Al-Haq Homoeopathic Clinic is managed by a team of 05 homeopathic doctors, including three homoeopathic Lady Doctors, especially for the female patients so that female patients can discuss their problems in courtesy and secrecy as well.
Homoeopathic Doctor Muhammad Mansoor-ul-Haq is the senior member of the whole team. In addition to treating the visiting patients, he provides online consultation to the far flong and abroad patients. He has been deeply associated with homeopathy since 1988, serving regularly since 1992. Since then, he has successfully treated a large number of acute, chronic and complicated cases of varying natures, at the clinic as well as through Internet. He is providing online consultation since 2000. His expertise especially in Diabeties and Non Healing Ulcers. Presently his timings are :
ON TUESDAY and THURSDAY (1830 to 2100 hrs) (NORMAL PATIENTS)
ON SATURDAY (1100 to 1400 and 1830 to 2100 hrs) (FOR DIABETIC & CHRONIC CASES)
Homoeopathic Doctor Muhammad Ashfaq
Timings are:
ON MONDAY , WEDNESDAY and FRIDAY (1830 to 2100 hrs)
Homeopathic Lady Doctor Aalia Mansoor is the senior member of homoeopathic Lady Doctors. She has an acumen knowledge of Homoeopathy. Her expertise especially in Female Diseases. She has successfully treated a large number of acute, chronic and complicated cases of different natures.
Presently Her timings are
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Amina NAsir
Timings are:
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Shazia
Timings are:
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Isma Riaz Shah
Timings are:
N SATURDAY to FRIDAY (1100 to 1400 hrs and 1830 to 2100 hrs)
Thursday, December 9, 2010
DIABETIC ULCERS / NON HEALING ULCERS
Non-Healing Wound / Ulcers
Diagnosis/Definition
Chronic Wound: Any non-healing wound and/or ulcer that has been present for 3-4 weeks duration and has not responded to conventional therapies.
Complex Wound: Wound in an area that is difficult to perform wound care, unusual wounds of unknown etiology or wounds that require advanced wound care treatment modalities for example the Wound VAC.
Initial Diagnosis and Management
Pressure Ulcers: Management involves assessment of systems, wound assessment and management, off loading with a specialty bed and evaluation by a plastic surgeon for Stage III or IV ulcers
Stage III - full thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend to, but not through, fascia.
Stage IV - full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (tendon, joint capsule).
Non-Healing Surgical Wounds: Wounds that are taking longer to heal because of underlying problems such as diabetes, poor nutritional status, immune compromised, or infection. Any surgical wound of 3-4 week duration that is not responding to conventional therapies. Management includes assessment of systems, wound management, and evaluation of a general surgeon.
Lower Extremity Ulcerations: Any non-healing ulcer of a lower extremity that has been present for 3-4 week duration and has not responded to conventional therapies. The wounds may be arterial, venous, mixed ulcers or pressure ulcers in diabetic patients.
ARTERIAL ULCER - caused by ischemia; related to the presence of arterial occlusive disease; generally present on the foot, typically the distal appendages; very painful; onset can be precipitated by trauma. Management involves assessment of blood flow to the extremity, wound management, and evaluation by a vascular surgeon.
VENOUS STASIS ULCER - result of edema and impaired venous return; loss of epidermis and various levels of dermis and subcutaneous tissue occurring on the medial or lateral aspect of the distal 1/3 of the lower extremity. Often found in combination with an edematous and indurated lower extremity. Management involves assessment of venous system with a venous duplex scan, wound management, compression stockings and/or wraps, and evaluation by a vascular surgeon. If pedal pulses are not palpable, an evaluation of the arterial system should be performed prior to initiating compressive therapy. A dermatologist consult may be obtained if chronic dermatitis is present.
MIXED VESSSEL (ARTERIAL AND VENOUS ULCER) - presence of arterial insufficiency and venous disease. Typically, ulcers are found on the lower extremity including the foot. Management includes assessment of arterial and venous blood flow to the lower extremity, wound management, and evaluation by a vascular surgeon.
All patients should be encouraged to decrease their risk factors (e.g., smoking, etc.) and to manage co-existing conditions such as diabetes.
DIABETIC NEUROPATHIC FOOT ULCERS – generally occur in diabetic patients with significant sensory neuropathy with unrecognized repetitive trauma. Management includes stopping the trauma with special shoes (off loading), assessment of arterial blood supply and wound care. Patients should be referred to the Limb Preservation Service.
MISCELLANEOUS EXTREMITY WOUND OR ULCERS - All other ulcerations assessed individually and treated according to the underlying etiology.
Neurogenic ulcers, also known as diabetic ulcers, are ulcers that occur most commonly on the bottom of the foot. People with diabetes are predisposed to peripheral neuropathy, which involves a decreased or total lack of sensation in the feet. Feet are naturally stressed from walking, and someone who has decreased sensation will not necessarily feel that they have an area of skin breakdown occurring. Coupled with this lack or absence of sensation is a decrease in circulation to the feet as well. Wounds that do not get proper blood flow are not only slower to heal but also at an increased risk for infection. A small cut, scrape, or irritated area in a diabetic can turn into an ulcer for these reasons. It is common for these types of ulcers to keep coming back in diabetics.
Diagnosis/Definition
Chronic Wound: Any non-healing wound and/or ulcer that has been present for 3-4 weeks duration and has not responded to conventional therapies.
Complex Wound: Wound in an area that is difficult to perform wound care, unusual wounds of unknown etiology or wounds that require advanced wound care treatment modalities for example the Wound VAC.
Initial Diagnosis and Management
Pressure Ulcers: Management involves assessment of systems, wound assessment and management, off loading with a specialty bed and evaluation by a plastic surgeon for Stage III or IV ulcers
Stage III - full thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend to, but not through, fascia.
Stage IV - full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (tendon, joint capsule).
Non-Healing Surgical Wounds: Wounds that are taking longer to heal because of underlying problems such as diabetes, poor nutritional status, immune compromised, or infection. Any surgical wound of 3-4 week duration that is not responding to conventional therapies. Management includes assessment of systems, wound management, and evaluation of a general surgeon.
Lower Extremity Ulcerations: Any non-healing ulcer of a lower extremity that has been present for 3-4 week duration and has not responded to conventional therapies. The wounds may be arterial, venous, mixed ulcers or pressure ulcers in diabetic patients.
ARTERIAL ULCER - caused by ischemia; related to the presence of arterial occlusive disease; generally present on the foot, typically the distal appendages; very painful; onset can be precipitated by trauma. Management involves assessment of blood flow to the extremity, wound management, and evaluation by a vascular surgeon.
VENOUS STASIS ULCER - result of edema and impaired venous return; loss of epidermis and various levels of dermis and subcutaneous tissue occurring on the medial or lateral aspect of the distal 1/3 of the lower extremity. Often found in combination with an edematous and indurated lower extremity. Management involves assessment of venous system with a venous duplex scan, wound management, compression stockings and/or wraps, and evaluation by a vascular surgeon. If pedal pulses are not palpable, an evaluation of the arterial system should be performed prior to initiating compressive therapy. A dermatologist consult may be obtained if chronic dermatitis is present.
MIXED VESSSEL (ARTERIAL AND VENOUS ULCER) - presence of arterial insufficiency and venous disease. Typically, ulcers are found on the lower extremity including the foot. Management includes assessment of arterial and venous blood flow to the lower extremity, wound management, and evaluation by a vascular surgeon.
All patients should be encouraged to decrease their risk factors (e.g., smoking, etc.) and to manage co-existing conditions such as diabetes.
DIABETIC NEUROPATHIC FOOT ULCERS – generally occur in diabetic patients with significant sensory neuropathy with unrecognized repetitive trauma. Management includes stopping the trauma with special shoes (off loading), assessment of arterial blood supply and wound care. Patients should be referred to the Limb Preservation Service.
MISCELLANEOUS EXTREMITY WOUND OR ULCERS - All other ulcerations assessed individually and treated according to the underlying etiology.
Neurogenic ulcers, also known as diabetic ulcers, are ulcers that occur most commonly on the bottom of the foot. People with diabetes are predisposed to peripheral neuropathy, which involves a decreased or total lack of sensation in the feet. Feet are naturally stressed from walking, and someone who has decreased sensation will not necessarily feel that they have an area of skin breakdown occurring. Coupled with this lack or absence of sensation is a decrease in circulation to the feet as well. Wounds that do not get proper blood flow are not only slower to heal but also at an increased risk for infection. A small cut, scrape, or irritated area in a diabetic can turn into an ulcer for these reasons. It is common for these types of ulcers to keep coming back in diabetics.
Thursday, October 28, 2010
Dengue Virus Prevention
DENGUE FEVER – PREVENTION, TREATMENT AND HOMEOPATHIC MEDICINES.
Homoeopathic medicines work like Vaccines.
DENGUE FEVER indicates a lack of preventive measures by the civic agencies, and now peoples are challenged as mosquito breeding was detected on their premises!
WHAT IS DENGUE FEVER?
Dengue is a mosquito-borne disease caused by any one of four closely related dengue viruses (DENV-1, -2, -3, and -4). Infection with one serotype of DENV provides immunity to that serotype for life, but provides no long-term immunity to other serotypes. Thus, a person can be infected as many as four times, once with each serotype.
