Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Dobrivoje S. Stokic is active.

Publication


Featured researches published by Dobrivoje S. Stokic.


Journal of Clinical Investigation | 1994

N-acetylcysteine inhibits muscle fatigue in humans.

Michael B. Reid; Dobrivoje S. Stokic; Stephen M. Koch; Fadi A. Khawli; A. Arturo Leis

N-acetylcysteine (NAC) is a nonspecific antioxidant that selectively inhibits acute fatigue of rodent skeletal muscle stimulated at low (but not high) tetanic frequencies and that decreases contractile function of unfatigued muscle in a dose-dependent manner. The present experiments test the hypothesis that NAC pretreatment can inhibit acute muscular fatigue in humans. Healthy volunteers were studied on two occasions each. Subjects were pretreated with NAC 150 mg/kg or 5% dextrose in water by intravenous infusion. The subject then sat in a chair with surface electrodes positioned over the motor point of tibialis anterior, an ankle dorsiflexor of mixed-fiber composition. The muscle was stimulated to contract electrically (40-55 mA, 0.2-ms pulses) and force production was measured. Function of the unfatigued muscle was assessed by measuring the forces produced during maximal voluntary contractions (MVC) of ankle dorsiflexor muscle groups and during electrical stimulation of tibialis anterior at 1, 10, 20, 40, 80, and 120 Hz (protocol 1). Fatigue was produced using repetitive tetanic stimulations at 10 Hz (protocol 1) or 40 Hz (protocol 2); intermittent stimulations subsequently were used to monitor recovery from fatigue. The contralateral leg then was studied using the same protocol. Pretreatment with NAC did not alter the function of unfatigued muscle; MVC performance and the force-frequency relationship of tibialis anterior were unchanged. During fatiguing contractions stimulated at 10 Hz, NAC increased force output by approximately 15% (P < 0.0001), an effect that was evident after 3 min of repetitive contraction (P < 0.0125) and persisted throughout the 30-min protocol. NAC had no effect on fatigue induced using 40 Hz stimuli or on recovery from fatigue. N-acetylcysteine pretreatment can improve performance of human limb muscle during fatiguing exercise, suggesting that oxidative stress plays a causal role in the fatigue process and identifying antioxidant therapy as a novel intervention that may be useful clinically.


Emerging Infectious Diseases | 2003

Acute Flaccid Paralysis and West Nile Virus Infection

James J. Sejvar; A. Arturo Leis; Dobrivoje S. Stokic; Jay A. Van Gerpen; Anthony A. Marfin; Risa M. Webb; Maryam B. Haddad; Bruce C. Tierney; Sally Slavinski; Jo Lynn Polk; Victor Dostrow; Michael Winkelmann; Lyle R. Petersen

Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a peripheral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic features of this paralysis syndrome, we evaluated acute flaccid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hospitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnormalities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropriate treatment and diagnostic testing.


Electroencephalography and Clinical Neurophysiology | 1995

Electric source localization of the auditory P300 agrees with magnetic source localization

Ina M. Tarkka; Dobrivoje S. Stokic; Luis F.H. Basile; Andrew C. Papanicolaou

The event-related cortical potential elicited in the context of auditory target detection tasks includes the N1, P2 and P3 components. The aim of the present study was to identify the sources of these scalp-recorded components using an electrical multiple dipole model. Nine healthy adults volunteered for the study. An auditory oddball paradigm was used. Stimuli (18% target and 82% non-target tones) were delivered through ear-phones and subjects were required to silently count the targets. Event-related potentials (ERPs) to these stimuli were recorded by 30 electrodes placed on the scalp. The identification of the sources of the ERP was attempted using the brain electric source analysis (BESA) program. The instantaneous source locations of N1, P2 and P3 reported in magnetoencephalographic (MEG) literature were used as initial starting locations for the spatio-temporal multiple dipole modeling of the EEG data. First the auditory long latency responses were modeled separately. Bilateral superior temporal plane sources with almost vertical orientations explained the first 250 msec window of the non-target tone recording including N1/P2 complex. This agrees with MEG source localization of N1m/P2m. Two slightly deeper dipoles in superior temporal gyri and bilateral dipoles in hippocampi or parahippocampal areas explained P3 (analysis window 250-600 msec). The final model explained the complete epoch of 600 msec with 6 dipoles and the residual variances of individual models ranged from 3.83% to 7.77%. The concordance between MEG and BESA source localization results supports the notion of generators in temporal lobes for the N1/P2 complex and generators in temporal and hippocampal areas for the P3 component.


