Increased availability and greater access to  medical imaging  has caused a rising number of asymptomatic, unruptured cerebral aneurysms to be  discovered incidentally  during medical imaging investigations. [ 47 ]  Unruptured aneurysms may be managed by  endovascular  clipping or stenting. For those subjects that underwent follow-up for the unruptured aneurysm,  computed tomography angiography  (CTA) or  magnetic resonance angiography  (MRA) of the brain can be done yearly. [ 48 ]  Recently, an increasing number of aneurysm features have been evaluated in their ability to predict aneurysm rupture status, including aneurysm height, aspect ratio, height-to-width ratio, inflow angle, deviations from ideal spherical or elliptical forms, and  radiomics  morphological features. [ 49 ]


The  prevalence  of intracranial aneurysm is about 1–5% (10 million to 12 million persons in the United States) and the  incidence  is 1 per 10,000 persons per year in the United States (approximately 27,000), with 30- to 60-year-olds being the age group most affected. [ 10 ] [ 20 ]  Intracranial aneurysms occur more in women, by a ratio of 3 to 2, and are rarely seen in pediatric populations. [ 10 ] [ 17 ]


Cerebral angiography  is a form of  angiography  which provides images of blood vessels in and around the brain, thereby allowing detection of abnormalities such as  arteriovenous malformations  and  aneurysms . [ 1 ]
It was pioneered in 1927 by the Portuguese neurologist  Egas Moniz  at the  University of Lisbon , who also helped develop  thorotrast  for use in the procedure. [ 2 ]


Typically a  catheter  is inserted into a large artery (such as the  femoral artery ) and threaded through the circulatory system to the  carotid artery , where a  contrast agent  is injected.  A series of  radiographs  are taken as the contrast agent spreads through the brain's arterial system, then a second series as it reaches the venous system.


For some applications, [ citation needed ]  cerebral angiography may yield better images than less invasive methods such as  computed tomography angiography  and  magnetic resonance angiography .
In addition, cerebral angiography allows certain treatments to be performed immediately, based on its findings. In recent decades, cerebral angiography has so assumed a therapeutic connotation thanks to the elaboration of endovascular therapeutic techniques. Embolization (a minimally invasive surgical technique) over time has played an increasingly significant role in the multimodal treatment of cerebral MAVs, facilitating subsequent microsurgical or radiosurgical treatment. [ 3 ] [ 4 ]  Another type of treatment possible by angiography (if the images reveal an aneurysm) is the introduction of metal coils through the catheter already in place and maneuvered to the site of aneurysm; over time these coils encourage formation of  connective tissue  at the site, strengthening the vessel walls. [ 5 ] [ 6 ]


In some jurisdictions, cerebral angiography is required to confirm  brain death . [ citation needed ]


Prior to the advent of modern neuroimaging techniques such as  MRI  and  CT  in the mid-1970s, cerebral angiographies were frequently employed as a tool to infer the existence and location of certain kinds of lesions and hematomas by looking for secondary vascular displacement caused by the  mass effect  related to these medical conditions. This use of angiography as an  indirect  assessment tool is nowadays obsolete as modern non-invasive diagnostic methods are available to image many kinds of primary intracranial abnormalities directly. [ 7 ]  It is still widely used however for evaluating various types of vascular pathologies within the skull.


Cerebral angiography is used for diagnosis but may be followed by treatment procedures in the same setting. [ 8 ]  Cerebral angiography is used to image various intracranial (within the head) or extracranial (outside the head) diseases. [ 8 ]


Intracranial diseases are: non-traumatic  subarachnoid haemorrhage , non-traumatic  intracerebral haemorrhage ,  intracranial aneurysm ,  stroke ,  cerebral vasospasm ,  cerebral arteriovenous malformation  (for Spetzler-Martin grading and plan for intervention),  dural arteriovenous fistula ,  embolisation  of brain tumours such as  meningioma ,  cavernous sinus haemangioma , for  Wada test , and to obtain haemodynamics of cerebral blood flow such as cross flow, circulation time, and collateral flow. [ 8 ] [ 9 ]


Extracranial diseases are:  Subclavian steal syndrome , rupture of the carotid artery,  carotid artery stenosis , cervical spine trauma,  epistaxis  (nose bleeding) and plan for embolisation of  juvenile nasopharyngeal angiofibroma  before operation. [ 8 ] [ 9 ]


Although  computed tomography angiography  (CTA) and  Magnetic resonance angiography  (MRA) has been used widely in evaluation of intracranial disease, cerebral angiography provides higher resolution on the conditions of blood vessel lumens and vasculature. [ 10 ]  Cerebral angiography is also the standard of detecting intracranial aneurysm and evaluating the feasibility of  endovascular coiling . [ 11 ]  Performing a cerebral angiogram by gaining access through the femoral artery or radial artery is feasible in order to treat cerebral aneurysms with a number of devices [ 12 ]


Certain conditions such as contrast allergy, renal insufficiency, and coagulation disorders are contraindicated in this procedure. [ 8 ]


Before the procedure, focused history and neurological examination is performed, available imaging, and blood parameters are reviewed. [ 9 ]  When reviewing imaging, arch anatomy and variants are evaluated to select suitable catheters to assess the vessels.  Complete blood count  is reviewed to ensure adequate amount of  haemoglobin  in subject's body, and to rule out the presence of  sepsis . Serum  creatinine  is assessed to rule out renal dysfunction. Meanwhile,  prothrombin time  is assessed to rule out  coagulopathy . [ 8 ]  Informed consent regarding the risks of the procedure is taken. [ 9 ]  Anticoagulants are withheld if possible. [ 9 ]  Fasting is required 6 hours before the procedure and insulin requirement is reduced by half for those diabetics who are fasting. [ 9 ]  Bilateral  groins  (for  femoral artery  access) and left arm/forearm (for  brachial artery / radial artery  access) are prepared. Neurological status of the patient before  sedation  or  anesthesia  is recorded. [ 8 ]