Dengue viruses are transmitted from person to person by Aedes mosquitoes (most often Aedes aegypti) in the domestic environment.
Epidemics have occurred periodically in the Western Hemisphere for more than 200 years. In the past 30 years, dengue transmission and the frequency of dengue epidemics have increased greatly in most tropical countries like India, Bangladesh, Brazil, Cambodia, Indonesia, Malaysia, Mexico, Pakistan, Singapore, Sri Lanka, Thailand, Vietnam, etc.
WHAT ARE THE SYMPTOMS OF DENGUE FEVER?
Classic dengue fever, or “break bone fever,” is characterized by acute onset of high fever 3–14 days after the bite of an infected mosquito.
Symptoms include
frontal headache,
retro-orbital pain,
myalgias,
arthralgias,
hemorrhagic manifestations,
rash, and
low white blood cell count
The patient also may complain of anorexia and nausea.
Acute symptoms, when present, usually last about 1 week, but weakness, malaise, and anorexia may persist for several weeks.
Some patients with dengue fever go on to develop dengue hemorrhagic fever (DHF), a severe and sometimes fatal form of the disease.
DIAGNOSIS OF DENGUE FEVER
The diagnosis of dengue is usually made clinically.
The classic picture is high fever with no localizing source of infection, a patchily rash with thrombocytopenia and relative leucopenia – low platelet and white blood cell count.
LABORATORY DIAGNOSIS OF DENGUE INFECTION
One can get DENGUE FEVER ANTIBODY, IgM & IgG.
AIM OF TREATMENT OF DENGUE FEVER:
• Relieving symptoms of pain.
• Controlling fever.
• Telling patients to avoid aspirin and other non steroidal, anti-inflammatory medications because they may increase the risk for hemorrhage.
• Reminding patients to drink more fluids, especially when they have a high fever.
HOW TO TREAT DENGUE FEVER
• Drink plenty of fluids and get plenty of rest.
• Antipyretics to control temperature. Children with dengue are at risk for febrile seizures during the febrile phase of illness.
• Avoid aspirin / Disprin and other nonsteroidal, anti-inflammatory medications because they increase the risk of hemorrhage. People generally take Brufen or Combiflam tablets in such fever conditions, these are to be avoided.
• Get platelet counts.
PREVENTION OF DENGUE FEVER
- Homoeopathic medicines provide resistance in the human body.
- Primary prevention of dengue is mosquito control.
DENGUE FEVER AND HOMEOPATHY MEDICINES
In Homoeopathy, we have more than 20 medicines which can be taken based on human body and lifestyle prior to the attack and after the Dengue Fever attach based on different symptoms of fever in different stages. I would suggest you to please consult your homeopathic physician or homeopathic consultant for appropriate selection of the homeopathic drug for dengue fever before causing any damage.
Homoeo
Doctor.Muhammad Mansoor-ul-Haq
Master of Science in Information Technology,
B.Sc, D.H.M.S, R.H.M.P
http://al-haq-clinic.blogspot.com/
Homoeopathic medicines work like Vaccines.
DENGUE FEVER indicates a lack of preventive measures by the civic agencies, and now peoples are challenged as mosquito breeding was detected on their premises!
WHAT IS DENGUE FEVER?
Dengue is a mosquito-borne disease caused by any one of four closely related dengue viruses (DENV-1, -2, -3, and -4). Infection with one serotype of DENV provides immunity to that serotype for life, but provides no long-term immunity to other serotypes. Thus, a person can be infected as many as four times, once with each serotype.
Dengue viruses are transmitted from person to person by Aedes mosquitoes (most often Aedes aegypti) in the domestic environment.
Epidemics have occurred periodically in the Western Hemisphere for more than 200 years. In the past 30 years, dengue transmission and the frequency of dengue epidemics have increased greatly in most tropical countries like India, Bangladesh, Brazil, Cambodia, Indonesia, Malaysia, Mexico, Pakistan, Singapore, Sri Lanka, Thailand, Vietnam, etc.
WHAT ARE THE SYMPTOMS OF DENGUE FEVER?
Classic dengue fever, or “break bone fever,” is characterized by acute onset of high fever 3–14 days after the bite of an infected mosquito.
Symptoms include
frontal headache,
retro-orbital pain,
myalgias,
arthralgias,
hemorrhagic manifestations,
rash, and
low white blood cell count
The patient also may complain of anorexia and nausea.
Acute symptoms, when present, usually last about 1 week, but weakness, malaise, and anorexia may persist for several weeks.
Some patients with dengue fever go on to develop dengue hemorrhagic fever (DHF), a severe and sometimes fatal form of the disease.
DIAGNOSIS OF DENGUE FEVER
The diagnosis of dengue is usually made clinically.
The classic picture is high fever with no localizing source of infection, a patchily rash with thrombocytopenia and relative leucopenia – low platelet and white blood cell count.
LABORATORY DIAGNOSIS OF DENGUE INFECTION
One can get DENGUE FEVER ANTIBODY, IgM & IgG.
AIM OF TREATMENT OF DENGUE FEVER:
• Relieving symptoms of pain.
• Controlling fever.
• Telling patients to avoid aspirin and other non steroidal, anti-inflammatory medications because they may increase the risk for hemorrhage.
• Reminding patients to drink more fluids, especially when they have a high fever.
HOW TO TREAT DENGUE FEVER
• Drink plenty of fluids and get plenty of rest.
• Antipyretics to control temperature. Children with dengue are at risk for febrile seizures during the febrile phase of illness.
• Avoid aspirin / Disprin and other nonsteroidal, anti-inflammatory medications because they increase the risk of hemorrhage. People generally take Brufen or Combiflam tablets in such fever conditions, these are to be avoided.
• Get platelet counts.
PREVENTION OF DENGUE FEVER
- Homoeopathic medicines provide resistance in the human body.
- Primary prevention of dengue is mosquito control.
DENGUE FEVER AND HOMEOPATHY MEDICINES
In Homoeopathy, we have more than 20 medicines which can be taken based on human body and lifestyle prior to the attack and after the Dengue Fever attach based on different symptoms of fever in different stages. I would suggest you to please consult your homeopathic physician or homeopathic consultant for appropriate selection of the homeopathic drug for dengue fever before causing any damage.
Homoeo
Doctor.Muhammad Mansoor-ul-Haq
Master of Science in Information Technology,
B.Sc, D.H.M.S, R.H.M.P
http://al-haq-clinic.blogspot.com/
Wednesday, July 7, 2010
INTRADURAL OR PRIMARY SPINAL CORD TUMORS
(By Dr.Muhammad Mansoor-ul-Haq)
Patient awareness program.
Before talking about the Intradural or primary spinal cord tumors; brief discuss about CNS; central nervous system: the portion of the vertebrate nervous system consisting of the brain and spinal cord. The central nervous system (CNS) is the part of the nervous system that coordinates the activity of all parts of the bodies
Intradural or primary spinal cord tumors (neoplasms (Neoplasm is an abnormal mass of tissue as a result of neoplasia. Neoplasia (new growth in Greek) is the abnormal proliferation of cells)) are uncommon lesions (A lesion is any abnormal tissue found on or in an organism, usually damaged by disease or trauma.) and fortunately affect only a minority of the population. However, when lesions grow, they result in compression of the spinal cord, which can cause limb dysfunction, motor and sensation loss, and, possibly, lead to death. Spinal tumors are classified based on their anatomic location as related to the dura mater (lining around the spinal cord) and spinal cord (medullary) as epidural, intradural extramedullary, or intradural intramedullary. Primary spinal tumors are typically intradural in location, where extradural spinal tumors are typically due to metastatic disease.
This article focuses on the evaluation and management of intradural intramedullary spinal cord tumors. The typical histopathological types that account for 95% of these intramedullary neoplasms include astrocytomas, ependymomas, and hemangioblastomas. Spinal cord astrocytomas and ependymomas can be further classified as glial cell neoplasms.( Glia (or glial cells) and neurons (nerve cells) are the two major types of cells in the nervous system. While neurons are excitable — generating electrical impulses that transmit information throughout the central nervous system(CNS) and the peripheral nervous system (PNS) — glia are non-excitable cells that serve a wide range of essential functions in support of neurons.)
Problem
Spinal cord parenchyma consists of both gray (neurons and supporting glial cells (Nonconducting cells that serve as support cells in the nervous system and help to protect neurons)) and white matter (axonal(that part of a nerve cell through which impulses travel away from the cell body.)) and tracts that transmit impulses between the brain and body. These tracts, or circuits, control posture, movement, sensation, and autonomic system function, including bowel, bladder, and sexual function.
Neurologic dysfunction develops as the spinal cord tumors enlarge and compress adjacent healthy neural tissue, disrupting these pathways. Upon further compression, patients can lose complete motor function and sensation below the lesion. In addition to weakness and sensory loss, patients may experience pain, particularly at night. This pain is believed to be related to disturbances in venous outflow by the tumor, causing engorgement and swelling of the spinal cord.
Frequency
Intramedullary spinal cord tumors account for approximately 2% of adult and 10% of pediatric central nervous system neoplasms. In adults, 85-90% of intramedullary tumors are the glial subtypes, astrocytoma or ependymoma. Ependymomas account for approximately 60-70% of all spinal cord tumors found in adults, while, in children, 55-65% of intramedullary spinal cord tumors are astrocytomas. Hemangioblastomas account for 5% of tumors, whereas paragangliomas, oligodendrogliomas, and gangliogliomas account for the remaining lesions.