Experimental Brain Research | 1995

Focal depression of cortical excitability induced by fatiguing muscle contraction: a transcranial magnetic stimulation study

W. Barry McKay; Stephen M. Tuel; Arthur M. Sherwood; Dobrivoje S. Stokic; Milan R. Dimitrijevic

Motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the motor cortex were recorded in separate sessions to assess changes in motor cortex excitability after a fatiguing isometric maximal voluntary contraction (MVC) of the right ankle dorsal flexor muscles. Five healthy male subjects, aged 37.4±4.2 years (mean±SE), were seated in a chair equipped with a load cell to measure dorsiflexion force. TMS or TES was delivered over the scalp vertex before and after a fatiguing MVC, which was maintained until force decreased by 50%. MEPs were recorded by surface electrodes placed over quadriceps, hamstrings, tibialis anterior (TA), and soleus muscles bilaterally. M-waves were elicited from the exercised TA by supramaximal electrical stimulation of the peroneal nerve. H-reflex and MVC recovery after fatiguing, sustained MVC were also studied independently in additional sessions. TMS-induced MEPs were significantly reduced for 20 min following MVC, but only in the exercised TA muscle. Comparing TMS and TES mean MEP amplitudes, we found that, over the first 5 min following the fatiguing MVC, they were decreased by about 55% for each. M-wave responses were unchanged. H-reflex amplitude and MVC force recovered within the 1st min following the fatiguing MVC. When neuromuscular fatigue was induced by tetanic motor point stimulation of the TA, TMS-induced MEP amplitudes remained unchanged. These findings suggest that the observed decrease in MEP amplitude represents a focal reduction of cortical excitability following a fatiguing motor task and may be caused by intracortical and/or subcortical inhibitory mechanisms.


Muscle & Nerve | 2003

Clinical spectrum of muscle weakness in human west nile virus infection

A. Arturo Leis; Dobrivoje S. Stokic; Risa M. Webb; Sally Slavinski; Jonathan D. Fratkin

Poliomyelitis has recently been identified as a cause of muscle weakness in patients with West Nile virus (WNV) infection. However, the clinical spectrum of WNV‐associated weakness has not been described. We reviewed data on 13 patients with WNV infection. Patients with muscle weakness were classified into one of three distinct groups based on clinical features. Group 1 comprised five patients who developed acute flaccid paralysis, four with meningoencephalitis and one without fever or other signs of infection. Paralysis was asymmetric, and involved from one to four limbs in individual patients. Electrodiagnostic studies confirmed involvement of anterior horn cells or motor axons. Group 2 involved two patients without meningoencephalitis who developed severe but reversible muscle weakness that recovered completely within weeks. Muscle weakness involved both lower limbs in one patient and one upper limb in the other. Group 3 consisted of two patients who experienced subjective weakness and disabling fatigue, but had no objective muscle weakness on examination. In addition to the three distinct groups, two other patients developed exaggerated weakness in the distribution of preexisting lower motor neuron dysfunction. We conclude that the clinical spectrum of WNV‐associated muscle weakness ranges from acute flaccid paralysis, with or without fever or meningoencephalitis, to disabling fatigue. Also, preexisting dysfunction may predispose anterior horn cells to additional injury from WNV. Awareness of this spectrum will help to avoid erroneous diagnoses and inappropriate treatment. Muscle Nerve 28: 302–308, 2003


Neurology | 1996

Spinal motoneuron excitability after acute spinal cord injury in humans

A. Arturo Leis; M.F. Kronenberg; Ivana Stetkarova; W. C. Paske; Dobrivoje S. Stokic

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. NEUROLOGY 1996;47: 231-237


Neurorehabilitation and Neural Repair | 2004

Clinical neurophysiological assessment of residual motor control in post-spinal cord injury paralysis.

