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Douglas "Kit" Fox, MD, Neurosurgeon, Executive Medical Director
Monday, March 15, 2010
Trigeminal neuralgia (TN), also known as tic doloureux, is a paroxysmal lancinating pain that occurs in one or more of the distributions of the trigeminal nerve. The pain often occurs with sensory stimulation to the face or teeth, with patients being unable to eat or have anything touch their face. Spontaneous remission is common, with patient often having prolonged periods where they are symptom-free. This occurs in the general population in 4/100000 people but in those with multiple sclerosis have an incidence of 2/100. Vascular compression from an artery at the root entry zone, tumor involvement, and development of a plaque can cause trigeminal neuralgia, which is likely an ephaptic transmission in the nerve from demyelinated pain fibers. Of note, there is no correlation of TN with herpes zoster infection, as the pain with herpes zoster is constant and not paroxysmal.
Once determined to be the cause of a patient’s pain, multiple therapies are available. Medical therapy is usually with carbamazepine, baclofen, and/or gabapentin. Nearly 70% of patients will have complete or tolerable relief with medications. Surgical options include
nerve blocks or ablations, percutaneous rhizotomy with radiofrequency or glycerol, microvascular decompression (MVD), nerve sectioning, and stereotactic radiosurgery. MVD is the most durable treatment providing sustained relief at ten years in 70% of patients treated.
The incidence of facial anesthesia is reduced compared to percutaneous rhizotomy. This does require surgery, however, and the inherent risks that go along with the procedure including CSF leak and aseptic meningitis. Patients with multiple sclerosis that have a
plaque at the dorsal root entry zone will respond better to steretactic radiosurgery or percutaneous rhizotomy.
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Michael Hummer, MD, Neurologist
Tuesday, February 16, 2010
Chorea is a classical neurological illness, the name of which derives from both Latin and Greek referring to dance or choral dance. Chorea has been described since the Middle Ages and describes a syndrome of brief, rapid, abrupt, involuntary movements coming from random muscle contractions. The pattern of movement may at times give the impression that the patient is restless or fidgety. Chorea is an uncommon but nevertheless very interesting neurological condition. In the Middle Ages, the most common form of chorea was most likely Sydenham’s chorea, which is a postinfectious chorea related to side effects from rheumatic fever and antibodies in the bloodstream resulting from beta hemolytic group Streptococcus. The frequency of this disorder has declined continually over the years and it is very uncommon at this time.
Chorea can be caused by multiple conditions, the most important of which from a neurobiological perspective is Huntington disease or Huntington’s chorea. Huntington’s chorea is a slowly progressive, familial, neurogenetic disease that causes disorder of muscle control, emotional control, cognitive ability, and involuntary movements. Huntington disease was first well described by Dr. George Huntington when he concisely reported affected families in New York state in a paper "On Chorea and Choreiform Affectations" published in 1894. Chorea can also be caused by stroke, lupus erythematosus, or a variety of other less common genetic, infectious, and drug related causes.
Huntington disease is, arguably, one of the most important causes of chorea from neurobiological, social, and economic standpoints. Huntington disease is a genetic disorder of an autosomal dominant type which basically means that there is a 50% chance of inheriting the gene from an affected parent and, therefore, a 50% chance of inheriting the condition. These genes produce a protein called huntingtin which, with an abnormal huntingtin gene, is excessively produced and produces progressive neurodegeneration widely throughout the brain, but in particular in deep structures called the corpus striatum. Absence of the normal huntingtin gene causes embryonic death in mice and it seems that the normal huntingtin gene supports the normal health of nerve cells in the brain. It is felt that the excessive production of huntingtin gene produces its abnormal effects by a gain in function rather than a loss in function.