Etiology
The pathogenesis of spinal neoplasms is unknown, but most arise from normal cell types in the region of the spinal cord in which they develop. A genetic predisposition is likely, given the higher incidence in certain familial or syndromic groups (neurofibromatosis). Astrocytomas and ependymomas are more common in patients with neurofibromatosis type 2, which is associated with an abnormality on chromosome 22. In addition, spinal hemangioblastomas can develop in 30% of patients with von Hippel-Lindau syndrome, which is associated with an abnormality on chromosome 3.
Pathophysiology
The spinal cord consists of numerous nerve bundles that descend from and ascend to the brain. Electrical impulses are carried and transmitted to facilitate movement and sensation. With intramedullary spinal cord tumors, compression and stretching of these fiber tracts results in loss of the motor and sensory function. As the tumors grow, the patient's neurologic function further deteriorates.
Presentation
Patients with intramedullary glial spinal cord tumors (ie, ependymomas, astrocytomas) typically present with back pain referred from the level of the lesion, sensory changes, or worsening function. The symptoms can be of a long duration, since these lesions tend to grow slowly and typically have a benign histopathology. Patients with low-grade astrocytomas tend to experience symptoms over a mean duration of 41 months. This is in contrast to patients with malignant astrocytomas, whose symptoms persist for a mean duration of only 4-7 months before diagnosis.
Tumor-specific characteristics
• Ependymomas
o Mean age at presentation of 43 years
o Slight female predominance
o Pain localized to the spine (65%)
o Pain worse at night or upon awakening
o Dysesthetic pain (burning pain)
o Long history of symptoms
o Myxopapillary variant (mean age of presentation of 21 y; slight male predominance)
• Astrocytomas
o Equal male and female prevalence
o Pain localized to spine
o Pain worse at night or upon awakening
o Paresthesias (abnormal sensation)
• Hemangioblastomas
o Onset of symptoms by the fourth decade of life, 80% symptomatic by age 40 years
o Familial disorder (ie, von Hippel-Lindau syndrome) present in a third of patients
o Decreased posterior column sensation
o Back pain localized over lesion
Physical examination findings
• Motor weakness (late finding)
• Sensory
o Decreased touch, pain, and/or temperature sensation
o Hyperesthesias
o Decreased proprioception (inability to localize limbs in space)
o Abnormal sensation below the level of lesion
o Abnormal sensation only at level of lesion (suspended level)
• Hyperreflexia
o Hoffman sign for cervical lesions
o Clonus
o Extensor plantar response (Babinski sign)
• Spasticity
• Increased tone
• Muscle atrophy (late finding)
Indications
Intramedullary spinal cord neoplasms or tumors are typically histopathologically "benign" or slow growing. However, patients can have more aggressive neoplasms as well as morbidity due to the location of the lesion. Consequently, compared with similar intracranial neoplasms, patients may have a prolonged survival after diagnosis.
Optimal treatment options depend on the patient's clinical symptoms and neurologic finding. When and whether to treat these lesions as well as perform radiosurgery or surgical excision of lesions remains controversial. However, cures have been reported only after complete surgical resection. Therefore, patients with neurologic symptoms and confirmatory findings from imaging studies may benefit most from surgical excision, with the surgical goal of total gross resection of the lesion.
Relevant Anatomy
Arterial
Understanding the normal spinal cord vascular supply is essential to treating intramedullary spinal cord lesions; specifically because these vessels may have a variable and inconsistent distribution.
The great vessels (aorta, carotids) contribute arterial supply to the spinal cord via segmental arteries, which further branch into medullary and radicular arteries. The radicular artery provides extramedullary blood supply to the nerve root and dura; the medullary artery bifurcates into anterior and posterior divisions to form the spinal arteries. One anterior and 2 posterior spinal arteries then transverse the longitudinal axis of the spinal cord and provide the blood supply to the spinal cord. Neoplasms acquire their blood supply by leaching blood from these vessels.
Venous
The venous plexus of the spinal column, termed the Batson plexus, is unlike other venous systems in the body because the veins do not contain valves. Therefore, blood can have pathologic retrograde flow. This retrograde flow blood can back up and cause venous congestion. This can manifest as venous hypertension. Because oxygenated blood cannot pass through the spinal cord because of the congestion of outflow, patients present with progressive neurologic dysfunction.
Spinal cord
The spinal cord parenchyma consists of a central canal surrounded by an H-shaped gray matter region that contains neurons. Outer myelinated nerve tracts, termed white matter, surround the central gray matter. The central canal represents an embryologic remnant from neurulation of the neural plate and is lined with ependymal cells. Ependymomas arise from these cells and, therefore, are typically located centrally in the spinal cord parenchyma. In contrast, astrocytes support gray matter neurons and white matter axons. Neoplastic transformation of these supporting cells results in the development of astrocytomas and may occur almost anywhere within the cord.
Contraindications
Observation with serial imaging studies over a variable period is a treatment option for patients who pose a high surgical risk, who are elderly, and/or who only have minimal neurologic signs. Patients in whom pathology tissue shows a malignant neoplasm may be best treated with radiotherapy because they are expected to have an accelerated deterioration and complete surgical resection is not possible.
Intramedullary spinal cord tumors, like the one depicted in the image below, refer to a subgroup of intradural spinal tumors that arise from cells within the spinal cord, as opposed to adjacent structures such as the nerve roots or meninges. They are much less common than brain tumors and are thought to account for only 2-4% of all intrinsic tumors of the central nervous system. Their most common initial symptom is generalized back pain, which is very difficult to distinguish clinically from back pain from musculoskeletal conditions.
View of a cervical intramedullary ependymoma in situ after midline myelotomy and initial dissection (top left). The tumor was removed en bloc (right), and the postsurgical cavity in the spinal cord is shown (bottom left).
Patients are often diagnosed only after the development of neurologic signs and symptoms that may occur later in the course of the disease. Early diagnosis is important, however, because surgical removal for most tumors is curative, and surgical results are optimized when tumors are smaller. Also, neurological deficits resulting from intramedullary spinal cord tumors are seldom reversible. As such, functional outcomes after surgery are closely tied to the patient's preoperative neurologic condition.
History of the Procedure
Important events in the development of our understanding of spinal cord tumors are as follows:
• In 1887, Horsley performed the first successful removal of an intradural tumor.
• In 1907, Elsberg performed the first successful removal of an intramedullary tumor and subsequently published the seminal publication on spinal tumors. He developed a two-stage operation in which a myelotomy was performed and the dura was closed in the first stage. In the second stage, the tumor had partially extruded from the spinal cord for easier resection.
• In 1919, Dandy introduced air-contrast myelography.
• In 1940, Greenwald introduced bipolar coagulation.
• In 1964, Kurze introduced the operating microscope.
• In 1967, Greenwood published a large series detailing successfully removed tumors.
• In 1990, McCormick published a large surgical series demonstrating excellent long-term outcomes for surgery of ependymomas and established a clinical grading system.
Problem
Intramedullary spinal cord tumors are tumors that occur inside the spinal cord. They are relatively rare, compared with brain tumors, but still affect thousands of patients every year. They are generally slow growing, histologically benign tumors and are often definitely treated with surgery.
Frequency
Spinal tumors occur with an incidence of 1.1 case per 100,000 persons.
Intramedullary spinal tumors comprise approximately 2-4% of all CNS neoplasms.
The most common kinds of intramedullary tumors are ependymomas, astrocytomas, and hemangioblastomas.
In adults, ependymomas are the most common tumor type, accounting for 40-60% of all intramedullary spinal tumors, with the mean age of presentation being 35-40 years.
In children, astrocytomas are the most common tumor type, accounting for around 60% of all intramedullary spinal tumors, and the mean age of presentation is 5-10 years.
Intramedullary spinal tumors can arise anywhere in the spinal cord, from the cervicomedullary junction to the filum terminale, but they are found most frequently in the cervical cord, presumably because it contains more neural tissue than the thoracic or lumbar segments.
Etiology
The etiology of intramedullary spinal tumors remains obscure but undoubtedly varies according to histology. Most intramedullary spinal cord tumors are considered to be glial in origin because they are histologically and immunohistochemically similar to differentiated non-neuronal cell types, such as ependymal cells and astrocytes, which occur in nonpathological spinal cord tissue. The traditional thinking is that tumors occur when these differentiated cells, which normally stop propagating after spinal cord development, acquire mutations that cause them to divide again in an uncontrolled fashion.
Individuals with type I and type II neurofibromatosis (NF1 and NF2) have been recognized for some time as having an increased incidence of intramedullary spinal tumors, as well many other kinds of tumors, compared with the general population. This general predisposition to tumors has been linked to germline mutations in 2 different genes named for their associated diseases. Patients with the NF1 gene are predisposed to spinal astrocytomas, whereas patients with the NF2 gene are predisposed to spinal ependymomas. Relatively recent genetic analyses of spinal ependymomas from individuals without syndromic neurofibromatosis have shown somatic mutations in the NF2 gene in a subset of cases.
The identification of mitotically active neural stem cells and neural progenitor cells throughout the central nervous system has altered current thinking about how all intrinsic CNS tumors arise. Many lines of evidence point toward neural stem cells as the cells of origin in brain tumors. This line of inquiry is not nearly as advanced in the spinal cord, but some preliminary work has shown similarities between tumor cells from spinal ependymomas and neural stem cells from the spinal cord.