W.B. McKAY; H. K. Lim; Michael M. Priebe; Dobrivoje S. Stokic; Arthur M. Sherwood

Objective. This study was designed to characterize the rudimentary residual lower-limb motor control that can exist in clinically paralyzed spinal-cord-injured individuals. Methods. Sixty-seven paralyzed spinal-cord-injured subjects were studied using surface electromyography recorded from muscles of the lower limbs and analyzed for responses to a rigidly administered protocol of reinforcement maneuvers, voluntary movement attempts, vibration, or the ability to volitionally suppress withdrawal evoked by plantar surface stimulation. Results. Markers for the subclinical discomplete motor syndrome were found in 64% of the subjects. The tonic vibration response was recorded in 37%, volitional plantar surface stimulation response suppression in 27%, and reinforcement maneuver responses in 6% of the subjects. Three subjects, 4%, produced reliable but very low amplitude surface electromyography during the voluntary movement segment of the protocol. Surface electromyography recorded during passive leg movement was related to Ashworth scores as was the tonic vibration response marker (P < 0.05). Conclusions. Multimuscle surface electromyography patterns recorded during a rigidly administered protocol of motor tasks can be used to differentiate between clinically paralyzed spinal-cord-injured individuals using subclinical motor output to identify the translesional neural connections that remain available for intervention testing and treatment planning after spinal cord injury.


American Journal of Physical Medicine & Rehabilitation | 2008

Risk Factors for Falls During Inpatient Rehabilitation

Jae Eun Lee; Dobrivoje S. Stokic

Lee JE, Stokic DS: Risk factors for falls during inpatient rehabilitation. Am J Phys Med Rehabil 2008;87:341–353. Objective:To determine risk factors for falls during inpatient rehabilitation on the basis of admission data, and to assess the predictive value of the FIM instrument. Design:One thousand four hundred seventy-two patients consecutively admitted to a large tertiary care rehabilitation center during 18 mos were included in this retrospective study. Events surrounding falls were reported by clinical staff. Demographic data, prehospital socioeconomic status, medical condition at admission, and admission FIM scores were analyzed using log-logistic regression model for their association with falls. Results:One hundred forty (9.5%) patients fell at least once. Most falls occurred during daytime (85%), in a patient room (90%), and were unobserved (74%). About a half of all falls occurred during the first week of rehabilitation stay. Multivariate model revealed that diagnosis of stroke and amputation, age between 41 and 50 yrs, lower cognitive FIM scores, and a large number of medical comorbidities (≥9) were associated with a high risk for fall. The respective prevalence ratios were 1.79, 3.80, 2.01, 0.98, and 1.50. Conclusions:The rate of falls varies considerably among different diagnostic groups admitted to inpatient rehabilitation. Mid-aged people with stroke and amputation, worse cognitive functions, and greater medical complexity are at a higher risk for falling. Admission FIM score may be of value for predicting falls in rehabilitation setting, which warrants further investigation.


Frontiers in Neurology | 2012

Neuromuscular Manifestations of West Nile Virus Infection

A. Arturo Leis; Dobrivoje S. Stokic

The most common neuromuscular manifestation of West Nile virus (WNV) infection is a poliomyelitis syndrome with asymmetric paralysis variably involving one (monoparesis) to four limbs (quadriparesis), with or without brainstem involvement and respiratory failure. This syndrome of acute flaccid paralysis may occur without overt fever or meningoencephalitis. Although involvement of anterior horn cells in the spinal cord and motor neurons in the brainstem are the major sites of pathology responsible for neuromuscular signs, inflammation also may involve skeletal or cardiac muscle (myositis, myocarditis), motor axons (polyradiculitis), and peripheral nerves [Guillain–Barré syndrome (GBS), brachial plexopathy]. In addition, involvement of spinal sympathetic neurons and ganglia provides an explanation for autonomic instability seen in some patients. Many patients also experience prolonged subjective generalized weakness and disabling fatigue. Despite recent evidence that WNV may persist long-term in the central nervous system or periphery in animals, the evidence in humans is controversial. WNV persistence would be of great concern in immunosuppressed patients or in those with prolonged or recurrent symptoms. Support for the contention that WNV can lead to autoimmune disease arises from reports of patients presenting with various neuromuscular diseases that presumably involve autoimmune mechanisms (GBS, other demyelinating neuropathies, myasthenia gravis, brachial plexopathies, stiff-person syndrome, and delayed or recurrent symptoms). Although there is no specific treatment or vaccine currently approved in humans, and the standard remains supportive care, drugs that can alter the cascade of immunobiochemical events leading to neuronal death may be potentially useful (high-dose corticosteroids, interferon preparations, and intravenous immune globulin containing WNV-specific antibodies). Human experience with these agents seems promising based on anecdotal reports.


