rise in H-reflex amplitude despite evidence of persistent hyperpolarization is due to enhanced transmission at Ia fiber-motoneuron connections below the SCI. Finally, the observation that the stretch reflex is proportionally more depressed than the H-reflex is consistent with fusimotor drive also being depressed after SCI.
The physiologic mechanisms generating the cutaneous silent period (CSP) remain uncertain. It is not known whether the CSP occurs because of inexcitability of the spinal motor neuron. We therefore, assessed excitability of the motor neuron during the CSP using F-wave responses. H-reflexes were also elicited during the CSP. Electrical stimulation to the fifth digit produced the CSP in the voluntarily contracting abductor pollicis brevis muscle (APB). Median nerve stimulation at the wrist elicited control F or H responses during isometric APB contraction (condition 1) and in resting muscle (condition 2). Control amplitudes were compared to those elicited in the midst of the CSP. In Condition 1, F-wave amplitudes and frequency during the CSP were unchanged compared with controls. However, F-waves were increased in amplitude and frequency during the CSP (P < 0.001) relative to responses elicited in resting muscle (condition 2). H-reflexes during the CSP were suppressed (P < 0.001) compared with controls elicited during contraction (condition 1), but facilitated relative to the resting state (condition 2) in which no H-reflexes were elicitable. We conclude that spinal motor neurons remain excitable to antidromic volleys at the same time that the corticospinal volley is inhibited to produce the CSP. Moreover, motor neuron excitability appears to be increased during the CSP compared to the relaxed state.
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Cutaneous and mixed nerve silent periods (SPs) were analyzed in 2 patients with pure sensory neuropathy and in 5 healthy controls. In patients, sensory nerve action potentials (SNAPs) and somatosensory evoked potentials (SEPs) were absent, but digital and mixed nerve stimulation evoked complete SPs in voluntarily contracting thenar muscles. Marked differences in SP latencies were found between the patients, despite shared diagnoses and virtually identical nerve conduction studies. When compared with controls, SPs were normal in the first patient and markedly delayed in the second. Such findings suggest that SPs can identify conduction abnormalities not detected by routine studies. The pathologic correlate to these abnormalities remains uncertain, although electrophysiologic data suggest that the smaller, slower conducting delta fibers carry the impulses that generate these SPs.