- Common Spinal Procedures
- Don't Forget Your Brain
- Brain Cancer
- Brain and Spinal Cord Injuries
Some of the patients afflicted with disease will require surgery. When indicated, conservative treatments will be trialed (and exhausted) firstly however. This mostly applies to spinal pathology. Often times, pain and motor deficits (weakness) associated with a "herniated disc" in the neck or low back will resolve given time, aggressive anti-inflammatory treatments and physical therapy, so-called active rest. A subset of individuals will not respond to the prescribed treatments and therefore be deemed surgical. The recommended procedure will be dictated by the patient's presenting symptoms in the context of the imaging study findings. The diagnosis of "disc herniation" by no means mandates surgery. In fact, only a minority of clinic patients with spinal pathology come to surgery.
Low back pain in isolation is nearly always treated non-surgically except in the rare case of an unstable fracture, mobile spondylolisthesis or cancer with vertebral involvement. Those individuals may benefit from fusion surgery (during which the bones of the spine are fused together with titanium hardware or "rods and screws"). The same rules apply for axial neck pain. It is ill-advised to undergo surgery primarily for neck or low back pain unless the pain generator has been definitively isolated. Outcomes otherwise are typically poor.
That said, neck or low back pain may be an associated symptom or harbinger of degenerative disease. Often, patients with a radicular syndrome or radiculopathy have axial pain. It may accompany arm or leg pain (sciatica) that results from compression of a nerve root. The resultant inflammation causes the sensation of shooting pain in the affected extremity. A cervical radiculopathy is associated with arm pain, motor (weakness) or sensory loss (numbness). That affecting the low back (lumbar radiculopathy) is associated with lower extremity symptomatology. Both lumbar are cervical radicular syndromes are usually caused by an inflammatory condition known as spondylosis (arthritis or degenerative disease) which encompasses those all-too-often-heard words of coffee table discussions: "disc bulges," "herniations," "stenosis," "facet disease." You get the picture. And guess what? The mechanism by which they produce symptoms is exactly the same: pressure on adjacent neural structures (nerves). Said pressure causes an inflammatory response within the nerve which sends pain signals via the spinal cord to the brain. So while the leg or arm may hurt, the offending pathology is in the spine. Leg pain or arm pain, the difference is simply a matter of geography. The treatment is identical however.
Aggressive anti-inflammatory treatments and active rest (under the supervision of a trained professional) are the first-line measures. In the absence of worsening pain, such non-surgical options are continued. Natural history studies suggest that in the majority of cases, symptoms will improve and eventually resolve given time. Ever hear the saying, "Time heals all wounds"? It applies here as well. For those patients with refractory pain or progressive neurologic deficit, surgery is an option. Whether surgery is performed to address radiculopathy (nerve root problem) or myelopathy (spinal cord dysfunction), the principle is the same (go figure): alleviate pressure on (or decompress) the affected structure (nerve or spinal cord). How? Through various procedures with fancy names such as "laminotomy," "laminectomy," or "anterior cervical decompression and fusion." No matter. They all accomplish the same thing. Some of the described procedures require adjuvant fusion ("screws and rods"), adding complexity to the operation. Typically, these too are well-tolerated despite their more extensive nature.
Dr. Osborn has performed over 1,000 major spine operations and is also well-versed in the nonsurgical management of cervical and lumbar radicular syndromes and low back pain. In addition to elective spine procedures for degenerative disease, he routinely performs stabilization procedures in the context of trauma. All spine procedures are performed in a hospital setting, except injections and dorsal column stimulator trials (both falling under the guise of pain management). These are performed in an office-based operating suite under fluoroscopic guidance.
- Anterior Cervical Discectomy and Fusion (ACDF)
- Cervical Laminectomy +/- Lateral Mass Fusion
- Dorsal Column Stimulation (trial and permanent implantation)
- Interspinous Fusion
- Lumbar Laminectomy
- Lumbar Hemilaminotomy
- Lumbar Microdiscectomy
- Lumbar epidural steroid injections and facet blocks
- Posterior Lumbar Interbody Fusion (PLIF)
- Transforaminal Lumbar Interbody Fusion (TLIF)
It's your most precious asset. The most complex computer in the universe. In the confines of your rigid skull, this gelatinous collection of a-billion-plus neurons resides. Comprised predominantly of fat (which ensheaths the neurons or nerve cells), your brain is subject to oxidative stress and free-radical damage like other bodily organs. Similarly the brain degenerates, plain and simple. Functionally, it falters over time. Memory and coordination become impaired. Cognition slows. Often times the body follows suit. Disease sets in.
But you can do something about the degenerative process before it starts. Caring for your brain is no different than that for other areas of the body. All age-related diseases have common underpinnings, right? Take exercise for example. We're all aware of the beneficial effects exercise has on one's heart. Your brain benefits from exercise as well however. Physiologically, mechanistically and structurally, it is no way related to muscle. But it can be worked as muscle is worked during exercise.
Exercise forges neural pathways in the brain. Let's face it, there is a component of learning in exercise. As you learn to write with your left hand for example, you learn to properly execute a squat. The process of learning literally rewires the brain. That's why it takes time. You cannot master the squat overnight. Why? The brain has to change. Neuronal connections or "synapses" are formed through very complex biophysical mechanisms under the influence of growth factors such as NGF (nerve growth factor) and BDNF (brain-derived neurotrophic factor). These exert anti-inflammatory effects on the brain and by virtue, reverse age-associated spatial memory loss and enhance learning. NGF and BDNF also act as free-radical scavengers.
But don't wait until you develop Alzheimer's dementia to start exercising. Start now! Increased physical activity is protective of the brain as it prevents the progression of age-related brain atrophy. And this is not only inclusive of the brain memory centers, but of every region of the brain. Yes, neuronal death is inhibited by physical activity. This too is likely a function of stimulated expression of nerve growth factors. There is also recent evidence that the augmented blood flow to the brain during exercise promotes neurogenesis. Exercise can enhance both your learning abilities and memory!
How else can you turbo charge your brain? In addition to following an anti-inflammatory diet rich in green vegetables, omega-3 and omega-9 fatty acids, supplementing aggressively with anti-oxidant and anti-inflammatory agents, practicing stress relief and strength training, one could learn a new skill (like a properly executed squat or deadlift). Or what about a new language? Try holding your fork in your non-dominant hand. Can you juggle three balls? No? Well then learn. Switch on those genes that regulate neurogenesis (the formation of new neurons) and the synthesis of the aforementioned "neurotrophins," which happen to overlap with those associated with health and longevity. Yes, you are in control, not the genes as was once thought!
Health and longevity are associated with optimal gene expression. "Show your genes" the proper stimuli (with sound nutrition and exercise for example) to avoid illness. Fail to do so and age-related disease sets in. This includes atherosclerotic heart disease, osteoporosis, degenerative disease of the spine, dementia and even cancer.
We are exposing our DNA to environmental toxins (in many forms) and guess what? Mutations form. Mutations in tumor suppressor genes. These protective genes normally function is a variety of ways to assure that cells with mutated DNA (from a spontaneous event, UV radiation, etc.) do not divide or reproduce. But when these suppressor genes are mutated, our cells in essence have lost their guardians. Mutations in the p53 suppressor gene, for example, are associated with various types of cancers, namely breast, colorectal, liver lung and ovarian cancers.
As a neurosurgeon, I often treat the lethal brain cancer known as glioblastoma multiforme, also associated with a p53 mutation. Sadly, by the time these patients present to the hospital with symptoms such as headache and weakness, their very aggressive tumors have infiltrated large areas of the brain, limiting the efficacy of even the best treatment options. It is of utmost importance therefore that we detect such tumors earlier or better yet, prevent them, in light of their environmental origin. Easier said than done, unfortunately. It takes just a single cancer cell to slip through the body's robust surveillance system and wreak havoc.