Lancet Infectious Diseases | 2003

West Nile poliomyelitis.

A. Arturo Leis; Jonathan D. Fratkin; Dobrivoje S. Stokic; Theresa Harrington; Risa M. Webb; Sally Slavinski

gen, and alpha fetoprotein, were negative. The x-ray films of the chest and computed tomography scan of the thorax and abdomen were normal. The patient was treated with subcutaneous heparin and diclophenac, and fever and migratory thrombophlebitis subsided. Because the patient had been working with manure several days before his initial symptoms, Q fever serologic testing was requested. The antibody levels measured by complement fixation (CF) against phase II Coxiella burnetii antigen was 1:512. By indirect immunofluorescence, the titers of IgM and IgG against phase I and II were 1:64 and 1:512 and 1:256 and >2,048, respectively. Antibody titers against Mycoplasma, Chlamydia, Legionella, enterovirus, and influenza were negative. Recovery was uneventful and the patient was asymptomatic during a follow-up visit 3 weeks later. Antiphospholipid antibodies were negative. Three months after the acute phase of the infection, new titers of antibodies (CF) against C. burnetii were 1:128. Two years after the episode the patient was asymptomatic. This patient is unique in that he had acute Q fever with migratory thrombophlebitis. A diagnosis of Trousseau’s syndrome associated with an occult malignancy was considered on admission, but it was excluded soon. The recent history of exposure to manure was the key for the clinical diagnosis. Although specific anti-coxiella treatment was not given, the patient followed a self-limited course, and both clinical and laboratory abnormalities promptly subsided. Microscopic vasculitis and thrombosis are commonly found in patients with other rickettsial infections (5), but vascular phenomena must be considered an exceptional event in patients with Q fever. However, thrombophlebitis and pulmonary embolisms have been occasionally reported (6–8). These unusual manifestations have been associated with aPL during the course of acute Q fever (7,8). Antibodies to phospholipids have been found in 80% of patients in a large series of acute Q fever (9). None of the patients in the study showed thrombotic events or cardiac valve involvement in contrast to patients with lupus or primary aPL syndrome in whom clinical manifestations attributed to aPL developed (9). This observation could be explained by the fact that aPL found in patients with lupus and primary aPL syndrome are directed against a complex antigen that includes a lipid-binding inhibitor of coagulation, which has been characterized as a β2-glycoprotein I (apolipoprotein H). This glycoprotein seems to inhibit the activation of the contact phase system of the intrinsic pathway of blood coagulation (10). On the other hand, apolipoprotein H is not necessary for the aPL activity observed in patients with Q fever and other infectious diseases (10). According to these studies, the observation of low titers of aPL in the serum of our patient during the acute phase of Q fever must be seen as a finding of uncertain importance not necessarily associated with migratory thrombophlebitis. In short, migratory thrombophlebitis (Trousseau’s syndrome) should be added to the evergrowing list of unusual manifestations of Q fever.

Collaboration


Dive into the Dobrivoje S. Stokic's collaboration.

Top Co-Authors

Avatar

A. Arturo Leis

University of Mississippi Medical Center

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Stuart A. Yablon

Glenrose Rehabilitation Hospital

View shared research outputs
Top Co-Authors

Avatar

Fengwei Bai

University of Southern Mississippi

View shared research outputs
Top Co-Authors

Avatar

Amber M. Paul

University of Southern Mississippi

View shared research outputs
Top Co-Authors

Avatar

Jonathan D. Fratkin

University of Mississippi Medical Center

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Markus Kofler

Baylor College of Medicine

View shared research outputs
Top Co-Authors

Avatar

Sally Slavinski

New York City Department of Health and Mental Hygiene

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge