St. Francis Medical Technologies has developed a minimally invasive surgical procedure for the treatment of lumbar spinal stenosis (LSS) that has already been used in Europe. The FDA approved the procedure this past Spring 2006. Spinal stenosis can be either congenital or acquired and is characterized by narrowing of the spinal canal or neural foramen resulting in neural compression. Symptoms of spinal stenosis can present as back pain, radiculopathy, gait abnormalities, neurogenic claudication, and bowel/bladder dysfunction. The spinal canal size varies between flexion and extension. Flexion increases and extension decreases the spinal canal size.
Degenerative disc disease is the most common cause for spinal stenosis and is the most common indication for lumbar spine surgery in the elderly. Decompressive surgery consisting of laminotomy, laminectomy and/or foraminotomy is the only option for symptomatic LSS if patients fail conservative treatment (Sept/Oct 2006 The Pain Journal). Unfortunately there are comorbidities associated with spine surgery including mechanical failure and a success rate of only 65% for good and excellent outcomes.
St. Francis Technologies has developed an innovative minimally invasive surgical device, the X-Stop®, for the treatment of spinal stenosis. The X-Stop is indicated for spinal stenosis when symptoms increase with extension and decrease with flexion. The X-Stop is a titanium spacer inserted under local anesthesia anterior to interspinous ligament over the lamina between the spinous processes at symptomatic segmental levels.
The device distracts the disc space and maintains it in a slightly flexed position that reduces extension at symptomatic level(s), while maintaining the dynamic structure of the spine.
The X-Stop has demonstrated a 59% one year success rate (comparable to traditional spine surgery), early mobility, reduced morbidity, and decreased recovery time compared to more invasive surgery. The procedure is non-destructive and completely reversible if more extensive surgery is required at a later time. The X-Stop is contraindicated in patients with severe osteoporosis.
Sunday, January 11, 2009
Monday, January 5, 2009
Percutaneous Radiofrequency – Treating Hepatic Tumors
The two most common malignant tumors of the liver are hepatocellular carcinoma (HCC) and colorectal carcinoma metastases (CCM) to the liver. The prognosis is poor with zero percent survival rate at five years without treatment. In general, systemic chemotherapy and/or radiation are not effective. Surgical resection is the only option for cure but only five to 15% of patients with HCC or CCM are eligible for resection. The success rate for those who are eligible for resection is compromised by post operative morbidity, cost, and only a slight improvement in the long term prognosis with a survival rate of approximately 20% at five years. Furthermore, these patients are not suitable for additional resections. Unfortunately, most patients die from recurrent tumors.
Radiofrequency ablation (RFA) of hepatic tumors can be performed by a percutaneous, laproscopic or open surgical approach. Inclusion criteria for RFA consist of preoperative imaging demonstrating fewer than five tumors with diameters less than five centimeters and no evidence of extrahepatic tumor. Exclusion criteria include patients who are eligible for surgical resection of tumors; tumors that are too close to vital structures such as the diaphragm, gallbladder and subcapsular tumors abutting against other visceral structures. Contraindications to performing RFA include excessive intrahepatic tumor load, untreatable extrahepatic tumor, cirrhosis, and active infection.
Percutaneous RFA of HCC has demonstrated a 90% necrosis rate for tumors less than three cm at six months, but one-third of these patients will develop recurrent tumors at 15 months. The rate of necrosis for HCC is 50 to 70% at six months for three to five centimeter tumors and only 25% for tumors greater than five centimeters. The success rate of RFA in CCM is not as good as in HCC with a necrosis rate ranging from 50 to 90%. Recurrent tumor develops in 70% of these patients at 12 months and 90% at 18 months.
Complications include post-operative bleeding and a flu-like syndrome post ablation that typically begins three to five days after the ablation and lasts up to five days. RFA of the liver is otherwise a safe procedure with an extremely low rate of major complications.