Sedation drug such as  intravenous   midazolam  and  painkiller  such as  fentanyl  can be used if the subject is restless or painful. The subject is then lie down on supine position with arm at the sides. Uncooperative subjects may have their forehead tapped to reduce motion. The subject is advised to stay as still as possible especially when  fluoroscopy  images are taken. The subject is also advised to avoid swallowing when images of neck are taken. These measures are taken to reduce motion artifact in the images. [ 8 ]


Right common  femoral artery  (RFA) is the preferred site of access. If RFA access is not optimal, then brachial artery access is chosen. Either a micropuncture system or an 18G access needle can be used with or without ultrasound guidance. There are four types of catheters that can be used: angled vertebral catheter for usual cases, Judkins right coronary catheter (Terumo) for tourtous vessels, Simmons's catheter and Mani's head hunter catheter (Terumo) for extremely tortous vessels. A 5Fr sheath is also placed within and flushed with heparinised saline to prevent clotting around the sheath. [ 8 ]  In terms of guidewire, Terumo hydrophilic Glidewire 0.035 inches can be used. [ 8 ]


To prevent  embolism  (either due to blood clot or  air embolism , "double flush" and "wet connect" techniques are used. [ 8 ]  In "double flush" technique, a saline syringe is used to  aspirate  blood from the catheter. Then, a second heparinised saline syringe is used to flush the catheter. [ 13 ]  "Wet connect" is the technique that connects syringe to a sheath without air bubbles within. [ 8 ]


Digital subtraction angiography  is the main technique of imaging the cerebral blood vessels. Catheter should be advanced over the guidewire. Rotating the catheter during advancement is also helpful. Roadmap (superimposing previous image on live  fluoroscopic  image) is used to advance catheters or guidewires before any vessel bifurcation can help to prevent vessel  dissection . [ 8 ]  After the catheter is in position, guidewire is removed slowly with heparinised saline dripping into the catheter at the same time to prevent air embolism. Prior to contrast injection, backflow of the catheter should be established to ensure there is no wedging, dissection, or intracatheter clotting. During the catheterisation of  vertebral artery , extra care should be taken to prevent vessel dissection or vasospasm. Delayed or incomplete contrast washout may indicate vasospasm or dissection. [ 8 ]


Cervical arch angiogram is taken if there is any suspicion of  aortic arch  narrowing, or any anatomical variants such as bovine arch ( brachiocephalic trunk  shares a common origin with left  common carotid artery ). If such abnormality is present, it results it difficulty in  cannulation  of the main branches of the aortic arch. [ 8 ]  The catheter of choice to cannulate this area is pigtail catheter with multiple side holes. Contrast injection rate of 20 to 25ml/sec is given with total volume of 40 to 50 ml of contrast. The frame rate of fluoroscopy is 4 to 6 frames per second. [ 8 ]  The image is taken in with the x-ray tube in left anterior oblique position. [ 8 ]


To image the vessels of the neck such as common carotid, internal and external carotid arteries, AP, lateral, and 45 degrees bilateral oblique positions are taken. Contrast injection rate is 3 to 4 ml/sec with total volume of 7 to 9 ml. The frame rate of fluoroscopy is 3 to 4 frames/sec. [ 8 ]


To image the anterior cerebral circulation such as internal and external carotid arteries and its branches, AP, Towne's and lateral views are taken. [ 8 ]  The petrous part of the  temporal bone  should be superimposed at the mid or lower orbits when taking the AP/Towne's view. Contrast injection rate is 6 to 7 ml/sec with total volume of contrast at 10 ml. [ 8 ] [ 9 ]  The frame rate of fluoroscopy is 2 to 4 frames/sec. [ 8 ]  Neck extension can help to navigate into tortous cerival part of the  internal carotid artery . [ 14 ] [ 15 ]


At the level of carotid bifurcation, AP and oblique images are taken. At the cavernous (C4) and ophthalmic segments (C6) of the internal carotid artery, Caldwell and lateral views are taken. [ 8 ]  At the supraclinoid segment (C5-clinoid, C6-ophthalmic, and C7-bifurcation to  posterior communicating artery  (PCOM) segments), AP view is used to access the terminal branches such as  anterior cerebral artery  (ACA),  middle cerebral artery  (MCA) while oblique view (25 to 35 degrees) is used to access the ACA,  anterior communicating artery  (ACOM), and MCA bifurcations. [ 8 ]  Lateral view is useful to visualise the PCOM while submentovertical view is useful to project ACOM above the nasal cavity, thus making it easier to access the anatomy of ACOM. Transorbital oblique view is useful to access the MCA anatomy. [ 8 ]


The anatomy of external carotid artery is access via AP and lateral views. [ 8 ]


To image the posterior circulation, such as vertebral and basilar arteries, AP, Towne's view, lateral projections near the back of the head and upper part of the neck is taken. In this case, petrous bone should be projected at the bottom or below the orbits to visualise the  basilar artery  and its branches in AP/Towne's view. The rate of injection is 3 to 5 ml/sec, for a total of 8ml. The fluoroscope will be catching images at a rate of 2 to 4 frames per second. [ 8 ]   Posterior cerebral artery  (PCA) can be seen in AP view. [ 8 ]  The left vertebral artery is easier to cannulate than the right vertebral because of the straightforward anatomy of the left vertebral artery. [ 16 ]


Any activation of primary collateral system (ACOM and PCOM arteries) or secondary collateral system (pial-pial and leptomeningeal-dural) in case of occlusion of internal carotid artery should also be documented. [ 8 ] [ 17 ]  Leptomeningeal collaterals or pial collaterals are the small arterial connections that join the terminal branches of ACAs, MCAs, and PCAs on the surface of the brain. [ 18 ]


Manual compression or percutaneous closure device can be used to stop the bleeding from common femoral artery. Groin  haematoma  should be monitored during  intensive care unit  (ICU) monitoring. The puncture should be immobilised (to prevent movement) for 24 hours post puncture. [ 8 ]  Neurological examination should be performed and new neurological deficit should be documented. Significant neurological changes should be evaluated with MRI scan or a repeat cerebral angiography to rule out acute stroke or vessel dissection. Painkiller should be administered if there is any puncture site pain. [ 8 ]


The most common complication is groin haematoma which occurs in 4% of those affected. Neurologic complications such as  transient ischemic attack  in 2.5% of the cases. There is also the risk of stroke with permanent neurological defect in 0.1% of the cases and may lead to death in 0.06%. [ 8 ]  Rarely, 0.3 to 1% of the cases experience cortical blindness from 3 minutes to 12 hours after the procedure. It is a condition where those affected experienced loss of vision with normal  pupillary light reflex , and normal  extraocular muscles  movement. The condition can sometimes be accompanied by headaches, mental state changes, and memory losses. [ 19 ]


Some risk factors of complications are if the subject is having  subarachnoid haemorrhage , atherosclerotic cerebrovascular disease, frequent transient ischemic attacks, age more than 55 years, and poorly controlled diabetes. Besides, longer procedures, increased in number of catheter exchanges, and the use of larger size of catheters also increases the risk of complications. [ 8 ]


In 1896, E. Haschek and O.T. Lindenthal in Vienna, Austria, reported angiography of blood vessels by taking a series of X-rays after injecting a mixture of petroleum, quicklime, and mercuric sulfide into the hand of a cadaver. [ 1 ]


Cerebral angiography was first described by  Egas Moniz , a Portuguese physician and politician, in 1927. He performed this procedure on six patients. Two developed  Horner's syndrome  due to leaking of contrast material around the carotid artery, one developed temporary  aphasia , and another died due to thromboembolism to the anterior circulation of the brain. [ 20 ]


Prior to the 1970s the typical technique involved a needle puncture directly into the carotid artery, [ 21 ] [ 22 ]  as depicted in the 1973 horror film  The Exorcist , [ 23 ]  which was replaced by the current method of threading a catheter from a distant artery due to common complications caused by trauma to the artery at the puncture site in the neck (particularly hematomas of the neck, with possible compromission of the airway). [ 24 ] [ 25 ]


Cerebral salt-wasting syndrome  ( CSWS ), also written  cerebral salt wasting syndrome , is a  rare   endocrine condition  featuring a  low blood sodium concentration  and  dehydration  in response to injury (trauma) or the presence of tumors in or surrounding the  brain . In this condition, the kidney is functioning normally but excreting excessive sodium. [ 1 ]  The condition was initially described in 1950. [ 2 ]  Its cause and management remain controversial. [ 3 ] [ 4 ]  In the current literature across several fields, including  neurology ,  neurosurgery ,  nephrology , and  critical care medicine , there is controversy over whether CSWS is a distinct condition, or a special form of  syndrome of inappropriate antidiuretic hormone secretion (SIADH) . [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ]


Signs and symptoms of CSWS include  large amounts of urination  (polyuria, defined as over three liters of urine output over 24 hours in an adult), high amounts of sodium in the urine, low blood sodium concentration, [ 1 ]   excessive thirst  (polydipsia), extreme  salt  cravings,  dysfunction of the autonomic nervous system  (dysautonomia), and  dehydration .  Patients often self-medicate by consuming high amounts of sodium and by dramatically increasing their water intake. Advanced symptoms include  muscle cramps , lightheadedness, dizziness or  vertigo , feelings of anxiety or panic,  increased heart rate  or  slowed heart rate ,  low blood pressure  and  orthostatic hypotension  which can result in  fainting . [ 12 ]  Other symptoms frequently associated with dysautonomia include  headaches ,  pallor ,  malaise , facial flushing,  constipation  or  diarrhea ,  nausea ,  acid reflux , visual disturbances, numbness,  nerve  pain,  trouble breathing , chest pain, loss of consciousness, and  seizures . [ 12 ]


Although the pathophysiology of CSWS is not fully understood, it is usually caused by neurological injury, most commonly  aneurysmal   subarachnoid hemorrhage . [ 5 ]  It is also reported after surgery for pituitary tumor, acoustic neuroma,  calvarial  remodeling,  glioma  and with infections including  tuberculous meningitis ,  viral meningitis ,  metastatic carcinoma , and  cranial trauma . [ 5 ]


CSWS is a  diagnosis of exclusion  and may be difficult to distinguish from the  syndrome of inappropriate antidiuretic hormone  (SIADH), which develops under similar circumstances and also presents with hyponatremia. [ 1 ]  The main clinical difference is that of total fluid status of the patient: CSWS leads to a relative or overt  low blood volume [ 3 ]  whereas SIADH is consistent with a normal or high blood volume (due to water reabsorption via the V2 receptor). [ 1 ]  If blood-sodium levels increase when fluids are restricted, SIADH is more likely. [ 13 ]  Additionally, urine output is classically low in SIADH and elevated in CSWS. [ 1 ]


While CSWS usually appears within the first week after brain injury and spontaneously resolves in 2–4 weeks, it can sometimes last for months or years. In contrast to the use of fluid restriction to treat SIADH, CSWS is treated by replacing the urinary losses of water and sodium with hydration and sodium replacement. [ 1 ]  The  mineralocorticoid  medication  fludrocortisone  can also improve the low sodium level. [ 1 ] [ 14 ]


In 1858,  Claude Bernard  first raised the possibility of a direct relationship between the central nervous system and renal excretion of osmotically active solutes. He found that a unilateral lesion in the reticular substance at the floor of the fourth ventricle produced a diuresis of chloride, but not glucose. Bernard reproduced this syndrome through renal denervation. [ 15 ]  Through medullary lesioning in animals, Jungmann and Meyer from Germany induced polyuria and increased urinary salt excretion in 1913. Water intake restriction did not stop the polyuria, and salt continued to be excreted in the urine despite. [ 16 ]  In 1936, McCance defined the consequences of salt depletion in normal human. Patients with extra-renal salt losses complicated by hyponatremia were found to be common-place, and consistent with McCance's description, they excreted urine virtually free of sodium. [ 17 ]


Shortly after World War II, the  flame photometer  was developed. The availability of the flame photometer made clinical determinations of the serum sodium concentration possible. Berry, Barnes and Richardson shared the production of this new device to measure sodium and potassium in solution of biological materials by means of the flame photometer in 1945. [ 18 ] [ 19 ] [ 20 ]  Yale was one of the first medical centers to have that new device, the flame photometer, so some of the first published observations about hyponatremia came from Yale. [ 21 ]


Almost a century after the pioneering work of Bernard in animals, Peters et al., in 1950, reported three patients seen at Yale New Haven Hospital with hyponatremia associated with varying cerebral pathologies and severe dehydration. In each patient, urine sodium losses persisted despite hyponatremia and a high-salt diet. All three patients were unable to prevent urinary sodium loss despite low serum sodium levels and no evidence of extrarenal sodium loss. Their hyponatremia responded to salt therapy. They postulated that this provided evidence of an extra-pituitary cerebral structure mediating normal sodium metabolism but were unsure of its location or mechanism of action. A subsequent paper from the group at Yale attributed hyponatremia in neurologic disease to SIADH. [ 22 ]


The normal regulatory mechanism of renal adjustment of salt and water balance was better understood in 1950s. The responsibility for the maintenance of a normal volume and tonicity of the body fluids devolves on the kidneys. This modern concept of renal physiology described the transformation of a large volume of glomerular filtrate to a much smaller volume of bladder urine which has been altered. The proximal portion of renal tubule is largely responsible for the decrease in volume of the filtrate and, to less extent, for alterations in composition. However, it is in the distal tubule that induced fine adjustment of water and sodium balance. [ 23 ]  In 1953, Leaf et al., demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain. This was not "salt wasting"; it was a physiologic response to an expanded intravascular volume. Vasopressin-ADH administration to normal humans was shown to result in water retention and urinary loss of electrolytes (primarily sodium) in other studies at the time. [ 24 ]


The term "cerebral salt wasting" (CSW) was coined by Cort in 1954. The title of a paper by Cort describing a patient with a thalamic glioma resulting in hydrocephalus and raised intracranial pressure (although it is prudent to note that the earlier-described work by Peters, Welt and colleagues in 1950 was presented in a paper entitled "A salt-wasting syndrome associated with cerebral disease"). This patient was hyponatremic and clinically dehydrated with initial salt therapy not reversing this. Salt restriction resulted in ongoing natriuria. Recommencement of salt therapy subsequently increased serum sodium. Treatment with adrenocorticotropic hormone (ACTH) and deoxycortone acetate (having potent mineralocorticoid activity) had no effect. The author postulated an external influence on renal function not adrenal or pituitary in origin. Unfortunately, the patient died three and a half weeks later in "circulatory failure with terminal shock". At autopsy, the pituitary and adrenal glands were normal. Given Bernard's ability to create a chloride diuresis without glycosuria though renal denervation, Cort postulated the existence of a neuronal connection between the hypothalamus and proximal tubule of the kidney influencing electrolyte reabsorption. In all above-described cases, there was evidence of hyponatremia and dehydration. In the ensuing years, however, hyponatremia in cerebral pathology was described without clinical or laboratory evidence of dehydration. Renal and adrenal function appeared intact, but, unlike in the earlier case of "cerebral salt wasting" described by Cort, an increase in renal absorption and plasma concentration of sodium occurred with administration of ACTH and deoxycortone acetate. [ 25 ] [ 26 ]  A study on a 5-month-old female infant with diffuse cerebral damage and hyponatremia in 1957 suggested that on normal fluid intakes the child was unable to excrete solute-free water in a normal manner. This may represent the result of damage to the cerebral osmoreceptors as part of generalized brain damage. The data do not support the concept that the hyponatremia resulted from true salt-wasting, either cerebral or renal in mediation. If correction of such a state is desirable, the most useful therapeutic measure would appear to be limitation of the intake of fluid to slightly more than the amount needed to cover water expenditure from insensible losses, obligatory urine volume and growth requirements. [ 27 ]


The term "cerebral hyponatremia" was suggested in the work of Epstein, et al. 1961. Inappropriate release of endogenous vasopressin is probably responsible for hyponatremia in tuberculous meningitis. Inability to excrete water normally is also a feature of the salt wasting of certain hyponatremic patients with pulmonary tuberculosis. Similarly, it has been suggested that inappropriate release of vasopressin is the cause of hyponatremia and renal salt wasting in certain diseases, including bronchogenic carcinoma, cerebral injuries, and malformations. [ 28 ]


In 1981, Nelson et al. studied hyponatremia in neurosurgical patients, primarily subarachnoid hemorrhage, and found that isotopically measured blood volumes were contracted; he attributed this finding to cerebral salt wasting (CSW). Following these publications, the term "CSW" vanished from the literature for over two decades with hyponatremia in patients with cerebral pathology assumed to result from SIADH. Then, in 1981, a study of twelve neurosurgical patients mainly with SAH found ten to have decreased red blood cell mass, plasma volume, and total blood volume despite "fulfilling laboratory criteria" for SIADH. [ 29 ]  Other authors associated hyponatremia in subarachnoid hemorrhage with increased levels of natriuretic peptides, negative sodium balance, and low central venous pressure. [ 30 ] [ 31 ] [ 32 ]


A valid diagnosis of "salt wasting" requires evidence of inappropriate urinary salt losses and a reduced "effective arterial blood volume". Unfortunately, there is no gold standard to define inappropriate urinary sodium excretion. "Effective arterial blood volume" is a concept, not a measurable variable; in fact, we often define it clinically by looking at urine sodium excretion. [ 33 ]


William Schwartz  (1922–2009) attended Duke University after serving in the US Army in World War II. He observed that sulfanilamide increased excretion of sodium in patients with heart failure. This observation was the basis for the discovery and development of modern diuretic drugs.  Frederic Bartter  (1914–1983) worked on hormones affecting the kidney that led to the discovery of  syndrome of inappropriate antidiuretic hormone  (SIADH) in 1957 and Bartter syndrome in 1963. Schwartz-Bartter syndrome is named after these two scientists. The first reports of hyponatremia and renal sodium loss corrected by fluid restriction in patients with bronchogenic carcinoma were published by Bartter. At that time, no direct measurement of vasopressin was done. [ 34 ]


Clipping  is a  surgical procedure  performed to treat an  aneurysm . If the aneurysm is intracranial, a  craniotomy  is performed, and afterwards an  Elgiloy (Phynox)  or  titanium  Sugita clip is affixed around the aneurysm's neck.
Surgical clipping was introduced by  Walter Dandy  of the  Johns Hopkins Hospital  in 1937. It consists of performing a  craniotomy , exposing the aneurysm, and closing the base of the aneurysm with a clip chosen specifically for the site. The surgical technique has been modified and improved over the years. Surgical clipping has a lower rate of aneurysm recurrence after treatment. Titanium Aneurysm Clips are being used to clip aneurysms and the procedure is known as aneurysm clipping. [ 1 ]


ROSA  is a medical robotic technology, designed to minimize invasiveness of surgeries of the  central nervous system . ROSA robots assist health professionals during surgical procedures.


The ROSA technology, developed by the French company  Zimmer Biomet Robotics , is used in 120 hospitals across Europe, North America, Asia and the Middle East. [ 1 ]


The device allows frameless  stereotactic procedures  increasing accuracy  [ 2 ]  and reducing operative time. [ 3 ] [ 4 ]  It is especially effective for  SEEG ,  DBS , endoscopic procedures, brain tumor resection and pediatric surgery. [ 5 ] [ 6 ]


The ROSA device combines software for neurosurgical planning and navigation, with a robotic arm of high technology. [ 7 ]


The system was designed by  Zimmer Biomet Robotics  (Montpellier, France) and is currently used in Europe, North America, Asia and Australia. [ 8 ] [ 9 ]


Cordotomy  (or  chordotomy ) is a surgical procedure that disables selected  pain -conducting tracts in the  spinal cord , in order to achieve loss of  pain  and  temperature   perception . This procedure is commonly performed on patients experiencing severe pain due to  cancer  or other incurable diseases. Anterolateral cordotomy is effective for relieving unilateral, somatic  pain  while bilateral cordotomies may be required for visceral or bilateral pain.


Cordotomy is performed as for patients with severe intractable pain, usually but not always due to  cancer .  Being irreversible and relatively invasive, cordotomy is used exclusively for pain where treatment to level 3 of the  World Health Organization   pain ladder  (i.e., use of major opiates such as  morphine ) has proved inadequate. Cordotomy is especially indicated for pain due to  asbestos -related cancers such as  pleural  and  peritoneal mesothelioma .


Most cordotomies are now performed  percutaneously  with  fluoroscopic  or CT guidance while the patient is awake under  local anesthesia .  The  spinothalamic tract  is normally divided at the level C1-C2.


Open cordotomy, which requires a  laminectomy  (removal of part of one or more vertebrae), takes place under  general anaesthetic  and has a longer recovery time and a higher risk of side-effects including permanent weakness.  However, it is still sometimes used where percutaneous cordotomy is unfeasible, especially in children or other patients who are unable to co-operate.  In open cordotomy, a  thoracic  approach is normally used so that the spinal cord tracts controlling the breathing muscles are not put at risk.


Cordotomy can be highly effective in relieving pain, but there are significant side effects.  These include  dysesthesia  (abnormal sensation), [ 1 ]  urinary retention and (for bilateral cervical cordotomy) apnea during sleep ( acquired central hypoventilation syndrome ) caused by inadvertent division of the  reticulospinal tracts . [ 2 ]


Cordotomy was first performed in 1912 by the American Neurosurgeons, William Gibson Spiller (1863–1940) and Edward Martin (1859–1938). [ 3 ]   Due to the surgical risks, it remained a rare procedure until the percutaneous technique was developed in 1965. [ 4 ]   During the 1990s the procedure became less widely used, partly because medical pain-control options had improved, and partly due to concern about side-effects.  Nevertheless, it is still considered an effective treatment for severe pain.


A number of alternative surgical procedures have evolved in the 20th century. These include:


Commissural myelotomy , for bilateral pain arising from pelvic or abdominal malignancies  [ 5 ]


Punctate  or  limited midline myelotomy  for pelvic and abdominal visceral pain, [ 6 ] [ 7 ]


Other options for medically intractable pain which do not involve open surgery include implantation of an  intrathecal  pump (a  syringe driver  delivering medication into the space around the spinal cord) administering  local anaesthetics  and/or  opiates [ 8 ]


A  corpectomy   or  vertebrectomy  is a  surgical procedure  that involves removing all or part of the  vertebral body  ( Latin :  corpus vertebrae , hence the name corpectomy), usually as a way to decompress the  spinal cord  and nerves. Corpectomy is often performed in association with some form of  discectomy . [ 1 ]


When the vertebral body has been removed, the surgeon performs a  vertebral fusion . Because a space in the column remains from the surgery, it must be filled using a block of bone taken from the  pelvis  or one of the leg bones or with a manufactured component such as a cage. This  bone graft  holds the remaining vertebrae apart. As it heals, the vertebrae grow together and  fuse . [ 1 ]


Auscultation , a  medical neurological procedure , can be performed upon the skull to check for intracranial  bruits . Such a bruit may be found in such conditions as cerebral angioma, tumour of the  glomus jugulare ,  intracranial aneurysm ,  meningioma , occlusion of the internal carotid artery, or  increased intracranial pressure . [ citation needed ]


The following extract details a method of performing cranial auscultation:


A bruit should be listened for, in quiet surroundings, over the skull and eyeballs, the latter situation being the most favourable for hearing the softest ones. The patient should be asked to close both eyes gently and the stethoscope firmly applied over one eye. During auscultation the other eye should be opened as in this way there is considerable diminution of eyelid flutter, which may cause confusion if rhythmical. Auscultation is then carried out over the other eye in a similar manner. If a murmur is not readily heard the patient should be asked to hold his breath. Finally auscultation should be carried out over the  temporal fossæ  and  mastoid processes . [ 1 ]


The  CyberKnife  system is a  radiation therapy  device manufactured by  Accuray . The system is used to deliver  radiosurgery  for the treatment of  benign tumors ,  malignant tumors  and other medical conditions. [ 1 ]


The device consists of a small  linear accelerator  attached to a  robotic arm , along with an integrated  image guidance  system. During treatment, the image guidance system captures  3D images , tracks the movement of  tumors , and guides the robotic arm to accurately aim the treatment beam at the moving tumor. [ 2 ]


The system is designed for  stereotactic radiosurgery  (SRS) and stereotactic body  radiation therapy  (SBRT). The system is also used for select 3D conformal radiotherapy (3D-CRT) and  intensity modulated radiation therapy  (IMRT).


The development of the system began in 1989 with contributions from  John R. Adler , a surgeon at  Stanford University , and Peter and Russell Schonberg of Schonberg Radiation Corporation. [ 3 ]  This work expanded upon earlier efforts in the 1980s to adapt standard  linear accelerators  for  radiosurgery . The inaugural CyberKnife system was installed at Stanford University in 1991, receiving clearance for clinical investigation by the  U.S. Food and Drug Administration  (FDA) in 1994. Following extensive  clinical research , the FDA granted approval for the treatment of  intracranial tumors  in 1999 and for  tumors  throughout the body in 2001. Subsequently, Accuray has introduced seven CyberKnife System models, including the CyberKnife G3 System (2005), CyberKnife G4 System (2007), CyberKnife VSI System (2009), CyberKnife M6 System (2012), and CyberKnife S7 System (2020).


The system is used to treat  tumors  of the  pancreas ,  liver ,  prostate ,  spine , cancer of the  throat  and  brain , and  benign tumors .


In neurosurgery,  Dandy's point  is a common entry point for  occipital   burr hole . Originally described by  Walter Dandy  in 1918 as a way to perform ventriculography via occipital approach. [ 1 ] [ 2 ]  It is located 2 centimetres (0.79 in) lateral to the  midline  and 3 centimetres (1.2 in) above the  inion . The catheter tip is directed toward a point 2 cm above the glabella and passed to a distance of 4 to 5 cm or until CSF is encountered. [ 2 ] [ 3 ]


Decerebellate  rigidity is caused by a  lesion  in the  cerebellum . The function of the cerebellum is to coordinate  muscular  activity. Animals with decerebellate rigidity show  opisthotonus  with  thoracic limb  extension, flexion of the  pelvic limbs  rigidly extended.  Mentation  of decerebellate animals is generally adequate.


This article about a medical condition affecting the nervous system is a  stub . You can help Wikipedia by  expanding it .


Decerebration  is the elimination of cerebral brain function in an animal by removing the  cerebrum , cutting across the  brain stem , or severing certain arteries in the brain stem.