The other relatively common type of intramedullary spinal tumor is hemangioblastoma. Hemangioblastomas are thought to arise from red blood cell precursors and are not intrinsic spinal cord tumors, but they are often anatomically intramedullary because of their association with the blood vessels that penetrate and nourish the spinal cord. Hemangioblastomas occur as a result of mutations in a tumor suppressor gene called vhl, which was found to be altered in patients with the neurocutaneous disorder von Hippel-Lindau disease(VHL). Patients are predisposed to form hemangioblastomas in the brain and spinal cord, and somatic mutations in the in the vhl gene have been found in tumors from patients without syndromic VHL.
Pathophysiology
The pathophysiology of intramedullary spinal cord tumors varies according to tumor type. Ependymomas are usually indolent, encapsulated tumors that are histologically benign. Pain and neurologic deficits arise as a result of a progressive stretching and distortion of nerve fibers. Usually a clear anatomical plane is present at surgery, and a gross visual anatomic resection results in a cure. Rare anaplastic subtypes can be invasive, however, and are more likely to recur or spread through CSF spaces. Even histologically benign–appearing spinal ependymomas can metastasize in this way.
Although malignant forms do exist, most spinal astrocytomas are low grade (WHO grade II) and less aggressive than astrocytomas in the brain. Pain and neurologic defects arise from a combination of nerve fiber stretching and from invasion of cord parenchyma. Because they are infiltrative tumors, complete surgical removal without damage to functional tissue is usually not possible. Exceptions to this general rule may include some pilocytic astrocytomas of the spinal cord (WHO grade I) that are more common in children.
Hemangioblastomas are highly vascular tumors with capillaries that display an increased permeability thought to be related to a hypersensitivity to vascular endothelial growth factor (VEGF). Lesions usually become symptomatic because this capillary hyperpermeability leads to fluid collections or syringes, which are often larger than the tumor itself, causing mass effect in addition to stretching of neural pathways. These fluid spaces are not lined with tumor cells, however, and only the tumor nidus needs to be removed at surgery.
Presentation
Symptoms
The clinical features of intramedullary spinal cord tumors are variable. Symptoms are not specific to spinal cord tumors and may be present in any myelopathic process.
Because of the slow-growing nature of many of these tumors, symptoms precede diagnosis an average of 2 years. Patients with malignant or metastatic spinal cord tumors present in the range of several weeks to a few months after symptoms develop.
Pain and weakness are the most common presenting symptoms of intramedullary spinal cord tumors. Pain is often the earliest symptom, classically occurring at night when the patient is supine. The pain is typically local over the level of the tumor but may radiate.
Progressive weakness may occur in the arms (cervical tumors) or legs (cervical, thoracic, conus tumors). Impaired bowel, bladder, or sexual function often occurs early. Patients may have poor balance. Rarely, symptoms of subarachnoid hemorrhage may be present.
Intratumoral hemorrhage can cause an abrupt deterioration, a presentation most often associated with ependymomas.
Examination
Examination may reveal a combination of upper and lower motor neuron signs. Lower motor signs may be at the level of the lesion and may aid in localization. Other signs evident upon physical examination may include spine tenderness, stiffening of gait, trophic changes of extremity, sensory loss, hyperreflexia, clonus, and scoliosis ortorticollis (generally in children).
Indications
The first-line treatment for intramedullary tumors is open surgical resection. Surgery is indicated for all symptomatic lesions. Small asymptomatic lesions may be followed clinically and radiographically because the majority of intramedullary tumors are relatively benign and slow growing. However, this approach carries the risk of the development of neurological deficits that are likely not recoverable and the uncertainty that comes with undetermined diagnosis.
At surgery, aggressiveness with respect to resection depends on the histological diagnosis of a frozen section and the ability to find and maintain a surgical plane. Given the difficulty in determining many ependymomas from astrocytomas on frozen section, the presence or absence of a clear surgical plane is usually the key determining factor in defining the surgical goal. If, after analysis of all available data including imaging characteristics, frozen section, and intraoperative appearance, a diagnosis of ependymoma is perceived, a complete surgical resection should be attempted. If a diagnosis of astrocytoma is perceived, most clinicians advocate a more limited debulking of only the tissue that is clearly abnormal.
External beam radiation is generally reserved for disseminated ependymomas and infiltrative astrocytomas but remains an option whenever radiographic residual or recurrent ependymoma is found. Stereotactic radiosurgery for intramedullary tumors remains untested.
Relevant Anatomy
The spinal cord originates at the foramen magnum and extends to the conus medullaris, which terminates at the L1-L2 vertebral body junction in adults. The pia matter condenses caudally to this area, extending to the sacrum as the filum terminale. It is an ovoid structure, most narrow in the anterior-posterior direction. At every vertebral level paired ventral and dorsal nerve roots exit the lateral aspect of the cord and coalesce to form 31 pairs of spinal nerves.
In contrast to the brain, the white matter of the spinal cord surrounds the interior gray matter. The spinal cord is covered by a supporting connective tissue layer called the pia matter that acts as a trellis for the vascular supply. A vestigial extension of the ventricular system, the central canal runs the length of the spinal cord. Dilation of the central canal may be pathologic in some instances. In general, ventral portion of the spinal cord parenchyma subserves motor function, whereas the dorsal portion subserves sensation. The spinal cord contains the same cell types as the brain, but these are highly specialized to their niche in the spinal cord.
The vascular supply for the spinal cord comes from the anterior spinal artery, the paired posterior spinal arteries, and the 31 radicular arteries. The anterior and posterior spinal arteries form off branches of the vertebral arteries at the cervicomedullary junction and course inferiorly along the length of the spinal cord. The anterior spinal artery is relatively constant and runs in the middle of the ventral surface of the cord, sending deep penetrating branches into the anterior median sulcus. These branches then send arterial twigs radially to the deepest portions of the spinal cord.
The paired posterior spinal arteries are relatively inconstant, course along the posterolateral surface of the cord, medial to the dorsal root entry zones, and send short penetrating end arterioles into the dorsal cord parenchyma. Thus, the anterior spinal artery supplies the ventral two thirds of the cord, whereas the posterior spinal artery supplies the dorsal third.
The spinal arteries form the nexus of an arterial network that is replenished by the radicular arteries that enter the spinal canal through the spinal nerve root sleeves. The radicular supply to the spinal cord is highly variable, but a few vital feeding arteries are usually present. The most important of these is the artery of Adamkiewicz, which is usually found on the left side, from T9 to L2.
Contraindications
Absolute contraindications to surgical intervention include uncorrected coagulopathy and systemic infection.
Relative contraindications to surgical intervention include complete neurologic deficit over 24 hours and short life expectancy
Patient awareness program.
Before talking about the Intradural or primary spinal cord tumors; brief discuss about CNS; central nervous system: the portion of the vertebrate nervous system consisting of the brain and spinal cord. The central nervous system (CNS) is the part of the nervous system that coordinates the activity of all parts of the bodies
Intradural or primary spinal cord tumors (neoplasms (Neoplasm is an abnormal mass of tissue as a result of neoplasia. Neoplasia (new growth in Greek) is the abnormal proliferation of cells)) are uncommon lesions (A lesion is any abnormal tissue found on or in an organism, usually damaged by disease or trauma.) and fortunately affect only a minority of the population. However, when lesions grow, they result in compression of the spinal cord, which can cause limb dysfunction, motor and sensation loss, and, possibly, lead to death. Spinal tumors are classified based on their anatomic location as related to the dura mater (lining around the spinal cord) and spinal cord (medullary) as epidural, intradural extramedullary, or intradural intramedullary. Primary spinal tumors are typically intradural in location, where extradural spinal tumors are typically due to metastatic disease.
This article focuses on the evaluation and management of intradural intramedullary spinal cord tumors. The typical histopathological types that account for 95% of these intramedullary neoplasms include astrocytomas, ependymomas, and hemangioblastomas. Spinal cord astrocytomas and ependymomas can be further classified as glial cell neoplasms.( Glia (or glial cells) and neurons (nerve cells) are the two major types of cells in the nervous system. While neurons are excitable — generating electrical impulses that transmit information throughout the central nervous system(CNS) and the peripheral nervous system (PNS) — glia are non-excitable cells that serve a wide range of essential functions in support of neurons.)
Problem
Spinal cord parenchyma consists of both gray (neurons and supporting glial cells (Nonconducting cells that serve as support cells in the nervous system and help to protect neurons)) and white matter (axonal(that part of a nerve cell through which impulses travel away from the cell body.)) and tracts that transmit impulses between the brain and body. These tracts, or circuits, control posture, movement, sensation, and autonomic system function, including bowel, bladder, and sexual function.
Neurologic dysfunction develops as the spinal cord tumors enlarge and compress adjacent healthy neural tissue, disrupting these pathways. Upon further compression, patients can lose complete motor function and sensation below the lesion. In addition to weakness and sensory loss, patients may experience pain, particularly at night. This pain is believed to be related to disturbances in venous outflow by the tumor, causing engorgement and swelling of the spinal cord.