Radiofrequency ablation (RFA) of hepatic tumors can be performed by a percutaneous, laproscopic or open surgical approach. Inclusion criteria for RFA consist of preoperative imaging demonstrating fewer than five tumors with diameters less than five centimeters and no evidence of extrahepatic tumor. Exclusion criteria include patients who are eligible for surgical resection of tumors; tumors that are too close to vital structures such as the diaphragm, gallbladder and subcapsular tumors abutting against other visceral structures. Contraindications to performing RFA include excessive intrahepatic tumor load, untreatable extrahepatic tumor, cirrhosis, and active infection.
Percutaneous RFA of HCC has demonstrated a 90% necrosis rate for tumors less than three cm at six months, but one-third of these patients will develop recurrent tumors at 15 months. The rate of necrosis for HCC is 50 to 70% at six months for three to five centimeter tumors and only 25% for tumors greater than five centimeters. The success rate of RFA in CCM is not as good as in HCC with a necrosis rate ranging from 50 to 90%. Recurrent tumor develops in 70% of these patients at 12 months and 90% at 18 months.
Complications include post-operative bleeding and a flu-like syndrome post ablation that typically begins three to five days after the ablation and lasts up to five days. RFA of the liver is otherwise a safe procedure with an extremely low rate of major complications.
Thursday, January 1, 2009
Intradiscal Electrothermal Therapy (IDET) – Treating Discogenic LBP
Discogenic low back pain (DLBP) is responsible for at least 40% of chronic LBP. Radial or circumferential tears (IDD) in the outer third of the posterior annulus lead to nociceptor stimulation through inflammatory or mechanical means resulting in acute DLBP. Over time, subsequent nerve in-growth into the annular tears is correlated with the expression of substance P leading to chronic DLBP.
DLBP results from IDD that leads to nerve irritation within the disc. In contrast, a herniated disc leads to mechanical or chemical irritation of nerve roots within the spinal canal resulting in LBP and sciatica.
The symptoms of DLBP are LBP worse with axial loading (sitting, standing or lifting) and better with recumbency. The pain can be referred into the legs but not in a sciatic distribution. Exam findings include muscle spasms, painful range of motion, and painful palpation. The neurological exam and imaging studies are often unremarkable. Discography is the only reliable means of diagnosing DLBP.
The IDET procedure consists of placing a semi-rigid catheter within the posterior annular tear of the painful disc. The area is then heated from 65 to 90°C over 16.5 minutes. The IDET mechanism of action in reducing DLBP is unknown at this time.
Indications for the IDET procedure mandate a positive lumbar discogram. Contraindications include disc degeneration with >50% disc height loss and a previously operated disc. Potential complications include bleeding, infection, and nerve root injury.
DLBP results from IDD that leads to nerve irritation within the disc. In contrast, a herniated disc leads to mechanical or chemical irritation of nerve roots within the spinal canal resulting in LBP and sciatica.
The symptoms of DLBP are LBP worse with axial loading (sitting, standing or lifting) and better with recumbency. The pain can be referred into the legs but not in a sciatic distribution. Exam findings include muscle spasms, painful range of motion, and painful palpation. The neurological exam and imaging studies are often unremarkable. Discography is the only reliable means of diagnosing DLBP.
The IDET procedure consists of placing a semi-rigid catheter within the posterior annular tear of the painful disc. The area is then heated from 65 to 90°C over 16.5 minutes. The IDET mechanism of action in reducing DLBP is unknown at this time.
Indications for the IDET procedure mandate a positive lumbar discogram. Contraindications include disc degeneration with >50% disc height loss and a previously operated disc. Potential complications include bleeding, infection, and nerve root injury.
Monday, December 22, 2008
Temporal Mandibular Joint Syndrome – A Common Source of Jaw and Facial Pain
Temporal Mandibular Joint (TMJ) Syndrome presently affects 10 million Americans and afflicts women four times more often than men between 20 and 40 years of age. TMJ syndrome is divided into three categories involving the mastication muscles and the joint.