Prevalence of affected individuals in the United States is approximately 1 in 10,000 and with a resultant approximately 30,000 people affected. Since it is an autosomal dominant disorder, both sexes are equally predisposed to this disease and the disease is present worldwide. There is some prevalence correlated with European ancestry and Huntington disease is rare in Japan and China. There are no proven ways to prevent the onset or progression of Huntington disease. The diagnosis can be made on the basis of clinical presentation, adequate family history, physical findings, and genetic testing. Prognosis is, for a slowly progressive course, over 10 to 25 years. Emotional symptoms such as depression tend to occur in the early to middle stages of the disease with sleep disruption and motor decline in the middle to late stages of the illness.
Various medications are available to treat symptoms in chorea and a new medication has been approved by the FDA for treatment of the muscle movements themselves. Other treatment is available for psychiatric symptoms. Luckily, Huntington’s chorea is a very uncommon condition, but this condition is being actively pursued with scientific investigations using electronic and genetic testing.
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Sara Austin, MD, Neurologist
Friday, January 08, 2010
Of the 3 nerves going to the forearm and hand that make the hand move, the ulnar nerve is arguably the most important as it provides all of the fine finger control, and much of the thumb movement. This nerve supplies the sensation to the 4th and 5th fingers, both the top and palm surface of the hand, and also the sensation of the hand just below the 5 finger.
The most common symptoms associated with a damaged ulnar nerve is numbness on the 5th finger side of the hand, aching in the hand, a feeling of coldness of the 4th and 5th fingers and possibly finger weakness. If the nerve damage is severe, the back of the hand will have a “hollowed out” appearance between the thumb and index finger because of muscle atrophy. Very severe ulnar nerve damage would cause the hand to look flat with the 4th and 5th fingers curled down.
The most common injury associated with the ulnar nerve is when the nerve is compressed as it travels around the elbow, either by direct pressure or prolonged positioning of the elbow joint at a 90 degree angle. Cellphone use is a common cause of ulnar nerve problems, as is sitting for long periods of time with the elbows on a hard surface.
Less commonly, the ulnar nerve can be compressed at the wrist, in which case the hand will be very weak but without the associated numbness that occurs with compression at the elbow.
Usually conservative treatment is the option of choice, but in cases of severe injury, a surgical consultation may be indicated. An electromyography (EMG) is a diagnostic for evaluating and recording the activation signal of muscles and is the preferred method of properly assessing an ulnar nerve injury, which can be facilitated by an EMG Board Certified neurologist.
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Juan Latorre, MD, Physical Medicine & Rehabilitation
Thursday, December 24, 2009
With approximately 12,000 new cases of spinal cord injury (SCI) each year with roughly 259,000 persons living with a traumatic SCI in the US, rehabilitation treatment plans must be individualized based on other factors such as age, co-morbidities, body habitus and level of motivation. It is also imperative to assess and manage the various affected systems. Muscle paralysis is often the most recognized sequela arising from SCI but other common complications include neuropathic pain, spasticity, heterotropic ossification, orthostatic hypotension, autonomic dysreflexia, DVT, CAD, atelectasis, pressure ulcers, depression, neurogenic bladder and bowel dysfunction, and in males neurogenic impotence and infertility.
The multisystem involvement of SCI makes the rehabilitation of these patient one that requires a comprehensive and multidisciplinary team approach, aimed at maximizing not only functional outcomes but also neurological recovery. Whatever the future in SCI holds we now know that people with SCI can live a happy and fulfilling life within the constrains of their impairments. With a collaborative effort of specialty physicians and a comprehensive rehabilitation program, the SCI patient stands to gain a more favorable outcome for achieving optimal clinical goals.
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Anant Patel, MD, Neurosurgeon
Wednesday, October 21, 2009
Movement disorder is a group of neurodegenerative diseases that primarily affects the motor and movement processes. The most common disorders include Parkinson’s disease (PD), Essential tremor (ET) and Dystonia.
Medications can be effective in the early treatment of these movement disorders. However, with the progression of disease, medications alone become ineffective. In PD, long-term management is often complicated with development of motor fluctuation and dyskinesia (involuntary dance like movement). In theses patient dyskinesias can be even more disabling then PD symptoms. Approximately 50 % of these patients will develop motor fluctuation and dyskinesia after 5 years of treatment with medication. Furthermore, only 50 % of tremor may respond to medication.
Surgical treatment for PD and ET has been around since the 1950’s. Early surgical intervention involved ablation of specific basal ganglia nuclei. However, lesioning became less effective with progression of the disease and bilateral lesions were often associated with severe complication involving speech, balance and walking. With further research, it was found that stimulation of these nuclei simulates the effects of a lesion without permanent destruction of tissue. In addition, the process is reversible and more importantly the stimulation is adjustable as the disease progresses. Therefore, Deep Brain Stimulation (DBS) has become the surgical treatment of choice for movement disorders.
DBS surgery is preformed in several stages using either the Frame or Frameless approach. The frameless approach uses infrared optics to achieve submillimeter accuracy needed in placement of the leads. The small stereotaxic frameless frame mounts on the skull over a small burr hole opening. This allows patients complete freedom to move their head and body on the operating table and thereby making it a comfortable experience. The DBS electrode is stereotaxically placed into the target nuclei. The patients are awake during this part of the surgery and intraoperative testing is preformed with stimulation of the electrode to ensure excellent response without any adverse side effects. The final stage of the procedure involves connection of the electrode leads to the implantable pulse generator (IPG), which is placed under the skin of the chest or abdomen. The IPG can be programmed to deliver electric stimulation to achieve desired results.
DBS is certainly not a cure for these neurodegenerative disorders by any means. However, it certainly gives us an incredible tool to modulate neuronal activity and thereby preserving function and quality of life for many of these patients with disabling symptoms.
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Bryan Atkinson, MD, Neurologist
Monday, October 05, 2009
Peripheral neuropathy is a common neurological condition. Neuropathy means "pathology of nerves" or "something wrong with the nerves" and peripheral neuropathy most often refers to symptoms of numbness or pain in the toes and feet or in the hands. Diabetes, including early or pre-diabetes, is the most common cause of peripheral neuropathy in the U.S. but many other conditions are associated with the diagnosis.
People with immunological disease such as Lupus may develop a peripheral neuropathy. Neuropathy can occur due to medications such as Chemotherapy or to toxicity from chronic alcohol use. Nutritional deficiencies, such as B12 deficiency, can cause neuropathy and infections such as AIDS or Lyme disease can injure the peripheral nerves. A genetic abnormality or Charcot-Marie-Tooth disease is at times identified as the cause. In over 30% of cases a specific cause of neuropathy cannot be identified and in these cases the neuropathy does not typically lead to any severe impairment.
The evaluation of symptoms suggestive of peripheral neuropathy includes laboratory testing for associated medical conditions, such as the conditions reviewed above, along with the direct evaluation of the peripheral nerves and muscles with NCS/EMG testing. Treatment depends on the underlying medical diagnosis with careful management of underlying conditions such as diabetes to help prevent further progression of the neuropathy. Medications such as elavil, neurontin, or lyrica may be used to help relieve the pain and burning that may be present. Ankle or wrist braces are at times needed for patients with weakness, and self-inspection of the feet for cuts or injuries is important in patients with significant sensory loss.
Peripheral neuropathy is common neurological condition and the physicians of the NeuroTexas Institute are able to provide expert evaluation and management of this often treatable diagnosis.
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Bhuvana Mandalapu, MD, Neurologist
Friday, October 02, 2009
No one over the age of 50, not even a lifelong athlete in seemingly excellent health, is free from the risk of stroke. With people living longer and the modern era of pre-made and pre-packaged foods, the rate of strokes has increased. Over the last several decades, stroke prevention measures have not changed much, but more awareness about stroke and its devastating nature are getting wider publicity.