As a result, the animal loses certain reflexes that are integrated in different parts of the brain. Furthermore, the reflexes which are functional will be hyperreactive (and therefore very accentuated) due to the removal of inhibiting higher- brain centers (e.g. the facilitatory area of the  reticular formation  will not receive regulating input from  cerebellum ,  basal ganglia  and the  cortex ).


Decerebration describes the ligation along the neural axis in distinct parts of the brain in experimental animals. Generally:


Lower decerebration results in a "bulbospinal" animal: reflexes which are integrated within the spinal cord and medulla oblongata are functional, reflexes integrated in midbrain and cortex are absent.


With difference to decortication there is pontine transection, thus sparing of the VestibuloSpinal (VS) and ReticuloSpinal (RES). The involved tracts are the corticospinal and rubrospinal tract. Decerebration in humans tends to have a worse prognosis than decortication. [ 1 ]


The most obvious accentuation is seen in the tonic labyrinthine reflexes, the  otolithic organs  mediate input about the gravitational force exerted on the body and the labyrinthine reflex acts on the extensor muscles in order to resist this gravitational force. In an animal where the cortical areas or the midbrain have been "cut off" from the neural axis, this reflex is hyperactive and the animal will maximally extend all four limbs. This phenomenon is known as  decerebrate rigidity . In humans, true decerebrate rigidity is rare since the damage to the brain centers it might be caused by usually are lethal. However,  decorticate rigidity  can be caused by bleeding in the  internal capsule  which causes damage to  upper motor neurons . The symptoms of decorticate rigidity are flexion in the upper limbs and extension in the lower limbs.


A  discectomy  (also called open discectomy, if done through a 1/2 inch or larger skin opening) is the surgical removal of abnormal disc material that presses on a  nerve root  or the  spinal cord . The procedure involves removing a portion of an  intervertebral disc , which causes pain, weakness or numbness by stressing the spinal cord or radiating nerves. The traditional open discectomy, or Love's technique, was published by Ross and Love in 1971. Advances have produced visualization improvements to traditional discectomy procedures (e.g. microdiscectomy, an open discectomy using an external microscope typically done through a 1-inch or larger skin opening), or endoscopic discectomy (the scope passes internally and typically done through a 2 mm skin opening or larger, up to 12 mm). In conjunction with the traditional discectomy or microdiscectomy, a  laminotomy  is often involved to permit access to the intervertebral disc. Laminotomy means a significant amount of typically normal bone (the lamina) is removed from the vertebra, allowing the surgeon to better see and access the area of  disc herniation .


Small or ultra-small endoscopic discectomy (called Nano Endoscopic Discectomy) does not have internal cutting or bone removal and, due to the small size, is not called "open". These procedures do not cause post-laminectomy syndrome ( failed back syndrome ). [ 1 ] [ 2 ]


Microdiscectomy is a spine operation with a smaller incision than traditional discectomy, in which a portion of a herniated nucleus pulposus is removed by way of a surgical instrument, while using an external operating microscope for lighting and magnification. They may be "open", i.e., with a larger incision, or minimally invasive, i.e., with a 1.5 to 2.0 cm surgical incision. [ 3 ] [ 4 ]


Microdiscectomy may be a surgical option for patients with a single-level  disc herniation  and evidence of nerve root compression with residual unremitting  radicular  symptoms after failed conservative treatment.  Cauda equina syndrome  and progressive or  new motor deficits  are among the urgent surgical indications for microdiscectomy. [ 3 ]


Contraindications  include additional pathologies, including infection, tumor, or segmental instability or vertebral fracture where fusion or instrumentation may be required. However, segmental instability and  spondylolisthesis  may be considered  relative contraindications  by some physicians. [ 3 ]


Degeneration caused by years of repetitive mechanical stress can cause the disc of an athlete to be herniated.  Lumbar disc herniation  (LDH) is a critical injury for elite athletes that could cause extreme pain and significantly hinder performance. To relieve the pain, athletes usually go through microdiscectomy. However, the results of treatments in elite athletes differ due to the demand for optimal treatment, short recovery period, and high performance after the operation. [ citation needed ]


Most athletes return to their pre-surgery level after a discectomy. A systematic review of 450 athletes shows that 75–100% of athletes return to play after surgery. [ 5 ]  The average recovery period ranged from 2.8 to 8.7 months. Athletes recovered an average of 64.4% to 103.6% of their preoperative performance and had reported career longevity of 2.6 to 4.8 years post-return. [ 5 ]
There are unsuccessful cases of discectomy for certain athletes like  Tiger Woods , a world-famous PGA Tour golfer. Woods underwent three microdiscectomy procedures from 2014 to 2015 which failed to alleviate his pain. [ 6 ]  The removal of disc material due to discectomy meant that Woods eventually had to go through  spinal fusion  to recover.


In the U.S., it has been estimated that the  Medicare  system spends over $300 million annually on lumbar discectomies. [ 7 ]


Howard Dully  (born November 30, 1948) is an American memoirist who is one of the youngest survivors of the  transorbital lobotomy , a procedure performed on him when he was 12 years old.


Dully received international attention in 2005, following the broadcasting of his story on  National Public Radio . Subsequently, in 2007, he published a  New York Times  Best Seller  memoir ,  My Lobotomy , a story of the hardships of his lobotomy, co-authored by  Charles Fleming .


Howard Dully was born on November 30, 1948, in  Oakland ,  California , the eldest son of Rodney and June Louise Pierce Dully. Following the death of his mother from  cancer  in 1954, Dully's father married single mother Shirley Lucille Hardin in 1955.