Treatment outcome is improved with early diagnosis. Some cases of TMJ syndrome are self-limiting but most progress to a chronic state especially those with coexisting ear symptoms.
Myofascial pain dysfunction (MPD) involves the mastication muscles and is considered the most common TMJ disorder. MPD is a stress related disorder with a centrally induced increase in mandibular muscle tension that results in muscle spasm, pain and dysfunction.
Internal Derangement (ID) refers to a mechanical dysfunction between the TMJ articular disc and the mandibular condyle, fossa and articular eminence. There is an organic problem with the joint. The mandibular muscle spasm is secondary to the mechanical joint dysfunction and is not the primary problem as seen in MPD.
Degenerative Joint Disease (DJD) describes the degeneration of the articular surfaces within the TMJ.
The primary symptoms of TMJ are dull jaw pain, increased pain with chewing, limited mouth opening, and jaw clicking or popping. Secondary symptoms include earache, headache, and neck pain. Examination findings demonstrate restricted mouth opening, facial muscle spasms, TMJ tenderness, TMJ clicking or popping, TMJ crepitus, and mandibular lateral deviation. Diagnostic evaluation includes x-rays, CT and/or MRI.
Conservative care consists of analgesics, muscle relaxants, moist heat, massage, and physical therapy. Interventional treatment includes intra-articular TMJ steroid injections, Botox injections of the temporalis muscle, and radiofrequency. TMJ joint arthroplasty is considered as a last result in appropriate candidates with refractory pain.
Treatment outcome is improved with early diagnosis. Some cases of TMJ syndrome are self-limiting but most progress to a chronic state especially those with coexisting ear symptoms.
Myofascial pain dysfunction (MPD) involves the mastication muscles and is considered the most common TMJ disorder. MPD is a stress related disorder with a centrally induced increase in mandibular muscle tension that results in muscle spasm, pain and dysfunction.
Internal Derangement (ID) refers to a mechanical dysfunction between the TMJ articular disc and the mandibular condyle, fossa and articular eminence. There is an organic problem with the joint. The mandibular muscle spasm is secondary to the mechanical joint dysfunction and is not the primary problem as seen in MPD.
Degenerative Joint Disease (DJD) describes the degeneration of the articular surfaces within the TMJ.
The primary symptoms of TMJ are dull jaw pain, increased pain with chewing, limited mouth opening, and jaw clicking or popping. Secondary symptoms include earache, headache, and neck pain. Examination findings demonstrate restricted mouth opening, facial muscle spasms, TMJ tenderness, TMJ clicking or popping, TMJ crepitus, and mandibular lateral deviation. Diagnostic evaluation includes x-rays, CT and/or MRI.
Conservative care consists of analgesics, muscle relaxants, moist heat, massage, and physical therapy. Interventional treatment includes intra-articular TMJ steroid injections, Botox injections of the temporalis muscle, and radiofrequency. TMJ joint arthroplasty is considered as a last result in appropriate candidates with refractory pain.
Monday, December 15, 2008
Herpes Zoster (Shingles) – A Painful and Disabling Disorder
Herpes Zoster (shingles) has a 10% to 20% lifetime incidence that increases with age. The incidence doubles with each decade after the age of 50 years. Shingles occurs from the reactivation of the varicella-zoster virus. The normal decrease in cell mediated immunity with age and diseases that affect cell mediated immunity (such as malignancy, HIV, and chronic corticosteroid use) are thought to be reasons for developing herpes zoster.
The varicella-zoster virus is a highly contagious DNA virus that enters the sensory dorsal root ganglion during the primary infection and remains dormant for decades. Virus reactivation occurs when there is a decrease in the virus specific cell mediated immunity. The reactivated virus travels down the sensory nerve leading to a rash and pain within the dermatomal distribution of the nerve.