Frequency
Intramedullary spinal cord tumors account for approximately 2% of adult and 10% of pediatric central nervous system neoplasms. In adults, 85-90% of intramedullary tumors are the glial subtypes, astrocytoma or ependymoma. Ependymomas account for approximately 60-70% of all spinal cord tumors found in adults, while, in children, 55-65% of intramedullary spinal cord tumors are astrocytomas. Hemangioblastomas account for 5% of tumors, whereas paragangliomas, oligodendrogliomas, and gangliogliomas account for the remaining lesions.
Etiology
The pathogenesis of spinal neoplasms is unknown, but most arise from normal cell types in the region of the spinal cord in which they develop. A genetic predisposition is likely, given the higher incidence in certain familial or syndromic groups (neurofibromatosis). Astrocytomas and ependymomas are more common in patients with neurofibromatosis type 2, which is associated with an abnormality on chromosome 22. In addition, spinal hemangioblastomas can develop in 30% of patients with von Hippel-Lindau syndrome, which is associated with an abnormality on chromosome 3.
Pathophysiology
The spinal cord consists of numerous nerve bundles that descend from and ascend to the brain. Electrical impulses are carried and transmitted to facilitate movement and sensation. With intramedullary spinal cord tumors, compression and stretching of these fiber tracts results in loss of the motor and sensory function. As the tumors grow, the patient's neurologic function further deteriorates.
Presentation
Patients with intramedullary glial spinal cord tumors (ie, ependymomas, astrocytomas) typically present with back pain referred from the level of the lesion, sensory changes, or worsening function. The symptoms can be of a long duration, since these lesions tend to grow slowly and typically have a benign histopathology. Patients with low-grade astrocytomas tend to experience symptoms over a mean duration of 41 months. This is in contrast to patients with malignant astrocytomas, whose symptoms persist for a mean duration of only 4-7 months before diagnosis.
Tumor-specific characteristics
• Ependymomas
o Mean age at presentation of 43 years
o Slight female predominance
o Pain localized to the spine (65%)
o Pain worse at night or upon awakening
o Dysesthetic pain (burning pain)
o Long history of symptoms
o Myxopapillary variant (mean age of presentation of 21 y; slight male predominance)
• Astrocytomas
o Equal male and female prevalence
o Pain localized to spine
o Pain worse at night or upon awakening
o Paresthesias (abnormal sensation)
• Hemangioblastomas
o Onset of symptoms by the fourth decade of life, 80% symptomatic by age 40 years
o Familial disorder (ie, von Hippel-Lindau syndrome) present in a third of patients
o Decreased posterior column sensation
o Back pain localized over lesion
Physical examination findings
• Motor weakness (late finding)
• Sensory
o Decreased touch, pain, and/or temperature sensation
o Hyperesthesias
o Decreased proprioception (inability to localize limbs in space)
o Abnormal sensation below the level of lesion
o Abnormal sensation only at level of lesion (suspended level)
• Hyperreflexia
o Hoffman sign for cervical lesions
o Clonus
o Extensor plantar response (Babinski sign)
• Spasticity
• Increased tone
• Muscle atrophy (late finding)
Indications
Intramedullary spinal cord neoplasms or tumors are typically histopathologically "benign" or slow growing. However, patients can have more aggressive neoplasms as well as morbidity due to the location of the lesion. Consequently, compared with similar intracranial neoplasms, patients may have a prolonged survival after diagnosis.
Optimal treatment options depend on the patient's clinical symptoms and neurologic finding. When and whether to treat these lesions as well as perform radiosurgery or surgical excision of lesions remains controversial. However, cures have been reported only after complete surgical resection. Therefore, patients with neurologic symptoms and confirmatory findings from imaging studies may benefit most from surgical excision, with the surgical goal of total gross resection of the lesion.
Relevant Anatomy
Arterial
Understanding the normal spinal cord vascular supply is essential to treating intramedullary spinal cord lesions; specifically because these vessels may have a variable and inconsistent distribution.
The great vessels (aorta, carotids) contribute arterial supply to the spinal cord via segmental arteries, which further branch into medullary and radicular arteries. The radicular artery provides extramedullary blood supply to the nerve root and dura; the medullary artery bifurcates into anterior and posterior divisions to form the spinal arteries. One anterior and 2 posterior spinal arteries then transverse the longitudinal axis of the spinal cord and provide the blood supply to the spinal cord. Neoplasms acquire their blood supply by leaching blood from these vessels.
Venous
The venous plexus of the spinal column, termed the Batson plexus, is unlike other venous systems in the body because the veins do not contain valves. Therefore, blood can have pathologic retrograde flow. This retrograde flow blood can back up and cause venous congestion. This can manifest as venous hypertension. Because oxygenated blood cannot pass through the spinal cord because of the congestion of outflow, patients present with progressive neurologic dysfunction.
Spinal cord
The spinal cord parenchyma consists of a central canal surrounded by an H-shaped gray matter region that contains neurons. Outer myelinated nerve tracts, termed white matter, surround the central gray matter. The central canal represents an embryologic remnant from neurulation of the neural plate and is lined with ependymal cells. Ependymomas arise from these cells and, therefore, are typically located centrally in the spinal cord parenchyma. In contrast, astrocytes support gray matter neurons and white matter axons. Neoplastic transformation of these supporting cells results in the development of astrocytomas and may occur almost anywhere within the cord.
Contraindications
Observation with serial imaging studies over a variable period is a treatment option for patients who pose a high surgical risk, who are elderly, and/or who only have minimal neurologic signs. Patients in whom pathology tissue shows a malignant neoplasm may be best treated with radiotherapy because they are expected to have an accelerated deterioration and complete surgical resection is not possible.
Intramedullary spinal cord tumors, like the one depicted in the image below, refer to a subgroup of intradural spinal tumors that arise from cells within the spinal cord, as opposed to adjacent structures such as the nerve roots or meninges. They are much less common than brain tumors and are thought to account for only 2-4% of all intrinsic tumors of the central nervous system. Their most common initial symptom is generalized back pain, which is very difficult to distinguish clinically from back pain from musculoskeletal conditions.
View of a cervical intramedullary ependymoma in situ after midline myelotomy and initial dissection (top left). The tumor was removed en bloc (right), and the postsurgical cavity in the spinal cord is shown (bottom left).
Patients are often diagnosed only after the development of neurologic signs and symptoms that may occur later in the course of the disease. Early diagnosis is important, however, because surgical removal for most tumors is curative, and surgical results are optimized when tumors are smaller. Also, neurological deficits resulting from intramedullary spinal cord tumors are seldom reversible. As such, functional outcomes after surgery are closely tied to the patient's preoperative neurologic condition.
History of the Procedure
Important events in the development of our understanding of spinal cord tumors are as follows:
• In 1887, Horsley performed the first successful removal of an intradural tumor.
• In 1907, Elsberg performed the first successful removal of an intramedullary tumor and subsequently published the seminal publication on spinal tumors. He developed a two-stage operation in which a myelotomy was performed and the dura was closed in the first stage. In the second stage, the tumor had partially extruded from the spinal cord for easier resection.
• In 1919, Dandy introduced air-contrast myelography.
• In 1940, Greenwald introduced bipolar coagulation.
• In 1964, Kurze introduced the operating microscope.
• In 1967, Greenwood published a large series detailing successfully removed tumors.
• In 1990, McCormick published a large surgical series demonstrating excellent long-term outcomes for surgery of ependymomas and established a clinical grading system.
Problem
Intramedullary spinal cord tumors are tumors that occur inside the spinal cord. They are relatively rare, compared with brain tumors, but still affect thousands of patients every year. They are generally slow growing, histologically benign tumors and are often definitely treated with surgery.
Frequency
Spinal tumors occur with an incidence of 1.1 case per 100,000 persons.
Intramedullary spinal tumors comprise approximately 2-4% of all CNS neoplasms.
The most common kinds of intramedullary tumors are ependymomas, astrocytomas, and hemangioblastomas.
In adults, ependymomas are the most common tumor type, accounting for 40-60% of all intramedullary spinal tumors, with the mean age of presentation being 35-40 years.
In children, astrocytomas are the most common tumor type, accounting for around 60% of all intramedullary spinal tumors, and the mean age of presentation is 5-10 years.
Intramedullary spinal tumors can arise anywhere in the spinal cord, from the cervicomedullary junction to the filum terminale, but they are found most frequently in the cervical cord, presumably because it contains more neural tissue than the thoracic or lumbar segments.
Etiology
The etiology of intramedullary spinal tumors remains obscure but undoubtedly varies according to histology. Most intramedullary spinal cord tumors are considered to be glial in origin because they are histologically and immunohistochemically similar to differentiated non-neuronal cell types, such as ependymal cells and astrocytes, which occur in nonpathological spinal cord tissue. The traditional thinking is that tumors occur when these differentiated cells, which normally stop propagating after spinal cord development, acquire mutations that cause them to divide again in an uncontrolled fashion.
Individuals with type I and type II neurofibromatosis (NF1 and NF2) have been recognized for some time as having an increased incidence of intramedullary spinal tumors, as well many other kinds of tumors, compared with the general population. This general predisposition to tumors has been linked to germline mutations in 2 different genes named for their associated diseases. Patients with the NF1 gene are predisposed to spinal astrocytomas, whereas patients with the NF2 gene are predisposed to spinal ependymomas. Relatively recent genetic analyses of spinal ependymomas from individuals without syndromic neurofibromatosis have shown somatic mutations in the NF2 gene in a subset of cases.