The most important part of stroke prevention is what is known as primary prevention. Other than genetically predisposing components (family genetics), the way we eat, live and care for our bodies are the primary ways we can decrease the risks for stroke. Other than regular check-ups with a primary care physician, the people who may be most important in stroke prevention are parents – and how they supervise what their children eat, help develop dietary habits, choose active daily lifestyles and make a conscious effort to keep the body and mind healthy.
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Amy Pope, RN, MSN, FNP
Thursday, September 24, 2009
Clinical pathways are interdisciplinary plans of care that outline the sequencing and timing of therapeutic interventions and expected patient outcomes as derived from available evidence and current best practices. They are comprehensive, integrated clinical process tools, employed to optimize patient care and to help ensure positive patient outcomes. The implementation process generally requires that they be continuously evaluated and improved upon in real time.
Pathways are designed to provide benefits to patient care by increasing patient awareness of their condition and recovery timeframe with streamlined interventions from multiple disciplines throughout their stay. This decreases the amount of time a patient has to stay in the hospital.
Caregivers also derive benefits from pathways because of encouraged interdisciplinary collaboration and communication. A clearly written set of goals reduces variability in practice, while providing ongoing provider education and practice evaluation.
In a time when national accreditation and evidence-based quality standards have become key to both a provider’s licensure and an institution’s viability, clinical pathways help to show how hospitals are meeting these standards. By optimizing resource utilization at correct times, pathways make the most of clinical resources at hand.
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David Morledge, MD, Neurologist
Thursday, September 17, 2009
Parkinson's disease, first described by James Parkinson in 1817, is a debilitating, neurodegenerative disease that presents late in life, manifested by slowness of movement, rigidity, and resting tremor. The diagnosis of Parkinson's disease is based on clinical findings; there are no reliable biologic markers or radiologic features to confirm the diagnosis.
An estimated 1 million persons in the United States suffer from PD, and there are a reported 60,000 new cases each year. Unlike most neurological disorders, the disease is more prevalent in males compared to females. Ninety-two percent of Americans are Caucasian, with only 3% being African American and 3 % being Hispanic.
The motor complications in Parkinson's disease occur because of degeneration of dopaminergic neurons in the substantia nigra, leading to loss of dopamine and cell death. Loss of greater than 60 % of normal dopaminergic innervation leads to the appearance of Parkinson's symptoms such as rigidity, bradykinesia, and tremor.
We don't know what causes Parkinson's disease, however environmental causative factors mentioned in the medical literature include exposure to pesticides, rural living, and drinking well water. Although it is more common in certain families, Parkinson's disease is not considered a genetic disease that follows usual inheritance patterns.
New research through postmortem studies has shown us that changes in the brain occur 3 to 5 years before the motor symptoms develop. These motor symptoms can cause sleep disorders, loss of smell, and bowel motility problems. Our focus is on diagnosing early and starting treatment, before the disease starts affecting mobility.
Neurologists who specialize in the treatment of Parkinson's disease now rely on a step-care approach with regard to what medications to recommend. We no longer recommend starting on carbidopa/levodopa early in the course of the disease. Once symptoms develop and start affecting the patient's quality of life, we tend to use MAO-b inhibitors and dopamine agonists before prescribing carbidopa/levodopa.
When medications stop working due to disease progression, deep brain stimulator surgery is a viable treatment option for certain patients. This form of surgery is performed by highly trained neurosurgeons who specialize in stereotactic surgery. The patient is then followed by a neurologist after the surgery for programming of the deep brain stimulator. This surgery is performed frequently at NeuroTexas Institute at St. David's Medical Center.
Medications and surgery alone are not the answer in optimizing treatment for PD. A regular exercise program, along with a balanced diet should also be followed. Communication with your physician is crucial in helping you understand more about the disease process and improving your quality of life.