A maculopapular rash evolves into vesicles with an erythmatous base. The vesicles eventually crust over in 7 to 10 days. Scars and pigment changes occur when the crusts fall off. Shingles pain is described as burning, stinging, and unrelenting. The T5 and T6 spinal nerves are the most commonly affected vertebral dermatomes and the ophthalmic division of the trigeminal nerve is the most commonly affected cranial nerve dermatome.
Post herpetic neuralgia (PHN) occurs in 20% of those with herpes zoster. Age is the most established risk factor for PHN with an incidence 15 times more often in those over age 50. Other risk factors include ophthalmic zoster, prodromal pain, and an immunocompromised state. Prodromal pain presents as hyperesthesias, paresthesias, burning dysethesias, or pruritis along the affected dermatome lasting one to two days and up to three weeks before the rash. PHN tends to be self-limited over time with 25% having pain at six months and five percent having pain at one year.
Shingles treatment is aimed at the acute viral infection, pain, and preventing post herpetic neuralgia. Oral antiviral agents (acyclovir, famciclovir, valacyclovir) decrease the duration and pain of the rash if used within the first 72 hours and can reduce the incidence of PHN. Oral prednisone has variable results for the acute viral infection, but reduces the acute pain when combined with acyclovir. Prednisone can diminish the onset of PHN and is often recommended in those over the age of 50 who are at a greater risk for PHN.
Treatment of the acute pain associated with Shingles includes the use of OTC medications, calamine lotion on vesicles, capsaicin cream for crusted lesions, opioids, prednisone, steroid injections of vesicles, epidurals and nerve root blocks. The same medications used for acute Shingles pain are used to treat PHN along with anticonvulsants and tricyclic antidepressants. Peripheral nerve stimulation is an effective last resort if other measures for pain control fail.
The varicella-zoster virus is a highly contagious DNA virus that enters the sensory dorsal root ganglion during the primary infection and remains dormant for decades. Virus reactivation occurs when there is a decrease in the virus specific cell mediated immunity. The reactivated virus travels down the sensory nerve leading to a rash and pain within the dermatomal distribution of the nerve.
A maculopapular rash evolves into vesicles with an erythmatous base. The vesicles eventually crust over in 7 to 10 days. Scars and pigment changes occur when the crusts fall off. Shingles pain is described as burning, stinging, and unrelenting. The T5 and T6 spinal nerves are the most commonly affected vertebral dermatomes and the ophthalmic division of the trigeminal nerve is the most commonly affected cranial nerve dermatome.
Post herpetic neuralgia (PHN) occurs in 20% of those with herpes zoster. Age is the most established risk factor for PHN with an incidence 15 times more often in those over age 50. Other risk factors include ophthalmic zoster, prodromal pain, and an immunocompromised state. Prodromal pain presents as hyperesthesias, paresthesias, burning dysethesias, or pruritis along the affected dermatome lasting one to two days and up to three weeks before the rash. PHN tends to be self-limited over time with 25% having pain at six months and five percent having pain at one year.
Shingles treatment is aimed at the acute viral infection, pain, and preventing post herpetic neuralgia. Oral antiviral agents (acyclovir, famciclovir, valacyclovir) decrease the duration and pain of the rash if used within the first 72 hours and can reduce the incidence of PHN. Oral prednisone has variable results for the acute viral infection, but reduces the acute pain when combined with acyclovir. Prednisone can diminish the onset of PHN and is often recommended in those over the age of 50 who are at a greater risk for PHN.
Treatment of the acute pain associated with Shingles includes the use of OTC medications, calamine lotion on vesicles, capsaicin cream for crusted lesions, opioids, prednisone, steroid injections of vesicles, epidurals and nerve root blocks. The same medications used for acute Shingles pain are used to treat PHN along with anticonvulsants and tricyclic antidepressants. Peripheral nerve stimulation is an effective last resort if other measures for pain control fail.
Monday, December 8, 2008
Trigeminal Neuralgia — A Common Cause of Facial Pain
Trigeminal neuralgia (TN), tic douloreaux, is a common painful condition of the face that usually affects one side of the face producing brief, severe, sharp, and electric pain.