Malignant brain tumors, whether primary (from the brain) or secondary (metastatic or from remote areas of the body), are generally treated with open surgery. Surgery is performed for three reasons (and three reasons only):
- To establish diagnosis: In order to render appropriate treatment postoperatively, your medical team must have a histologic (tissue or cellular) diagnosis. This is obtained only by physically sampling the tumor tissue. The diagnosis carries with it a specific prognosis (prospect of recovery).
- To alleviate neurologic deficit: Patients will often come to medical attention by virtue of signs/symptoms referable to the area of the brain in which the tumor resides. For example, if the mass lies within (or adjacent to) the motor cortex, one may present with weakness on one side of the body. Similarly, one may have sensory loss (numbness or pins and needles) or visual disturbances. Other more general symptoms may include headaches, nausea, vomiting or seizures.
- In order to potentially remedy or reduce the severity of the presenting neurological symptoms, surgeons resect as much of the tumor as is deemed safe. In general, tumors that are highly invasive (and are overtly malignant radiographically) will not be resected in favor of the less invasive stereotactic biopsy. Surgical resection in such cases does not confer any survival benefit and may in fact, be neurologically devastating to the patient. That said, those tumors that are amenable to resection, should be approached in an aggressive manner, as gross total resection (> 95% removal of tumor volume) is typically associated with a more favorable prognosis, oncologically speaking.
- To reduce tumor burden: In the context of what was stated above, the greater the tumor volume safely resected, the more favorable the outcome (time until disease progression or recurrence, survivability, etc.). This is related to the reduction in so called "mass effect" on adjacent brain (as discussed above) and the so-called "cytoreduction" (reduction in the quantity or volume of tumor cells). Make sense, right? Logic would dictate that the less resident tumor cells, the better.
- The same rules apply for benign tumors of the brain and tumors of the spine. Those of the spine are treated via a laminectomy (discussed elsewhere) and microsurgical resection. Relatively speaking, spinal tumors are less common than those of the brain.
The most common brain tumors are metastatic in nature or those from elsewhere in the body. These comprise slightly more than half of brain tumors seen clinically. In the U.S., the annual incidence of new cases of metastases is > 100,000, compared to 17,000 for primary brain tumors (those originating from the brain). The most common source of metastatic disease to the brain is the lung (bronchogenic carcinoma). Breast cancer is high on the differential in women as well.
Primary brain tumors originate from neuroepithelial tissue and have complex names which, for the most part, bespeak their cell of origin. They are benign and malignant subtypes. As stated above, the most common primary brain tumor is glioblastoma multiforme (GBM), unfortunately the most aggressive of all tumor types. Treatment (in amenable cases) consists of surgical resection followed by adjuvant chemotherapy and radiation (XRT). Metastatic tumors, in the case of solitary lesions, are often treated with surgery followed by XRT (which may involve whole brain radiation). In some cases, stereotactic radiosurgery (SRS) of focused-beam radiation is recommended. Tumors of lower grade (and subtype) are often treated surgically, but may not warrant postoperative chemotherapy or radiation.
Such is the case with the vast majority of meningiomas that originate from the covering of the brain. These tumors are nearly always histologically benign and account for approximately 15% of primary intracranial neoplasms. Patients typically present with headaches, seizures or symptoms referable to the area of the brain affected (compressed) by the mass. Surgical resection is the mainstay of treatment in symptomatic patients. Sometimes, because of their indolent growth rates, these tumors (if found incidentally) are managed expectantly with observation. The diagnosis of a meningioma does not necessarily commit one to surgery.
Should you require surgery for any type of brain tumor, Dr. Osborn will perform a craniotomy. This involves making a small opening in the skull through which the tumor is removed. This is typically performed under magnification (either with loupes or a microscope). Future treatments will be dictated by the type of tumor (determined by the pathologist) and the extent of surgical resection. You may require reoperative surgery in the event of recurrent or residual tumor. Chemotherapy or postoperative radiotherapy may be prescribed as well (depending upon the tumor histology).
In accordance with that stated previously, Dr. Osborn often prescribes these medications as adjuvants to traditional chemotherapies. Why? Well think about it. The genesis of age-related disease, including cancer, is free-radical damage to cellular structures within an inflammatory milieu under the influence of growth factors. Metformin (yes, the diabetic drug) tempers pancreatic release of insulin, a very potent growth factor. Aspirin reduces bodily inflammation, as does gancyclovir (indirectly). Interestingly, both aspirin and statin usage have an inverse relation with glioma (brain tumor) risk. Surprised? You shouldn't be, as BOTH have extremely robust anti-inflammatory properties.
Patients may also require placement of what is referred to as a shunt. Are you familiar with this term? It may conjure images of children with large heads due to over-accumulation of spinal fluid. Yes, congenital hydrocephalus is treated with CSF (cerebrospinal fluid) shunting or diversion of spinal fluid from the head to another bodily compartment, typically the abdomen. Same procedure, albeit applied to the adult population. Sometimes patients that have undergone tumor surgery will develop obstruction to the normal flow of spinal fluid with a resultant increase in intracranial pressure. Patients typically develop headache, nausea and vomiting, and may lapse into a coma if the "hydrocephalus" (accumulation of excessive spinal fluid) goes untreated. Shunt surgery typically takes less than 1 hour and involves the insertion of a silastic (silicone-plastic) catheter into the fluid spaces of the brain. The other end of the catheter (distal terminus) is placed into the abdominal cavity (where the fluid is diverted and absorbed by the large surface area of the peritoneum). Spinal fluid flow (from brain to abdomen) is regulated by a programmable valve that may be adjusted non-invasively (should it be deemed necessary postoperatively). Dr. Osborn is assisted by a general surgeon who performs the abdominal portion of the procedure laparoscopically. This minimizes incision size, postoperative pain and allows for more accurate placement of the catheter (in a region free of potentially obstructive fat).
The identical procedure is performed on aged patients who have been diagnosed with NPH or normal pressure hydrocephalus. Patients develop an accumulation of cerebrospinal fluid for reasons unknown. It is theorized that there is a blockage of CSF absorption (into the venous system of the body) or flow through the channels around the brainstem. 50% of the cases are identified in the wake of a remote infection (meningitis) or head injury. 50% are idiopathic (of unknown cause or etiology). Is there an occult predisposing inflammatory process at hand similar to other age-related diseases? This remains unclear. Regardless of its cause, NPH is treated with CSF shunting as the accumulated fluid (under low or normal pressure) causes a cluster of potentially debilitating symptoms otherwise known as the "clinical triad of NPH": gait ataxia (imbalance), dementia (memory loss) and urinary incontinence (an inability to control one's urine).
The diagnosis of NPH may be somewhat elusive, as Parkinson's disease and Alzheimer's disease can cause similar symptoms. NPH is uniformly associated with early onset gait ataxia. This is the first symptom to appear and the most common complaint offered by patients. The dementing illness and the urinary symptoms manifest later, and are classically less responsive to surgical treatment (than is the gait dysfunction). Patients with Alzheimer's disease present with memory problems first and gait deterioration secondarily. Often they do not have the associated hydrocephalus of the NPH patient either. Accordingly, patients with Alzheimer's disease do not respond to shunting. The pathogenesis is not that of excess fluid accumulation within the brain (which is thought to cause stretching of critical brain structures). Alzheimer's disease is a neurodegenerative disease caused by free-radical damage/oxidative stress in the context of both insulin resistance (it is referred to as type III diabetes, right?) and inflammation. The treatment therefore is prevention.
A similar line of logic applies to concussions, as the pathogenesis of Alzheimer's disease and dementia pugilistica (the dementing illness brought to the forefront by the recent NFL lawsuits) are similar. Granted, the cause of the latter is more well-defined: serial impacts to the head, but the resultant changes seen in the brain (microscopically) bear striking resemblance to one another. Those in the Alzheimer's brain have been induced over long periods of time, while those in the serially head-injured, at a more accelerated rate. Concussive and sub-concussive impacts catalyze cascades of biochemical events akin to the degenerative disease of aging. Here's the kicker (pun intended): Football players are not old, chronologically speaking!
Dr. Osborn has been cited as an expert in nearly 100 publications in the wake of the recent media concussion frenzy. As an avid athlete, he is acutely aware of the inherent dangers of sport, particularly impact sports. Given this, he recommends baseline cognitive testing for all athletes engaged in such activities and yearly studies to track brain function (even in the absence of an interim concussion). The results of such tests help direct "return to play" (RTP) recommendations in head-injured patients as well. Erring on the side of caution is always the best policy as the brain is extremely sensitive to impact, particularly those structures that are responsible for memory. And even more so in children and adolescents.
It is imperative therefore that patients (many of whom are parents) are acutely aware not only of the signs and symptoms of a concussion (which include but are not limited to a transient loss of consciousness, confusion, headache, nausea and vomiting in the wake of a bodily impact), but also of the preventive measures that must be instituted to prevent concussion. Listed are some things you can do to reduce your chances of sustaining a concussion or alert you as to the severity of an impact:
- Protect your head with a well-fit helmet.
- Utilize accelerometer technology (i.e. Reebok Checklight) to help gauge the severity of the impact. The data can help formulate RTP decisions.
- Strengthen your neck musculature to dampen the ‘to and fro' movement of the head at time of impact. Remember, you don't have to sustain a direct blow to the head to experience a concussion, as the brain is accelerated and decelerated within the rigid confines of the skull (essentially rattling back and forth). How do you strengthen your neck? Weight train with basic movements. Skip the cardio. It offers NO benefit in this regard.
- In the case of organized sports, be sure that the coaching staff is well-versed in the management of concussion. This usually equates to formal training. imPACT testing (or a like test) is a must. Ask Dr. Osborn or his staff for details about this.
- You are not Superman. Err on the side of sitting the game out and not returning to play for at least several weeks in the event of a concussion. You may otherwise end up in a local emergency with far more serious injuries such as "second impact syndrome," subdural or epidural hematoma.
Dr. Osborn spends a large percentage of time evaluating trauma patients at St. Mary's Medical Center, a Level I trauma center in the heart of West Palm Beach. There, a talented multi-disciplinary team of surgeons are positioned to receive all incoming trauma from the north end of Palm Beach County. This includes, but is not limited to, victims of high-speed vehicular accidents, sports-related injuries, assault, gunshot wounds, and falls. A large percentage of these patients sustain injuries to the central nervous system (CNS) or the brain and spinal cord. The injuries range in severity from mild to severe and in the case of the former, may be managed non-operatively. Those with more serious, life-threatening injuries often times undergo immediate surgery. Typically this applies to those who have sustained head injuries.
Spinal cord injury is typically managed (surgically) in a more delayed manner after an MRI is obtained and in the case of cervical spine injury, alignment is restored with traction (if feasible). The goals of spinal surgery in the context of trauma are identical to those discussed previously: decompression of the neural elements (spinal cord and exiting nerve roots), reestablishment of spinal alignment and stabilization. The manner in which this is accomplished is dictated by the morphology of the injury (i.e. fracture) and surgeon preference. Volumes have been written on this topic. There are many different ways to skin a cat. Common to nearly all procedures however, is the stabilization (fusion) portion. Patients are typically maintained in a rigid brace for 6-12 weeks postoperatively during which time bony fusion is occurring. Those patients with significant neurologic deficit will concomitantly undergo inpatient rehabilitation.