The identification of mitotically active neural stem cells and neural progenitor cells throughout the central nervous system has altered current thinking about how all intrinsic CNS tumors arise. Many lines of evidence point toward neural stem cells as the cells of origin in brain tumors. This line of inquiry is not nearly as advanced in the spinal cord, but some preliminary work has shown similarities between tumor cells from spinal ependymomas and neural stem cells from the spinal cord.
The other relatively common type of intramedullary spinal tumor is hemangioblastoma. Hemangioblastomas are thought to arise from red blood cell precursors and are not intrinsic spinal cord tumors, but they are often anatomically intramedullary because of their association with the blood vessels that penetrate and nourish the spinal cord. Hemangioblastomas occur as a result of mutations in a tumor suppressor gene called vhl, which was found to be altered in patients with the neurocutaneous disorder von Hippel-Lindau disease(VHL). Patients are predisposed to form hemangioblastomas in the brain and spinal cord, and somatic mutations in the in the vhl gene have been found in tumors from patients without syndromic VHL.
Pathophysiology
The pathophysiology of intramedullary spinal cord tumors varies according to tumor type. Ependymomas are usually indolent, encapsulated tumors that are histologically benign. Pain and neurologic deficits arise as a result of a progressive stretching and distortion of nerve fibers. Usually a clear anatomical plane is present at surgery, and a gross visual anatomic resection results in a cure. Rare anaplastic subtypes can be invasive, however, and are more likely to recur or spread through CSF spaces. Even histologically benign–appearing spinal ependymomas can metastasize in this way.
Although malignant forms do exist, most spinal astrocytomas are low grade (WHO grade II) and less aggressive than astrocytomas in the brain. Pain and neurologic defects arise from a combination of nerve fiber stretching and from invasion of cord parenchyma. Because they are infiltrative tumors, complete surgical removal without damage to functional tissue is usually not possible. Exceptions to this general rule may include some pilocytic astrocytomas of the spinal cord (WHO grade I) that are more common in children.
Hemangioblastomas are highly vascular tumors with capillaries that display an increased permeability thought to be related to a hypersensitivity to vascular endothelial growth factor (VEGF). Lesions usually become symptomatic because this capillary hyperpermeability leads to fluid collections or syringes, which are often larger than the tumor itself, causing mass effect in addition to stretching of neural pathways. These fluid spaces are not lined with tumor cells, however, and only the tumor nidus needs to be removed at surgery.
Presentation
Symptoms
The clinical features of intramedullary spinal cord tumors are variable. Symptoms are not specific to spinal cord tumors and may be present in any myelopathic process.
Because of the slow-growing nature of many of these tumors, symptoms precede diagnosis an average of 2 years. Patients with malignant or metastatic spinal cord tumors present in the range of several weeks to a few months after symptoms develop.
Pain and weakness are the most common presenting symptoms of intramedullary spinal cord tumors. Pain is often the earliest symptom, classically occurring at night when the patient is supine. The pain is typically local over the level of the tumor but may radiate.
Progressive weakness may occur in the arms (cervical tumors) or legs (cervical, thoracic, conus tumors). Impaired bowel, bladder, or sexual function often occurs early. Patients may have poor balance. Rarely, symptoms of subarachnoid hemorrhage may be present.
Intratumoral hemorrhage can cause an abrupt deterioration, a presentation most often associated with ependymomas.
Examination
Examination may reveal a combination of upper and lower motor neuron signs. Lower motor signs may be at the level of the lesion and may aid in localization. Other signs evident upon physical examination may include spine tenderness, stiffening of gait, trophic changes of extremity, sensory loss, hyperreflexia, clonus, and scoliosis ortorticollis (generally in children).
Indications
The first-line treatment for intramedullary tumors is open surgical resection. Surgery is indicated for all symptomatic lesions. Small asymptomatic lesions may be followed clinically and radiographically because the majority of intramedullary tumors are relatively benign and slow growing. However, this approach carries the risk of the development of neurological deficits that are likely not recoverable and the uncertainty that comes with undetermined diagnosis.
At surgery, aggressiveness with respect to resection depends on the histological diagnosis of a frozen section and the ability to find and maintain a surgical plane. Given the difficulty in determining many ependymomas from astrocytomas on frozen section, the presence or absence of a clear surgical plane is usually the key determining factor in defining the surgical goal. If, after analysis of all available data including imaging characteristics, frozen section, and intraoperative appearance, a diagnosis of ependymoma is perceived, a complete surgical resection should be attempted. If a diagnosis of astrocytoma is perceived, most clinicians advocate a more limited debulking of only the tissue that is clearly abnormal.
External beam radiation is generally reserved for disseminated ependymomas and infiltrative astrocytomas but remains an option whenever radiographic residual or recurrent ependymoma is found. Stereotactic radiosurgery for intramedullary tumors remains untested.
Relevant Anatomy
The spinal cord originates at the foramen magnum and extends to the conus medullaris, which terminates at the L1-L2 vertebral body junction in adults. The pia matter condenses caudally to this area, extending to the sacrum as the filum terminale. It is an ovoid structure, most narrow in the anterior-posterior direction. At every vertebral level paired ventral and dorsal nerve roots exit the lateral aspect of the cord and coalesce to form 31 pairs of spinal nerves.
In contrast to the brain, the white matter of the spinal cord surrounds the interior gray matter. The spinal cord is covered by a supporting connective tissue layer called the pia matter that acts as a trellis for the vascular supply. A vestigial extension of the ventricular system, the central canal runs the length of the spinal cord. Dilation of the central canal may be pathologic in some instances. In general, ventral portion of the spinal cord parenchyma subserves motor function, whereas the dorsal portion subserves sensation. The spinal cord contains the same cell types as the brain, but these are highly specialized to their niche in the spinal cord.
The vascular supply for the spinal cord comes from the anterior spinal artery, the paired posterior spinal arteries, and the 31 radicular arteries. The anterior and posterior spinal arteries form off branches of the vertebral arteries at the cervicomedullary junction and course inferiorly along the length of the spinal cord. The anterior spinal artery is relatively constant and runs in the middle of the ventral surface of the cord, sending deep penetrating branches into the anterior median sulcus. These branches then send arterial twigs radially to the deepest portions of the spinal cord.
The paired posterior spinal arteries are relatively inconstant, course along the posterolateral surface of the cord, medial to the dorsal root entry zones, and send short penetrating end arterioles into the dorsal cord parenchyma. Thus, the anterior spinal artery supplies the ventral two thirds of the cord, whereas the posterior spinal artery supplies the dorsal third.
The spinal arteries form the nexus of an arterial network that is replenished by the radicular arteries that enter the spinal canal through the spinal nerve root sleeves. The radicular supply to the spinal cord is highly variable, but a few vital feeding arteries are usually present. The most important of these is the artery of Adamkiewicz, which is usually found on the left side, from T9 to L2.
Contraindications
Absolute contraindications to surgical intervention include uncorrected coagulopathy and systemic infection.
Relative contraindications to surgical intervention include complete neurologic deficit over 24 hours and short life expectancy
Wednesday, April 28, 2010
FROZEN SHOULDERS
What is a frozen shoulder?
Frozen shoulder, or adhesive capsulitis, is a condition that causes restriction of motion in the shoulder joint. The cause of a frozen shoulder is not well understood, but it often occurs for no known reason. Frozen shoulder causes the capsule surrounding the shoulder joint to contract and form scar tissue.
What causes frozen shoulder?
Most often, frozen shoulder occurs with no associated injury or discernible cause. There are patients who develop a frozen shoulder after a traumatic injury to the shoulder, but this is not the usual cause. Some risk factors for developing a frozen shoulder include:
• Age & Gender
Frozen shoulder most commonly affects patients between the ages of 40 to 60 years old, and it is twice more common in women than in men.
• Endocrine Disorders
Patients with diabetes are at particular risk for developing a frozen shoulder. Other endocrine abnormalities, such as thyroid problems, can also lead to this condition.
• Shoulder Trauma or Surgery
Patients who sustain a shoulder injury, or undergo surgery on the shoulder can develop a frozen shoulder joint. When injury or surgery is followed by prolonged joint immobilization, the risk of developing a frozen shoulder is highest.
• Other Systemic Conditions
Several systemic conditions such as heart disease and Parkinson's disease have also been associated with an increased risk for developing a frozen shoulder.
•
What happens with a frozen shoulder?
No one really understands why some people develop a frozen shoulder. For some reason, the shoulder joint becomes stiff and scarred. The shoulder joint is a ball and socket joint. The ball is the top of the arm bone (the humeral head), and the socket is part of the shoulder blade (the glenoid). Surrounding this ball-and-socket joint is a capsule of tissue that envelops the joint.
Normally, the shoulder joint allows more motion than any other joint in the body. When a patient develops a frozen shoulder, the capsule that surrounds the shoulder joint becomes contracted. The patients form bands of scar tissue called adhesions. The contraction of the capsule and the formation of the adhesions cause the frozen shoulder to become stiff and cause movement to become painful.