Trigeminal neuralgia is defined by the International Headache Society as "intermittent attacks of facial or frontal pain that last a few seconds to less than two minutes without neurological deficits or any other causes of facial pain." The pain has at least four of the following five characteristics: 1) distribution along the trigeminal nerve; 2) sharp, superficial, sudden, stabbing, or burning pain; 3) severe pain intensity; 4) precipitation from trigger areas or daily activities; and 5) no symptoms between attacks.
The prevalence of TN is 100 per 100,000 with an incidence of five per 100,000 per year. TN is twice as common in women. The average age on onset is 50 years of age. There is a family history of TN in five percent of patients who have subsequently have a greater likelihood of bilateral involvement.
Many cases of TN that were originally though to be idiopathic without any identifiable lesion are due to vascular compression. Fifty percent of these patients who undergo a decompression of the trigeminal nerve are pain free for an average period of 15 years. Additional types of lesions are found in up to 15% of TN patients.
TN must be differentiated from intracranial tumors, nasopharyngeal tumors, post herpetic neuralgia, dental disorders, cluster headaches, and migraine headaches.
Although the natural course of TN is not known, TN is considered to be a chronic condition that lasts a lifetime. Some patients can have long periods of remission lasting months to years.
Treatment for TN includes oral medications and surgical intervention. Tegretol is the drug of choice in treating TN. Other anticonvulsants have also been used to treat TN. The most frequent surgical treatments are gamma knife tractotomy, radiofrequency gangliolysis, retrogasserian glycerol injection and micro-vascular decompression.
Trigeminal neuralgia is defined by the International Headache Society as "intermittent attacks of facial or frontal pain that last a few seconds to less than two minutes without neurological deficits or any other causes of facial pain." The pain has at least four of the following five characteristics: 1) distribution along the trigeminal nerve; 2) sharp, superficial, sudden, stabbing, or burning pain; 3) severe pain intensity; 4) precipitation from trigger areas or daily activities; and 5) no symptoms between attacks.
The prevalence of TN is 100 per 100,000 with an incidence of five per 100,000 per year. TN is twice as common in women. The average age on onset is 50 years of age. There is a family history of TN in five percent of patients who have subsequently have a greater likelihood of bilateral involvement.
Many cases of TN that were originally though to be idiopathic without any identifiable lesion are due to vascular compression. Fifty percent of these patients who undergo a decompression of the trigeminal nerve are pain free for an average period of 15 years. Additional types of lesions are found in up to 15% of TN patients.
TN must be differentiated from intracranial tumors, nasopharyngeal tumors, post herpetic neuralgia, dental disorders, cluster headaches, and migraine headaches.
Although the natural course of TN is not known, TN is considered to be a chronic condition that lasts a lifetime. Some patients can have long periods of remission lasting months to years.
Treatment for TN includes oral medications and surgical intervention. Tegretol is the drug of choice in treating TN. Other anticonvulsants have also been used to treat TN. The most frequent surgical treatments are gamma knife tractotomy, radiofrequency gangliolysis, retrogasserian glycerol injection and micro-vascular decompression.
Monday, December 1, 2008
Interstitial Cystitis — An Uncommon But Incapacitating Condition
Interstitial cystitis (IC), also referred to as painful bladder syndrome (PBS), is a chronic inflammatory condition of the bladder wall of unknown etiology. The prevailing opinion is that IC is a constellation of signs and symptoms arising from bladder inflammation that is aggravated by infectious, chemical, mechanical, allergic, autoimmune, neurogenic, and other factors. Some believe that a defect in the epithelial barrier, glycosaminoglycan (GAG) layer, of the bladder is a part of the pathogenesis of interstitial cystitis. IC is not psychosomatic and is not caused by stress.
Although IC can strike anyone of any age, race or gender, women are most commonly afflicted by IC. There are more than 700,000 cases of IC in the United States.