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Mark Burnett, MD, Neurosurgeon
Friday, August 28, 2009
This week, the death of Senator Edward Kennedy again puts the spotlight on the struggle for victory over brain cancer. Fifteen months ago, Senator Kennedy was diagnosed with glioblastoma multiforme, the most common and most aggressive primary malignant brain tumor. The tumor was located near the area of the brain responsible for speech and he suffered several seizures due to the tumor.
Treatment of tumors such as his is determined by a multidisciplinary team of doctors including neurosurgeons, medical oncologists, and radiation oncologists. If the tumor size and location make complete or near complete removal possible, surgery is generally recommended as the initial treatment. If the tumor is located in a region of the brain that houses a function that is critical, such as speech, or is so large that it passes through several brain regions, surgery may not be recommended. At times, these tumors arise near, but not through, delicate areas of the brain and the decision is made to do surgery with the patient awake rather than asleep so that functions such as speech and movement can be observed during surgery in real time. Awake surgery is commonplace now in most neurosurgical centers.
Complete surgical removal of a glioblastoma multiforme is not felt to be possible since the tumor spreads through the brain like a brush fire. When surgeons talk about their goal of removing all of the tumor, they are referring to all of the tumor that is seen on the MRI. While this is the ultimate goal of surgery, we know from studies that microscopic “fingers” of tumor extend out from these tumors and that tumor cells can be found several inches away from the area of tumor seen on MRI (in brain areas which look normal and tumor-free on the scan). Therefore, treatment of glioblastoma requires additional treatment after surgery.
The mainstay of treatment after surgery at most centers involves chemotherapy and radiation treatment. While there continue to be many clinical trials of new therapies, the standard chemotherapy treatment involves administration of temozolamide (Temodar) in addition to radiation. More recently, addition of a new medication called Avastin has been added to the common treatment pathway.
We do not yet have a complete understanding of the genetics of these tumors. In rare cases, glioblastomas appear as part of familial diseases. Individual cases arise as a completely new tumor (as in Senator Kennedy’s case) or can develop when a less aggressive glial brain tumor transforms into glioblastoma. Many studies have looked at environmental factors that could be associated with development of glioblastoma and none have been solidly linked to the tumor except exposure to high-dose ionizing radiation.
When these tumors progress despite treatment, they tend to do so just next to the area where they first appeared. In some cases, additional surgery is considered when tumors grow back depending upon the health of the patient and long-term treatment plan of the oncological team. The unusual truth about surgery on the brain is that there is no such thing as an “inoperable tumor” in the traditional sense of the term. Neurosurgeons can work in all areas of the brain, but removing tumors from some areas comes with too high of a cost in terms of functional loss. The real decision that neurosurgeons must make with each case is whether a patient’s quality of life will be too severely impacted by surgery to make it worthwhile, even if it could prolong survival.
Despite all of the technological advances we now have, overall survival for patients with glioblastoma has not been improved as much as we would like. Without any treatment, patients have a life expectancy measured in weeks. When surgery can safely remove all, or nearly all, of the tumor seen on MRI and patients undergo chemotherapy and radiation, the median survival extends to about 14 months (as with Senator Kennedy). The overall survival in patients receiving standard treatment is about 25% at the 2-year point from diagnosis.
While we have not won the war on glioblastoma, we have made surgery safer and less invasive and radiation treatments and chemotherapy less difficult for patients to endure. As new therapies are developed, we are going to slowly chip away at this devastating disease. I believe that one piece of good news for patients and families is that cutting edge cancer care for these tumors can be done at most centers. It used to be the case that patients needed to travel across the country to have access to the latest chemotherapy medications and treatments after surgery. The added stress of having doctors in different cities and constantly traveling could make care more disjointed and become an added burden for patients. Now, for instance, the same care plan that was carried out for Senator Kennedy is carried out each day in hospitals in every city across the country.
Our thoughts are with the Kennedy family this week, as well as all of those patients struggling with this disease.
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