Recovery rate. How quickly does one improve after sustaining a spinal cord injury? How much functional recovery can one expect? Two excellent questions.
The first: The rate of recovery from any neurologic insult is variable. It may take months or it may be years.
Rule: Younger individuals recover more quickly than older individuals. This phenomenon is likely multifactorial in etiology but undoubtedly related to the more robust vascular supply of a younger individual (less age-related atherosclerotic disease, right?). The more tenuous the blood supply to a structure (i.e., skin, brain or spinal cord) the less likely it is to recover from an injury or to heal.
And the second: The extent of recovery from a spinal cord injury is dependent on the severity of the injury. A "complete" injury or one with complete less of motor, sensory and sacral function (bowel/bladder control and perianal sensation) below the injured level (for > 24 hours) indicates that no distal function will recover. Patients with "incomplete" injuries have residual motor and sensory function below the injured level. In the context of that stated above, these patients tend to fare much better than those with complete injuries. In fact, many return to a normal lifestyle with minimal injury sequelae.
The same can be said about head injuries. Outcome is a direct correlate of injury severity. Head injuries range from mild to severe. A concussion (discussed above) is considered a mild traumatic brain injury (TBI). Typically with adequate rest (and absent repeat injury), patients will return to a normal lifestyle although many suffer from post-concussive syndrome: chronic headache, dizziness, memory loss, inattentiveness, emotional lability and disruption of the sleep/wake cycle. Non-steroidal anti-inflammatory medications, supplements such as omega-3 fatty acids and curcumin and targeted cognitive therapies are the mainstays of treatment.
Moderate to severe head injuries are associated with more prolonged loss of consciousness and neurologic deficit such as weakness of one side of the body, pupillary changes, eye deviation and abnormal reflexes, to name a few. These are clues as to the location of the insult (remember, the left side of the brain controls the right side of the body) that is ultimately confirmed by a CT scan of the brain. Also ascertained from the imaging study is specific type of pathology (discussed below), whether or not there is resultant "shifting" of the intracranial contents, the presence or absence of brain edema or swelling and the integrity of the calvarium (skull). Using the clinical and radiographic data, the neurosurgeon will formulate a treatment protocol. As with spine surgery, the goals of intervention are to alleviate pressure on the nervous tissue (brain in this case) as elevated intracranial pressure (ICP) can be lethal. The skull is similar to a closed box with a fixed volume. In response to an injury, the brain swells and ICP rises, compromising blood flow to the brain. The role of the neurosurgeon is to normalize perfusion (blood flow) to the brain by reducing intracranial pressure. This may entail inserting a drain (EVD) into the fluid spaces (ventricles) of the brain akin to the previously discussed "shunt" or surgically opening the skull (craniotomy) to evacuate a blood clot. Regardless, the goal is the same in the face of acute injury.
Neurosurgeons use fancy terms to describe various traumatic pathologies. In reality, most terms are nothing more than anatomical and structural descriptors.
- Hematoma: a collection of blood, plain and simple. Also sometimes referred to as a "clot."
- Subdural hematoma (SDH): a collection of blood located on the surface of the brain, underneath (or "sub") the dura, the leathery covering of the brain. Most often SDH are traumatic in origin but can occur spontaneously. The blood source is either the injured brain itself or what are known as "bridging veins" that are sheared/lacerated as a result of rapid acceleration/deceleration of the brain at time of impact.
- A subdural hematoma exerts pressure on the adjacent brain. If there is significant "mass effect" on the brain and resultant compromise of brain perfusion (elevations in intracranial pressure) or neurologic deficit, Dr. Osborn will typically intervene. The hematoma is drained either via "burr holes" or a "craniotomy."