IC has been associated with other chronic conditions, such as vulvar vestibulitis, irritable bowel syndrome, and fibromyalgia.
IC produces symptoms like a urinary tract infection (UTI), but is not caused by a bacterial infection. A UTI, unlike IC, can be successfully treated with antibiotics and a UTI should be considered as a cause for an exacerbation of IC symptoms.
The most common symptoms of IC are urinary frequency, urgency and pain. Frequency can be the first symptom of IC in early or mild cases. The frequency of urination can be astonishing and disabling in severe cases up to 60 times in a 24-hour period. Urgency can be seen with pain, pressure and/or spasms. Pain is often located in the pelvis, bladder, urethral, or vaginal areas. Pain is commonly associated with sexual intercourse. Men can experience genital and/or perineal pain as well as painful ejaculation. Some patients can complain of muscle and joint pain. IC is not excluded in the absence of night time urination or lack of pain.
The first step in diagnosing IC is ruling out other disorders that can mimic IC. Urine cultures can detect the presence or absence of a UTI. Other disorders to exclude include bladder cancer, bladder TB, STDs, vaginal infections, endometriosis, radiation cystitis, spinal cord/CNS conditions, and rheumatological diseases.
IC is diagnosed with the use of cystoscopy and hydrodistention of the bladder to identify pinpoint hemorrhages (glomerulations) in the bladder wall. These findings are characteristic of IC and are found in 90% of IC patients. Ulcers on the bladder wall are present in 5 to 10% of IC patients.
There are a variety of treatment options for the IC patient including diet, nutritional supplements, oral medications, physical therapy, bladder instillation techniques and surgery. Surgical options include laser treatment of bladder ulcers; sacral nerve root stimulation for treatment of bladder urgency and frequency; and only as a last resort internal pouch construction, urinary diversion or bladder augmentation. Urethral dilatation and urethrotomy are not surgical treatment options for IC.
Although IC can strike anyone of any age, race or gender, women are most commonly afflicted by IC. There are more than 700,000 cases of IC in the United States.
IC has been associated with other chronic conditions, such as vulvar vestibulitis, irritable bowel syndrome, and fibromyalgia.
IC produces symptoms like a urinary tract infection (UTI), but is not caused by a bacterial infection. A UTI, unlike IC, can be successfully treated with antibiotics and a UTI should be considered as a cause for an exacerbation of IC symptoms.
The most common symptoms of IC are urinary frequency, urgency and pain. Frequency can be the first symptom of IC in early or mild cases. The frequency of urination can be astonishing and disabling in severe cases up to 60 times in a 24-hour period. Urgency can be seen with pain, pressure and/or spasms. Pain is often located in the pelvis, bladder, urethral, or vaginal areas. Pain is commonly associated with sexual intercourse. Men can experience genital and/or perineal pain as well as painful ejaculation. Some patients can complain of muscle and joint pain. IC is not excluded in the absence of night time urination or lack of pain.
The first step in diagnosing IC is ruling out other disorders that can mimic IC. Urine cultures can detect the presence or absence of a UTI. Other disorders to exclude include bladder cancer, bladder TB, STDs, vaginal infections, endometriosis, radiation cystitis, spinal cord/CNS conditions, and rheumatological diseases.
IC is diagnosed with the use of cystoscopy and hydrodistention of the bladder to identify pinpoint hemorrhages (glomerulations) in the bladder wall. These findings are characteristic of IC and are found in 90% of IC patients. Ulcers on the bladder wall are present in 5 to 10% of IC patients.
There are a variety of treatment options for the IC patient including diet, nutritional supplements, oral medications, physical therapy, bladder instillation techniques and surgery. Surgical options include laser treatment of bladder ulcers; sacral nerve root stimulation for treatment of bladder urgency and frequency; and only as a last resort internal pouch construction, urinary diversion or bladder augmentation. Urethral dilatation and urethrotomy are not surgical treatment options for IC.
Subscribe to:
Posts (Atom)
