vicodin online
News Events Profiles Clinical Management Directory

Archive for October, 2013

Understanding and Treating Spasticity

Wednesday, October 30th, 2013

By Joshua Vova, M.D., FAAP, FAAPMR

The most common accepted definition of spasticity was characterized in 1980 by James Lance, who defined it as “a motor disorder characterized by a velocity dependent increase in (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex.(1)” In addition to increased muscle tone and hyperactive reflexes, spasticity can also contribute to weakness and poor coordination(2).

Spasticity results from an imbalance between the excitatory or inhibitory input from the alpha motor neurons and causes an increase in activation of the antagonist muscle due to damage to the central nervous system. Spasticity can also cause secondary changes to occur to muscle, tendon and collagen tissue properties such as stiffness, fibrosis and atrophy(3). Potential causes of spasticity include: spinal cord injury, traumatic brain injury, cerebral palsy, stroke, neoplastic syndromes and multiple sclerosis.

Uncontrolled spasticity may interfere with mobility, exercise, range of motion and activities of daily living as well as cause chronic pain and contribute to contractures and/or pressure sores(4). However, there are some positive effects associated with spasticity. It may may help maintain muscle tone in patients who are unable to ambulate, help support circulatory function, may prevent formation of deep venous thrombosis and may assist in ambulation or transfers(5).

When managing spasticity, the clinician must balance both the positive and negative effects of increases in muscle tone. Typically, spasticity does not increase over time. However there are external factors that can effect tone such as: infection, impaction, pressure sores, pain, deep vein thrombosis, increased intracranial pressure, stress, fatigue, sleep deprivation, environmental changes or even psychological factors.

Treatment of spasticity can be non-pharmacologic, pharmacologic or surgical. There are several factors that may influence the approach in treating spasticity: severity, chronicity, severity, distribution, locus of injury and co-morbidiites(6).

Spasticity may not necessarily develop immediately after an upper motor neuron injury, it may takes weeks or months to occur. Spasticity may improve as neurological recovery takes place. Spasticity of short-term duration may require a less aggressive approach than the patient who has had and contractures. However, one must address spasticity reduction immediately in order to maximize recovery during the period of CNS plasticity in the rehabilitation process.

An interdisciplinary team to design a treatment plan will often consist of physical therapists, occupational therapists, orthotists, physiatrists, neurologists, orthopedic surgeons and or neurosurgeons(4).


The cornerstone of treating all patients with spasticity is physical and occupational therapy. The goals of therapy are to help improve and maintain range of motion around a joint and strengthen muscles to improve function(4). When muscle become spastic, there is an imbalance of the muscle forces around a joint, which can lead to contracture and deformity. Techniques such as stretching, motor learning, strengthening exercises and constraint-induced therapy are often used to improve the properties of the muscle tendon units.

Serial casting can also be utilized to immobilize a spastic limb in a stretched position. Serial casting uses a series of casts in order to stretch the muscle and improve the passive range of motion. By using a cast, the muscle remains under slow, constant tension, which can modulate the muscles response to sensory stimulus and has also shown to improve the length and number of muscle fibers (sarcomeres), as well as the amount of connective tissue(7). Other possible techniques to help improve spasticity include kinesiotaping, which uses proprioceptive feedback and tension to influence movements, vibratory stimulation and electrical stimulation(4).

The use of orthotics, or braces, are frequently utilized in the treatment plan of spasticity. The goals of orthotics are to reduce pain, prevent contracture, improve function, compensate for loss of strength and sensation and reduce spasticity. An appropriately fitted orthotic can help to modify tone and reflexes to help a patient improve function and prevent deformity(4). Decisions regarding orthotic care are often a collaborative process between the physcian, therapist and orthotist to determine the appropriate design to help a patient accomplish a function and prevent further deformity.


Oral medications have demonstrated proven efficacy by inhibiting excitatory neurotransmitters or enhancing inhibitory neurotransmitters at the level of the spinal cord(3). Oral medications provide some advantages in the treatment of spasticity. They are noninvasive, not permanent and have proven to be clinically effective. However, some may be accompanied by side effects, including weakness and drowsiness, that may limit their effectiveness.

Many of the excitatory cortical spinal pathways that lead to spasticity are believed to be influenced by Gamma-aminobutyric acid (GABA), which is the main rationale for some of the pharmacologic options of treatment(5). There are currently two recognized GABA receptors: GABAA and GABAB. Benzodiazepines, medications like diazepam (Valium®) and clonazepam (Klonopin®) are the most common and oldest class of medications utilized medications to treat spasticity. Benzodiazepines act near the GABAA receptor to hyperpolarize the cell membrane and thus cause a presynaptic inhibition of polysynaptic and monosynaptic reflexes(2-4).

However, the effect that these medications have on the central nervous system is a limiting factor. These medications have the potential to cause sedation that can exacerbate potential cognitive deficits. Benzodiazepam overdose may also lead to somnolence, coma or death. These medications also carry the risk of physiologic addiction as well as a life-threatening withdrawal syndrome if they are abruptly weaned or discontinued. There also has been clinical evidence to demonstrate that these medications may interfere with neurologic recovery after brain injury and stroke, limiting their use as well(5).

Baclofen is a GABAB agonist. Baclofen acts both presynaptically and postsynaptically by crossing the blood brain barrier and acting at the spinal cord. Because of these properties, it is recommended for spasticity that is a result of cerebral and spinal cord origin(2).

Potential side effects can also include sedation, confusion, dizziness and nausea. Baclofen can also lower seizure threshold in patients who have seizures. Abrupt withdrawal can also lead to seizures, mental status changes or cardiovascular collapse. Gabapentin (Neurontin®) is an anticonvulsant with a chemical structure very similar to GABA. Although most commonly used now for neuropathic pain, it has shown some efficacy for decreasing spasticity at very high doses.(5) Its side effects include ataxia, headaches, tremors, somnolence, fainting and nystagmus(2, 3).

Another class of medications that has been used in treating spasticity is the imidazolines, alpha-2 adrenergic agents. These include the medications clonidine (Catapres®), which is known as a blood pressure medication, and tizanidine (Zanaflex®). These medications are believed to inhibit presynaptic afferents at the level of the spinal cord as well as inhibit the release of glutamate, an excitatory neurotransmitter(2). These agents are less utilized than the other medications mentioned above due to side effect profile and clinical efficacy(3, 5). Potential side effects include hypotension, sedation, dizziness, hallucinations, fatigue and hepatotoxicity(2, 3).

Dantrolene sodium is the only medication utilized for spasticity that does have its sight of action within the central nervous system but instead works directly on the muscle peripherally(3). Its mechanism of action is to block calcium release from the sarcoplasmic reticulum that results in decreased contractility of the muscle. Some clinicians feel that this may be better tolerated for patients who have spasticity of cerebral origin because it does not act centrally; lethargy and fatigue remain known side effects(2). Because it limits muscle contraction in all muscles, generalized weakness can also be a potential side effect. The major concern regarding dantrolene is that it has significant higher risks of hepatotoxicity compared with the other medications discussed. Risks for hepatotoxicity with dantrolene are increased at higher doses and in women older than 40(3).

Injectable Treatments

Injectable medications also play a significant role in spasticity management. There is an abundance of literature supporting their efficacy for treatment. Neuromuscular blocks are used to restore the balance between agonists and antagonist muscles. The spastic muscle can be come shortened and contracted as noted above. However, the antagonist muscle can become over lengthened and weakened, further contributing to the imbalance. There are several injectable medications that can be employed to provide neuromuscular blockades. Botulinum toxin will decrease spasticity by working directly on the muscle(8). Alcohol and phenol produce their effect through direct neural destruction(9).

The FDA first approved botulinum toxin in 1989 for use in blepharospasm. Commercially, there are three different types of botulinium toxin A available and one type of botulinum toxin B. When injected into a muscle, botulin toxin interferes with the release of acetylcholine at the neuromuscular junction. This will cause the muscle to become weaker, allowing the patient to potentially exert more control over the muscle, strengthen antagonist muscles and/or tolerate orthotics/casting.

It is strongly recommended that localization of muscles to be injected utilize a localization technique such as EMG, electrostimulation or ultrasound(8). Failure to utilize localization techniques even in experienced physicians can decrease accuracy by 25 percent to 50 percent in lower extremities and 40 percent to 70 percent in upper extremities(10). Injections can only be repeated after three months to reduce the risk of systemic effects and antibody formation. Four to 10 percent of patients will develop antibodies to botulin toxin over time, reducing the effectiveness of repeat injections(5). To maximize effectiveness and limit potential complications, I strongly recommend that a patient is referred to a physician who is knowledgeable on dosing, types and frequency of side effects and methods of localizing muscles for injections. Potential side effects can include bleeding, infection, pain, undesired weakness, swallowing problems, breathing problems and a flu-like illness(8).

Phenol and alcohol are neurolytic agents that are employed to reduce spasticity. The mechanism of action is reducing neural transmission by chemically denaturing nerve fibers. It requires the clinician to be able to localize the nerve using electrostimulation and/or ultrasound and slowly injecting the nerve directly until response to the stimulation abates(4).

The effects of phenol and alcohol have a longer duration of action than botulin toxin, but there are the risks for potentially more side effects. Injections can be very painful and especially in children require sedation. Other risks include dysesthesias, blood vessel sclerosis, compartment syndrome, venous thrombosis and skin necrosis(11). Commonly, these injections are used in conjunction with botulinum toxin. Due to dosing imitations of botulinum toxin, multiple injection sites may limit efficacy of the medication. The clinician can use phenol or alcohol to target larger muscles (i.e. adductors and hamstrings) that would normally require large doses of botulinum toxin and focus their botulinum toxin injection sites(9). Failure to recognize these limitations may result in under dosing of medication and subsequent failure of the treatment plan.

Surgical Treatments

Intrathecal Baclofen Pump. Intrathecal baclofen is used to treat spasticity by surgically implanting a mechanical device that directly infuses baclofen through a catheter into the intrathecal space around the spinal cord. Flexibility of the site of catheter implantation allows this to be an effective strategy for treating both upper and/or lower extremity spasticity.

This strategy is utilized when spasticity is refractory to the methods discussed above. The advantage is that higher concentrations of baclofen can be directly infused into the area of action around the spinal cord without the systemic side effects that accompany the oral medication. This allows for either a consistent dose of medication to be delivered or flexible programming based on a patient’s needs(12).

Although the initial implantation of the device requires a surgical procedure, adjustment to dosing and medication refills can be done noninvasively in a physician’s office. As with all medications, dosing requires an experienced physician to avoid potential side effects from overdose. In addition, risks from the surgical implantation include infection, headache from cerebrospinal fluid leak, catheter migration, disconnection or blockage(13).

Selective Dorsal Rhizotomy. Selective Dorsal Rhizotomy is a surgical intervention that targets lower extremity spasticity. This procedure is performed by a neurosurgeon who will perform a laminectomy orlaminotomy and selectively separate the L2-S2 motor and sensory nerve roots. Electrical stimulation of the individual sensory nerve roots is performed, and the ones that demonstrate abnormal patterns of sensory feedback are selectively ablated(14). The goal is to maintain a balance between reductions of spasticity and preservation of function.

Potential risks of this surgery include hyperesthesia, loss of bladder function and loss of previous ability to walk. Typically, in order to have the most benefit from his procedure, candidates for selective dorsal rhizotomy have to demonstrate some form of independent ambulation prior to surgery and not have any damage to the basal ganglia in the brain. Following this procedure, a patient must be able to participate in an extensive rehabilitation program usually requiring therapy four to five times a week for three to six months to maximize functional return.

Orthopedic Surgery. Orthopedic intervention for spasticity is mainly used to correct the effects
of spasticity or balance the forces caused by the spastic muscles. Over time, spasticity may cause
muscle and soft tissues contracture or bony deformity. By releasing muscles that cause a deformity, a more favorable balance can be achieved. Orthopedic surgeons may functionally lengthen a short muscle by tenotomy, lengthening the tendon alone or in- tramuscular lengthening of the fascia around the muscle. They may also consider transferring a muscle to compen- sate for a weaker antagonist muscle. Bones may also be repositioned or reshaped to help maintain motion(15).

The care for individuals with spasticity may be a complex process. Although the neurologic condition is usually static, the changes to muscle, bone, tendon and ultimately function over time is a dynamic process that needs to be actively managed. Appropriate management of the patient with spasticity requires a multidisciplinary team of experienced physicians and allied health professionals who are able to work together.


Joshua Vova, M.D., FAAP, FAAPMR, is a pediatric physiatrist. He graduated from University of South Florida Medical School in 2000 and completed his residency in pediatric at Jacobi Medical Center in New York. Following his pediatric residency, he completed a residency in physical medicine and rehabilitation at the Rehabilitation Institute of Chicago and a fellowship in Pediatric Rehabilitation Medicine at The Children’s Hospital in Denver. Dr. Vova currently serves as a pediatric physiatrist at Children’s Healthcare of Atlanta and fellowship director for the Pediatric Rehabilitation Medicine fellowship through Emory University and Children’s Healthcare of Atlanta.



1.    JW, L., The control of muscle tone, reflexes, and movement: Robert Wartenberg Lecture. Neurology, 1980. 30: p. 1303-1313.

2.    Zafonte, R., L. Lombard, and E. Elovic, Antispasticity Medications. American Journal of Physical Medicine & Rehabilitation, 2004. 83(Supplement): p. S50-S58.

3.    Watanabe, T.K., Role of oral medications in spasticity management. PM R, 2009. 1(9): p. 839-41.

4.    Ronan, S. and J.T. Gold, Nonoperative management of spasticity in children. Childs Nerv Syst, 2007. 23(9): p. 943-56.

5.    Thibaut, A., et al., Spasticity after stroke: Physiology, assessment and treatment. Brain Inj, 2013. 27(10): p. 1093-105.

6.    Gormley, M.E., Jr., C.F. O’Brien, and S.A. Yablon, A clinical overview of treatment decisions in the management of spasticity. Muscle Nerve Suppl, 1997. 6: p. S14-20.

7.    Preissner, K.S., The effects of serial casting on spasticity: a literature review. Occup Ther Health Care, 2002. 14(2): p. 99-106.

8.    Lim, E.C., A.M. Quek, and R.C. Seet, Accurate targeting of botulinum toxin injections: how to and why. Parkinsonism Relat Disord, 2011. 17 Suppl 1: p. S34-9.

9. Gooch, J.L. and C.P. Patton, Combining botulinum toxin and phenol to manage spasticity in children. Archives of Physical Medicine and Rehabilitation, 2004. 85(7): p. 1121-1124.

10. Chin, T.Y., et al., Accuracy of intramuscular injection of botulinum
toxin A in juvenile cerebral palsy: a comparison between manual needle placement and placement guided by electrical stimulation. J Pediatr Orthop, 2005. 25(3): p. 286-91.

11.Akkaya, T., et al., Neurolytic phenol blockade of the obturator nerve for severe adductor spasticity. Acta Anaesthesiol Scand, 2010. 54(1): p. 79-85.

12. Krach, L.E., R.L. Kriel, and A.C. Nugent, Complex dosing schedules for continuous intrathecal baclofen infusion. Pediatr Neurol, 2007. 37(5): p. 354-9.

13. Zdolsek, H.A., et al., Intrathecal baclofen therapy: benefits and complications. J Intellect Dev Disabil, 2011. 36(3): p. 207-13.

14. Hurvitz, E.A., et al., Functional outcomes of childhood dorsal rhizotomy in adults and adolescents with cerebral palsy. J Neurosurg Pediatr, 2013. 11(4): p. 380-8.

15. Sussman, M.D. and M.D. Aiona, Treatment of spastic diplegia in patients with cerebral palsy. J Pediatr Orthop B, 2004. 13(2): p. S1-12.


Physicians Help Make Children Functional in Spite of Disability

Wednesday, October 30th, 2013

by Maurice G. Sholas, M.D., Ph.D.

From ATLANTA Medicine Vol. 84, No. 4

Many of us fell in love with our profession while watching famous TV Doctors. Serious portrayals, like those on “Grey’s Anatomy” or “ER”, bring to life the real drama of helping patients cope with life altering health issues. Comedic portrayals, like those on “Scrubs”, shine light on the ironic aspects of the patient-doctor relationship. No matter the approach, all remind the viewer that doctors help patients on their journey through life.

As medicine has advanced, physicians and surgeons have become better able to provide more advanced treatment options for a variety of children and adolescents with catastrophic diagnoses. As a result, previously terminal findings have become more chronic conditions. Similarly, patients previously considered a success to simply be alive have the opportunity to seek out a better quality of life.

That evolving reality lead to the creation of the specialty of Pediatric Rehabilitation Medicine — officially recognized by the American Board of Medical Specialties in 2005. Specialists in Pediatric Physical Medicine and Rehabilitation (PM&R), called Pediatric Physiatrists, are specially trained to diagnose, manage and treat acquired or congenital physical disabilities in children. Most commonly, this includes injuries and the sequela of diseases of the musculoskeletal and neuromuscular systems.

Pediatric physiatrists are tertiary care sub-specialists who generally practice out of hospitals, private clinics or rehabilitation centers. They offer comprehensive, non- surgical treatment programs that help address the needs of the whole patient from a context of maximizing function. This approach of maximizing function can be applied to the non-disabled population as well through sports medicine.

The crux of Physiatry is the promotion of teamwork to address the functional concerns of a patient in a manner that is appropriate to their family, community and life context. As such, physiatrists coordinate a team consisting of: nurses, physical therapists, occupational therapists, speech-language pathologists, psychologists, neuropsychologists, prosthetists, orthotists, child life specialists, social workers and case managers. Pediatric physiatrists can serve as a very useful referral for primary care pediatricians and other specialists who provide care to children with special healthcare needs who have congenital or acquire physical disabilities.

Examples of congenital diagnoses that are treated by Pediatric Physiatrists include: cerebral palsy, spina bifida, brachial plexus lesions, muscular dystrophy and torticollis. The goal of the physiatrist is to manage the consequences of the patient’s disability. Thus, if a patient’s condition causes them to have muscle spasticity, the physiatrist uses medications like baclofen, botulinum toxin injections or specialized permanent nerve blocks to ameliorate these symptoms and promote easier care and comfort or better functional independence.

Another opportunity for physiatry management comes in using technology to maximize function. Physiatrists are experts at matching children with appropriate communication devices, braces (orthoses), prosthetic devices, wheelchairs, mobility devices or durable medical equipment essential in addressing caregiver or patient needs unique to this vulnerable population. Pediatric physiatrists blend non-operative musculoskeletal medicine with applied neurology to optimize the life trajectory for children born with physical disabilities.

Acquired conditions that are treated by pediatric physiatrists include: traumatic brain injuries, encephalitis, spinal cord injuries, pediatric burns, strokes and limb deficiency. In addition, they treat children who are deconditioned after oncological diagnoses (cancer rehab), cardiac anomalies (cardiac rehab) and those following complex musculoskeletal surgery.

Once the trauma team or the primary treating physicians stabilize the patient, the physiatrist works in a coordinated manner to restore function and optimize independence in patients as varied as those with brain tumors and others post complex spine and limb surgery. What makes the pediatric physiatry input unique is that it incorporates evidence-based medical care with functional optimization via therapy. Ultimately, this manages the child’s discoordination, poor endurance, altered cognitive status and altered functional independence following life-threatening insults. Pediatric physiatrists are critical in assisting patients and families to redefine and restore their definition of normal following a physical impairment.