- Epidural hematoma (EDH): a collection of blood located outside (or "epi") the dura, between it and the skull, often caused by laceration of a branch of the "middle meningeal artery". Typically there is an adjacent skull fracture. As the dura lines the inside of the skull, its resident arteries (branches of the middle meningeal) are susceptible to injury when the skull is fractured. Epidural hematomas usually occur in young adults and are associated with less severe brain injury than are acute subdural hematomas.
- Like their subdural counterpart, epidurals cause pressure-related damage to adjacent brain structures and a often treated surgically, particularly in the context of a depressed skull fracture (discussed below). Epidural hematomas, if deemed surgical, are uniformly treated with a craniotomy.
- Subarachnoid hemorrhage: The most common cause of subarachnoid hemorrhage is trauma, not a brain aneurysm. Subarachnoid hemorrhage is bleeding under the "arachnoid", the membrane of the brain that is under close approximation to the cortical surface of the brain. It is a very common radiographic finding in the wake of even mild head injuries. Subarachnoid hemorrhage in this setting is uniformly nonsurgical unless there is associated hydrocephalus (from disruption of the normal cerebrospinal fluid flow). This is rare however and much more often associated with aneurysmal subarachnoid hemorrhage.
- Aneurysm: What respectable neurosurgeon would exclude this from the discussion? An "aneurysm" is an outpouching in the wall of a blood vessel (due to a weakening in its muscular layer that is either congenital or degenerative in nature). Major risk factors for aneurysm formation are cigarette smoking and hypertension. Ruptured aneurysms leak into the subarachnoid space under high pressure (as the bleeding is arterial in origin), often times spilling large quantities of blood into a relatively small space. Intracranial pressure rises rapidly and many patients (10-15%) succumb prior to their arrival at a medical facility. Those that do survive the initial hemorrhage either undergo endovascular (catheter-based treatment) repair of the aneurysm (with "coils") or surgical "clipping". Endovascular technology is advancing at a breakneck pace and will ultimately supplant open surgery for intracranial aneurysms. A similar phenomenon occurred with the advent of laparoscopic surgery.
- Contusion: A bruise. Yes, your brain can be bruised just like any other area of the body as a result of an impact. Often managed non-operatively, isolated contusions tend to enlarge within the first 24-48 hours (30-40% of patients). Contusions may be identified on CT scan in conjunction with a subdural hematoma and can contribute to elevations in intracranial pressure (as they too are space-occupying, right?).
- Depressed skull fracture: Conjure up an image a smashed skull. A depressed fracture of the skull is a break in a cranial bone with depression of the bone in toward the brain. This may be the result of a blunt impact of missile injury (gunshot wound). Many cases are managed non-operatively. Indications for surgery (elevation of the fracture): neurologic deficit related to underlying brain, spinal fluid leak (in the case of an "open fracture" or that associated with an overlying scalp laceration), cosmesis (if the fracture is located in the frontal (forehead) region).
In the United States, more than 50,000 deaths occur annually due to traumatic brain injury. The brains of those that survive the insult experience a form of accelerated aging. Changes seen in the brains of TBI patients are similar to those seen in the brains of the severely demented. In fact, moderate and severe head injury is associated with a 2.3 and 4.5 times increased risk of Alzheimer's disease (respectively). And for this we have no cure.
As with Alzheimer's disease, risk factor modification is critical. Did you know that more than 85 percent of all TBIs are preventable? Did you know that over half of all brain injuries are related to alcohol and drug abuse? Did you know that seat belts are 57 percent effective in preventing traumatic and fatal brain injuries? Did you know that properly fitted helmets reduce the risk of brain injuries by 88 percent? Neglecting to wear your helmet and seatbelt therefore are risk factors for TBI.
Then apply a similar philosophy to age-related, non-communicable disease or NCD (inclusive of, but not limited to cardiovascular disease, type II diabetes and cancer), by far the leading cause of death in the world, and you'll be way ahead of the game.