Homeopathic Treatment for Frozen Shoulder
Homeopathy treats the person as a whole. It means that homeopathic treatment focuses on the patient as a person, as well as his pathological condition. The homeopathic medicines are selected after a full individualizing examination and case-analysis, which includes the medical history of the patient, physical and mental constitution etc. A miasmatic tendency (predisposition/susceptibility) is also often taken into account for the treatment of chronic conditions. Visit Al-Homoeopathic Clinic for the treatment of Frozen Shoulder.
Frozen shoulder, or adhesive capsulitis, is a condition that causes restriction of motion in the shoulder joint. The cause of a frozen shoulder is not well understood, but it often occurs for no known reason. Frozen shoulder causes the capsule surrounding the shoulder joint to contract and form scar tissue.
What causes frozen shoulder?
Most often, frozen shoulder occurs with no associated injury or discernible cause. There are patients who develop a frozen shoulder after a traumatic injury to the shoulder, but this is not the usual cause. Some risk factors for developing a frozen shoulder include:
• Age & Gender
Frozen shoulder most commonly affects patients between the ages of 40 to 60 years old, and it is twice more common in women than in men.
• Endocrine Disorders
Patients with diabetes are at particular risk for developing a frozen shoulder. Other endocrine abnormalities, such as thyroid problems, can also lead to this condition.
• Shoulder Trauma or Surgery
Patients who sustain a shoulder injury, or undergo surgery on the shoulder can develop a frozen shoulder joint. When injury or surgery is followed by prolonged joint immobilization, the risk of developing a frozen shoulder is highest.
• Other Systemic Conditions
Several systemic conditions such as heart disease and Parkinson's disease have also been associated with an increased risk for developing a frozen shoulder.
•
What happens with a frozen shoulder?
No one really understands why some people develop a frozen shoulder. For some reason, the shoulder joint becomes stiff and scarred. The shoulder joint is a ball and socket joint. The ball is the top of the arm bone (the humeral head), and the socket is part of the shoulder blade (the glenoid). Surrounding this ball-and-socket joint is a capsule of tissue that envelops the joint.
Normally, the shoulder joint allows more motion than any other joint in the body. When a patient develops a frozen shoulder, the capsule that surrounds the shoulder joint becomes contracted. The patients form bands of scar tissue called adhesions. The contraction of the capsule and the formation of the adhesions cause the frozen shoulder to become stiff and cause movement to become painful.
Homeopathic Treatment for Frozen Shoulder
Homeopathy treats the person as a whole. It means that homeopathic treatment focuses on the patient as a person, as well as his pathological condition. The homeopathic medicines are selected after a full individualizing examination and case-analysis, which includes the medical history of the patient, physical and mental constitution etc. A miasmatic tendency (predisposition/susceptibility) is also often taken into account for the treatment of chronic conditions. Visit Al-Homoeopathic Clinic for the treatment of Frozen Shoulder.
Monday, April 26, 2010
VITILIGO
What is vitiligo, and what causes it?
(DR.MUHAMMAD MANSOOR-UL-HAQ)
Vitiligo (vit-ill-EYE-go) is apigmentation disorder in which melanocytes (the cells that make pigment) in the skin are destroyed. As a result, white patches appear on the skin in different parts of the body. Similar patches also appear on both the mucous membranes (tissues that line the inside of the mouth and nose), and the retina (inner layer of the eyeball). The hair that grows on areas affected by vitiligo sometimes turns white.
The cause of vitiligo is not known, but doctors and researchers have several different theories. There is strong evidence that people with vitiligo inherit a group of three genes that make them susceptible to depigmentation. The most widely accepted view is that the depigmentation occurs because vitiligo is an autoimmune disease -- a disease in which a person's immune system reacts against the body's own organs or tissues. As such, people's bodies produce proteins called cytokines that alter their pigment-producing cells and cause these cells to die. Another theory is that melanocytes destroy themselves. Finally, some people have reported that a single event such as sunburn or emotional distress triggered vitiligo; however, these events have not been scientifically proven as causes of vitiligo.
Who is affected by vitiligo?
About 0.5 to 1 percent of the world's population, or as many as 65 million people, have vitiligo. In the United States, 1 to 2 million people have the disorder. Half the people who have vitiligo develop it before age 20; most develop it before their 40th birthday. The disorder affects both sexes and all races equally; however, it is more noticeable in people with dark skin.
Vitiligo seems to be somewhat more common in people with certain autoimmune diseases. These autoimmune diseases include hyperthyroidism (an overactive thyroid gland), adrenocortical insufficiency (the adrenal gland does not produce enough of the hormone called corticosteroid), alopecia areata (patches of baldness), and pernicious anemia (a low level of red blood cells caused by the failure of the body to absorb vitamin B12). Scientists do not know the reason for the association between vitiligo and these autoimmune diseases. However, most people with vitiligo have no other autoimmune disease.
Vitiligo may also be hereditary; that is, it can run in families. Children whose parents have the disorder are more likely to develop vitiligo. In fact, 30 percent of people with vitiligo have a family member with the disease. However, only 5 to 7 percent of children will get vitiligo even if a parent has it, and most people with vitiligo do not have a family history of the disorder.
What are the symptoms vitiligo?
People who develop vitiligo usually first notice white patches (depigmentation) on their skin. These patches are more commonly found on sun-exposed areas of the body, including the hands, feet, arms, face, and lips. Other common areas for white patches to appear are the armpits and groin, and around the mouth, eyes, nostrils, navel, genitals, and rectum.
Vitiligo generally appears in one of three patterns:
1. focal pattern -- the depigmentation is limited to one or only a few areas
2. segmental pattern -- depigmented patches develop on only one side of the body
3. generalized pattern -- the most common pattern. Depigmentation occurs symmetrically on both sides of the body.
In addition to white patches on the skin, people with vitiligo may have premature graying of the scalp hair, eyelashes, eyebrows, and beard. People with dark skin may notice a loss of color inside their mouths.
Will the depigmented patches spread?
Focal pattern vitiligo and segmental vitiligo remain localized to one part of the body and do not spread. There is no way to predict if generalized vitiligo will spread. For some people, the depigmented patches do not spread. The disorder is usually progressive, however, and over time the white patches will spread to other areas of the body. For some people, vitiligo spreads slowly, over many years. For other people, spreading occurs rapidly. Some people have reported additional depigmentation following periods of physical or emotional stress.
The diagnosis of vitiligo is made based on a physical examination, medical history, and laboratory tests.
A doctor will likely suspect vitiligo if you report (or the physical examination reveals) white patches of skin on the body-particularly on sun-exposed areas, including the hands, feet, arms, face, and lips. If vitiligo is suspected, the doctor will ask about your medical history. Important factors in the diagnosis include a family history of vitiligo; a rash, sunburn, or other skin trauma at the site of vitiligo 2 to 3 months before depigmentation started; stress or physical illness; and premature (before age 35) graying of the hair. In addition, the doctor will ask whether you or anyone in your family has had any autoimmune diseases, and whether you are very sensitive to the sun.
To help confirm the diagnosis, the doctor may take a small sample (biopsy) of the affected skin to examine under a microscope. In vitiligo, the skin sample will usually show a complete absence of pigment-producing melanocytes. On the other hand, the presence of inflamed cells in the sample may suggest that another condition is responsible for the loss of pigmentation.
Because vitiligo may be associated with pernicious anemia (a condition in which an insufficient amount of vitamin B12 is absorbed from the gastrointestinal tract) orhyperthyroidism (an overactive thyroid gland), the doctor may also take a blood sample to check the blood-cell count and thyroid function. For some patients, the doctor may recommend an eye examination to check for uveitis (inflammation of part of the eye), which sometimes occurs with vitiligo. A blood test to look for the presence of antinuclear antibodies (a type of autoantibody) may also be done. This test helps determine if the patient has another autoimmune disease.
How can people cope with the emotional and psychological aspects of vitiligo?
While vitiligo is usually not harmful medically, its emotional and psychological effects can be devastating. In fact, in India, women with the disease are sometimes discriminated against in marriage. Developing vitiligo after marriage can be grounds for divorce.
Regardless of a person's race and culture, white patches of vitiligo can affect emotional and psychological well-being and self-esteem. People with vitiligo can experience emotional stress, particularly if the condition develops on visible areas of the body, such as the face, hands, arms, and feet; or on the genitals. Adolescents, who are often particularly concerned about their appearance, can be devastated by widespread vitiligo. Some people who have vitiligo feel embarrassed, ashamed, depressed, or worried about how others will react.
Fortunately, there are several strategies to help people cope with vitiligo. Also, various treatments-which we will discuss a bit later-can minimize, camouflage, or, in some cases, even eliminate white patches. First, it is important to find a doctor who is knowledgeable about the disorder and takes it seriously. The doctor should also be a good listener and be able to provide emotional support. You must let your doctor know if you are feeling depressed, because doctors and other mental health professionals can help people deal with depression. You should also learn as much as possible about the disorder and treatment choices so that you can participate in making important decisions about medical care.
Talking with other people who have vitiligo may also help. The National Vitiligo Foundation can provide information about vitiligo and refer you to local chapters that have support groups of patients, families, and physicians. Contact information for the foundation is listed at the end of this brochure. Family and friends are another source of support.
Some people with vitiligo have found that cosmetics that cover the white patches improve their appearance and help them feel better about themselves. You may need to experiment with several brands of concealing cosmetics before finding the product that works best.