In addition to working with a team of nurses, therapists and para-medical professionals, pediatric physiatrists work with primary care doctors, neurologists, neurosurgeons, orthopedic surgeons, oncologists, rheumatologists and many other specialists. The patients of focus often are medically complex and require input across the spectrum of medical specialties – thus care coordination and “big picture” planning are of high value.

Two prime examples of physiatrist-led collaboration are pediatric cardiac rehabilitation and spasticity management. Cardiopulmonary rehabilitation involves optimizing function in those affected with heart or lung disease. Considerable efforts are made to manage a cardiac patients’ disease process under the direction of a cardiologist or cardiothoracic surgeon. Once that acute process is optimized, the physiatrist crafts a program that makes the child functional in spite of the limitation of their cardiopulmonary system – allowing them to rise from the proverbial couch and re-enter school, vocational interests and avocational activities.

Spasticity is a neurological finding resulting from damage to the central nervous system. Using medication, modalities, manual medicine and physical interventions, physiatrists participate in the care of children with these neuromuscular conditions to decrease this type of hypertonicity. Depending on the case, PM&R physicians may prescribe physical therapy to relax the muscles and improve strength.

For decades, adults who require rehabilitation have had access to Medical specialists who help them focus on function. Now that level of expertise is available to children and adolescents. Rehabilitation, the recovery of previously mastered skills, in addition to habilitation, the acquisition of new skills not previously mastered, are cornerstone concepts in pediatric physiatry.

In addition to understanding the disease process leading to disability, physiatrists appreciate the context under which interventions have to exist to be successful. These medical sub-specialists provide care in a collaborative manner that emphasizes practicality and teamwork. Practice models include inpatient and outpatient management as well as consultation.

Physiatrists can assist with studies that help identify a diagnosis, like when they perform electromyography or nerve conduction studies, but more often they focus on patient management for those children with the most complex diagnoses. Interventions can be medication optimization or procedural of coordination of care. Children with special healthcare needs are well-served by having a pediatric physiatrist among the specialists providing care for them.
For more information on physiatry and its subspecialty areas like pediatric rehabilitation medicine, go to The American Academy of Physical Medicine and Rehabilitation.

Maurice Sholas, M.D., Ph.D., is the Medical & Practice Director for Rehabilitation Services at Children’s Healthcare of Atlanta. He is one of 191 board-certified Pediatric Rehabilitation Medicine specialists in America. His professional focus is providing care to children with acquired or congenital physical disabilities. Dr. Sholas received an M.D. and Ph.D. from Harvard Medical School. He completed his residency training at the University of Texas HSC – San Antonio and fellowship training at the Rehabilitation Institute of Chicago. Dr. Sholas is active with Leadership Atlanta and the Medical Association of Atlanta.


Brain Tumor Specialist Erin Dunbar, M.D., Joins Piedmont Physicians Neuro-Oncology

Wednesday, October 30th, 2013

Erin M. Dunbar, M.D., a nationally renowned brain tumor specialist, has joined Piedmont Physicians Neuro-Oncology.

Dr. Dunbar, who is one of just a few hundred neuro-oncologists in the United States, will direct the medical neuro-oncology program and spearhead the clinical trial research program at the Piedmont Brain Tumor Center.

The National Cancer Institute estimates that 23,130 people will be diagnosed with brain and other nervous system cancers in 2013. Additionally, over 14,000 people will die from brain and spinal cord tumors.

Dr. Dunbar previously served as co-director of the Preston A. Wells, Jr. Center for Brain Tumor Therapy at the University of Florida.



Pediatrician Jose Rodriguez Recognized for Volunteer Work

Wednesday, October 30th, 2013

Jose Rodriguez, MD, MBA, FAAP, a pediatrician with WellStar Medical Group Kennestone Pediatric Associates, has been named Physician of the Year by the Georgia chapter of the American Academy of Pediatrics.

Dr. Rodriguez, a pediatrician for more than 20 years, is being recognized for his volunteer work with Ser Familia, a nonprofit founded in 2001 to help Latino families in the areas of family support and counseling, child abuse prevention, domestic violence prevention and crisis management.

Born and raised in Puerto Rico, Dr. Rodriguez completed his bachelor’s degree in science at the University of Puerto Rico, Rio Piedras Campus, and a medical degree from San Juan Bautista School of Medicine in San Juan, Puerto Rico. Dr. Rodriguez came to Georgia in 1981 to serve a residency in pediatrics at the Medical College of Medicine in Augusta. Since 1981, he has been practicing in Cobb County. In 1998, he received a master’s degree in Business Administration from Kennesaw State University. He is board certified in pediatrics.

Dr. Rodriguez holds two academic appointments in the pediatric departments of two medical schools. Since 2000, he has taught third and fourth year medical students as clinical professor at the Medical College of Georgia, and since 2005, he has taught third year medical students as adjunct associate clinical professor at Morehouse School of Medicine.

Dr. Rodriguez serves on the board of directors for the Georgia Chapter of the American Academy of Pediatrics as a District II Representative for Cobb County and Douglas County.


Consortium of Gynecologic Oncologists Participate in International Cooperative

Tuesday, October 29th, 2013

For more than five years, a unique consortium of gynecologic oncologists in Georgia have been participating in the Gynecologic Oncology Group (GOG), an international cooperative group that receives funding from the National Cancer Institute of the National Institutes for Health. The GOG studies gynecologic cancers through a menu of clinical trials. Developed and administered by Georgia CORE – the Center for Oncology, Research and Education – the Georgia working group is a unique statewide consortium recognized by NCI as a member of the GOG.

“Georgia affiliates in the GOG studies have exceeded the required participation goals by 200 percent,” said Sharad Ghamande, M.D., of Georgia Regents University and Principal Investigator of the Georgia CORE GOG. “And perhaps more importantly, one quarter of the patients who participated in the Georgia trials in the past three years are of racial and ethnic minorities – historically the groups least likely to receive the benefits of clinical cancer research.”

The GOG is administratively headquartered in Philadelphia, Pa. Approximately 45 individual clinical trials are active at any one time within GOG for patients with a variety of gynecologic malignancies, including cancers that arise from the ovaries, uterus, cervix, vagina, and vulva.

In addition to conducting trials, Georgia CORE GOG Investigators serve on several national committees and have co-authored papers.

Georgia CORE GOG Consortium affiliates include Central Georgia Gynecologic Oncology/The Medical Center of Central Georgia, Macon
; Emory University, Atlanta; 
Georgia Regents University, Augusta
; Columbus Regional Healthcare System/John B. Amos Cancer Center, Columbus;
 Memorial Health Medical Center, Savannah;
 Northeast Georgia Medical Center, Gainesville
; Northside Hospital, Atlanta
; Piedmont Healthcare, Atlanta; and 
Lewis Cancer & Research Pavilion at St. Joseph’s/Candler Health System, Savannah.



Lee Padove, M.D., Joins Northside Cardiology Practice

Tuesday, October 29th, 2013

Northside Hospital Cardiovascular Care has welcomed Lee Padove, M.D. to the full-service cardiology practice.  For more than 20 years, Dr. Padove has provided cardiovascular care in private practice in Atlanta and on the medical staff at Northside Hospital.

Board certified in cardiology, Dr. Padove received his Bachelor of Science degree from the University of Georgia, followed by his Doctorate of Medicine from the Medical College of Georgia.  He completed his internal medicine residency and cardiology fellowship at the Brooke Army Medical Center in Fort Sam Houston, Texas.  Dr. Padove’s special interests include cardiac evaluation and treatment during pregnancy, and he has been an invited lecturer at symposiums around the world.

Dr. Padove has been recognized by Super Doctors, Best Doctors, U.S. News & World Report “Top Doctors” and Atlanta Magazine “Top Doctors.”


Medical Association of Georgia’s 159th House of Delegates

Saturday, October 19th, 2013

October 19-20, 2013, Lake Lanier Islands Resort. For more information, visit MAG House of Delegates



Resources F T L Subscription Advertising About Us Past Issues Contact