(DR.MUHAMMAD MANSOOR-UL-HAQ)
Vitiligo (vit-ill-EYE-go) is apigmentation disorder in which melanocytes (the cells that make pigment) in the skin are destroyed. As a result, white patches appear on the skin in different parts of the body. Similar patches also appear on both the mucous membranes (tissues that line the inside of the mouth and nose), and the retina (inner layer of the eyeball). The hair that grows on areas affected by vitiligo sometimes turns white.
The cause of vitiligo is not known, but doctors and researchers have several different theories. There is strong evidence that people with vitiligo inherit a group of three genes that make them susceptible to depigmentation. The most widely accepted view is that the depigmentation occurs because vitiligo is an autoimmune disease -- a disease in which a person's immune system reacts against the body's own organs or tissues. As such, people's bodies produce proteins called cytokines that alter their pigment-producing cells and cause these cells to die. Another theory is that melanocytes destroy themselves. Finally, some people have reported that a single event such as sunburn or emotional distress triggered vitiligo; however, these events have not been scientifically proven as causes of vitiligo.
Who is affected by vitiligo?
About 0.5 to 1 percent of the world's population, or as many as 65 million people, have vitiligo. In the United States, 1 to 2 million people have the disorder. Half the people who have vitiligo develop it before age 20; most develop it before their 40th birthday. The disorder affects both sexes and all races equally; however, it is more noticeable in people with dark skin.
Vitiligo seems to be somewhat more common in people with certain autoimmune diseases. These autoimmune diseases include hyperthyroidism (an overactive thyroid gland), adrenocortical insufficiency (the adrenal gland does not produce enough of the hormone called corticosteroid), alopecia areata (patches of baldness), and pernicious anemia (a low level of red blood cells caused by the failure of the body to absorb vitamin B12). Scientists do not know the reason for the association between vitiligo and these autoimmune diseases. However, most people with vitiligo have no other autoimmune disease.
Vitiligo may also be hereditary; that is, it can run in families. Children whose parents have the disorder are more likely to develop vitiligo. In fact, 30 percent of people with vitiligo have a family member with the disease. However, only 5 to 7 percent of children will get vitiligo even if a parent has it, and most people with vitiligo do not have a family history of the disorder.
What are the symptoms vitiligo?
People who develop vitiligo usually first notice white patches (depigmentation) on their skin. These patches are more commonly found on sun-exposed areas of the body, including the hands, feet, arms, face, and lips. Other common areas for white patches to appear are the armpits and groin, and around the mouth, eyes, nostrils, navel, genitals, and rectum.
Vitiligo generally appears in one of three patterns:
1. focal pattern -- the depigmentation is limited to one or only a few areas
2. segmental pattern -- depigmented patches develop on only one side of the body
3. generalized pattern -- the most common pattern. Depigmentation occurs symmetrically on both sides of the body.
In addition to white patches on the skin, people with vitiligo may have premature graying of the scalp hair, eyelashes, eyebrows, and beard. People with dark skin may notice a loss of color inside their mouths.
Will the depigmented patches spread?
Focal pattern vitiligo and segmental vitiligo remain localized to one part of the body and do not spread. There is no way to predict if generalized vitiligo will spread. For some people, the depigmented patches do not spread. The disorder is usually progressive, however, and over time the white patches will spread to other areas of the body. For some people, vitiligo spreads slowly, over many years. For other people, spreading occurs rapidly. Some people have reported additional depigmentation following periods of physical or emotional stress.
The diagnosis of vitiligo is made based on a physical examination, medical history, and laboratory tests.
A doctor will likely suspect vitiligo if you report (or the physical examination reveals) white patches of skin on the body-particularly on sun-exposed areas, including the hands, feet, arms, face, and lips. If vitiligo is suspected, the doctor will ask about your medical history. Important factors in the diagnosis include a family history of vitiligo; a rash, sunburn, or other skin trauma at the site of vitiligo 2 to 3 months before depigmentation started; stress or physical illness; and premature (before age 35) graying of the hair. In addition, the doctor will ask whether you or anyone in your family has had any autoimmune diseases, and whether you are very sensitive to the sun.
To help confirm the diagnosis, the doctor may take a small sample (biopsy) of the affected skin to examine under a microscope. In vitiligo, the skin sample will usually show a complete absence of pigment-producing melanocytes. On the other hand, the presence of inflamed cells in the sample may suggest that another condition is responsible for the loss of pigmentation.
Because vitiligo may be associated with pernicious anemia (a condition in which an insufficient amount of vitamin B12 is absorbed from the gastrointestinal tract) orhyperthyroidism (an overactive thyroid gland), the doctor may also take a blood sample to check the blood-cell count and thyroid function. For some patients, the doctor may recommend an eye examination to check for uveitis (inflammation of part of the eye), which sometimes occurs with vitiligo. A blood test to look for the presence of antinuclear antibodies (a type of autoantibody) may also be done. This test helps determine if the patient has another autoimmune disease.
How can people cope with the emotional and psychological aspects of vitiligo?
While vitiligo is usually not harmful medically, its emotional and psychological effects can be devastating. In fact, in India, women with the disease are sometimes discriminated against in marriage. Developing vitiligo after marriage can be grounds for divorce.
Regardless of a person's race and culture, white patches of vitiligo can affect emotional and psychological well-being and self-esteem. People with vitiligo can experience emotional stress, particularly if the condition develops on visible areas of the body, such as the face, hands, arms, and feet; or on the genitals. Adolescents, who are often particularly concerned about their appearance, can be devastated by widespread vitiligo. Some people who have vitiligo feel embarrassed, ashamed, depressed, or worried about how others will react.
Fortunately, there are several strategies to help people cope with vitiligo. Also, various treatments-which we will discuss a bit later-can minimize, camouflage, or, in some cases, even eliminate white patches. First, it is important to find a doctor who is knowledgeable about the disorder and takes it seriously. The doctor should also be a good listener and be able to provide emotional support. You must let your doctor know if you are feeling depressed, because doctors and other mental health professionals can help people deal with depression. You should also learn as much as possible about the disorder and treatment choices so that you can participate in making important decisions about medical care.
Talking with other people who have vitiligo may also help. The National Vitiligo Foundation can provide information about vitiligo and refer you to local chapters that have support groups of patients, families, and physicians. Contact information for the foundation is listed at the end of this brochure. Family and friends are another source of support.
Some people with vitiligo have found that cosmetics that cover the white patches improve their appearance and help them feel better about themselves. You may need to experiment with several brands of concealing cosmetics before finding the product that works best.
Friday, April 16, 2010
INTRODUCTION
Al-Haq Homoeopathic Clinic is managed by a team of 05 homeopathic doctors, including three homoeopathic Lady Doctors, especially for the female patients so that female patients can discuss their problems in courtesy and secrecy as well.
Homoeopathic Doctor Muhammad Mansoor-ul-Haq is the senior member of the whole team. In addition to treating the visiting patients, he provides online consultation to the far flong and abroad patients. He has been deeply associated with homeopathy since 1988, serving regularly since 1992. Since then, he has successfully treated a large number of acute, chronic and complicated cases of varying natures, at the clinic as well as through Internet. He is providing online consultation since 2000. His expertise especially in Diabeties and Non Healing Ulcers. Presently his timings are :
ON TUESDAY and THURSDAY (1830 to 2100 hrs)
ON SATURDAY (1100 to 1400 and 1830 to 2100 hrs)
Homoeopathic Doctor Muhammad Ashfaq
Timings are:
ON MONDAY , WEDNESDAY and FRIDAY (1830 to 2100 hrs)
Homeopathic Lady Doctor Aalia Mansoor is the senior member of homoeopathic Lady Doctors. She has an acumen knowledge of Homoeopathy. Her expertise especially in Female Diseases. She has successfully treated a large number of acute, chronic and complicated cases of different natures.
Presently Her timings are
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Amina NAsir
Timings are:
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Shazia
Timings are:
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Isma Riaz Shah
Timings are:
N SATURDAY to FRIDAY (1100 to 1400 hrs and 1830 to 2100 hrs)
Homoeopathic Doctor Muhammad Mansoor-ul-Haq is the senior member of the whole team. In addition to treating the visiting patients, he provides online consultation to the far flong and abroad patients. He has been deeply associated with homeopathy since 1988, serving regularly since 1992. Since then, he has successfully treated a large number of acute, chronic and complicated cases of varying natures, at the clinic as well as through Internet. He is providing online consultation since 2000. His expertise especially in Diabeties and Non Healing Ulcers. Presently his timings are :
ON TUESDAY and THURSDAY (1830 to 2100 hrs)
ON SATURDAY (1100 to 1400 and 1830 to 2100 hrs)
Homoeopathic Doctor Muhammad Ashfaq
Timings are:
ON MONDAY , WEDNESDAY and FRIDAY (1830 to 2100 hrs)
Homeopathic Lady Doctor Aalia Mansoor is the senior member of homoeopathic Lady Doctors. She has an acumen knowledge of Homoeopathy. Her expertise especially in Female Diseases. She has successfully treated a large number of acute, chronic and complicated cases of different natures.
Presently Her timings are
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Amina NAsir
Timings are:
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Shazia
Timings are:
ON SATURDAY to FRIDAY (1100 to 1400 hrs)
Homoeopathic Lady Doctor Isma Riaz Shah
Timings are:
N SATURDAY to FRIDAY (1100 to 1400 hrs and 1830 to 2100 hrs)
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