Neurologist   Walter Freeman  had diagnosed Dully as suffering from childhood  schizophrenia  since age four, although numerous other medical and psychiatric professionals who had seen Dully did not detect a psychiatric disorder and instead blamed poor parenting by his stepmother. Freeman's notes stated that Dully's stepmother feared him, and that "He doesn't react either to love or to punishment... He objects to going to bed but then sleeps well. He does a good deal of daydreaming and when asked about it he says 'I don't know.' He turns the room's lights on when there is broad sunlight outside." [ 1 ]  In 1960, at 12 years of age, Dully was submitted by his father and stepmother for a trans-orbital lobotomy, performed by Freeman for $200 (equivalent to $2,060 in 2023). [ 2 ]  During the procedure, a long, sharp instrument called an  orbitoclast  was inserted through each of Dully's eye sockets 7 centimeters (2.8 in) into his brain.


Dully was institutionalized for years as a juvenile (in Agnews State Hospital as a minor); transferred to Rancho Linda School in San Jose, California, a school for children with behaviour-related problems;  incarcerated ; and was eventually  homeless  and an  alcoholic . After becoming  sober  and getting a college degree in  computer information systems , he became a California state certified behind-the-wheel instructor for a  school bus  company in  San Jose, California . [ 3 ] [ 4 ]


In his 50s, with the assistance of  National Public Radio   producer   David Isay , Dully started to research what had happened to him as a child. By this time, both his stepmother and Freeman were dead, and due to the aftereffects of the surgery, he was unable to rely on his own memories. He travelled the country with Isay and Piya Kochhar, speaking with members of his family, relatives of other lobotomy patients, and relatives of Freeman, and also gaining access to Freeman's archives. Dully first relayed his story on a  National Public Radio  broadcast in 2005, prior to co-authoring a memoir published in 2007. [ 5 ]


On November 16, 2005, David Isay broadcast Dully's search as a Sound Portraits  documentary  on NPR. According to  USA Today , the documentary, which  The New York Times  describes as "celebrated", [ 5 ]  "created a firestorm". [ 6 ]


The broadcast, aired on  All Things Considered , drew more listener response than any other program that had ever aired, [ citation needed ]  and by May 2006, the  Crown Publishing Group  had negotiated worldwide rights to publish Howard Dully's story in book form. [ 7 ]


In 2007, Dully published  My Lobotomy , a memoir co-authored by Charles Fleming.


The memoir relates Howard Dully's experiences as a child, the effect of the procedure on his life, his efforts as an adult to discover why the medically unnecessary procedure was performed on him and the effect of the radio broadcast on his life.


The book was critically well received.  The New York Times  described it as "harrowing", "one of the saddest stories you'll ever read". [ 5 ]   USA Today  called it "at once horrifying and inspiring". [ 6 ]  The  San Francisco Chronicle  critiqued it as "a gruesome but compulsively readable tale, ultimately redemptive". [ 8 ]  In the United Kingdom,  The Observer  characterized the book as "a forceful account of his survival" that "sheds light on the man who subjected him to one of the most brutal surgical procedures in medical history". [ 9 ]   The Times  described it as "uncomfortable reading", noting that "[i]t is, given the circumstances, astonishingly free of rancour." [ 10 ]


In the last section of the memoir, entitled "One Last Word", Dully compared his  lobotomy  to young children today who are diagnosed with  depression ,  bipolar disorder  or  attention deficit hyperactivity disorder  without a second opinion, and are subsequently  overmedicated . [ 11 ]


The  dura mater , (or just  dura ) is the outermost of the three  meningeal membranes . The dura mater has two layers, an outer  periosteal layer  closely adhered to the  neurocranium , and an inner meningeal layer known as the  dural border cell layer . [ 1 ]  The two dural layers are for the most part fused together forming a  thick fibrous tissue  membrane that covers the brain and the  vertebrae  of the  spinal column . [ 2 ]  But the layers are separated at the  dural venous sinuses  to allow blood to drain from the brain. [ 3 ]  The dura covers the  arachnoid mater  and the  pia mater  the other two meninges in protecting the  central nervous system .


At major boundaries of brain regions such as the  longitudinal fissure  between the  hemispheres , and the  tentorium cerebelli  between the posterior brain and the cerebellum the dura separates, folds and invaginates to make the divisions. These folds are known as dural folds, or reflections. [ 3 ]


The dura mater is primarily derived from  neural crest cells , with postnatal contributions from the  paraxial mesoderm . [ 4 ]


The dura mater has several functions and layers. The dura mater is a membrane that envelops the  arachnoid mater . It surrounds and supports the  dural venous sinuses  that reabsorbs  cerebrospinal fluid  and carries the cerebral  venous return , back toward the heart.


Cranial dura mater has two layers which include a superficial  periosteal  layer that is actually the inner  periosteum  of the  neurocranium  (the  calvarium  and  endocranium ); and a deep meningeal layer, which is the true dura mater. The dura mater covering the spinal cord is known as the  dural sac  or  thecal sac , and only has one layer (the meningeal layer) unlike cranial dura mater. The  potential space  between these two layers is known as the  epidural space , [ 5 ]  which can  accumulate blood  in the case of traumatic laceration to the  meningeal arteries .


The dura separates into two layers at  dural reflections  (also known as  dural folds ), places where the inner dural layer is reflected as sheet-like protrusions into the cranial cavity. There are two main dural reflections:


Two other dural infoldings are the cerebellar falx and the sellar diaphragm:


This depends upon the area of the cranial cavity: in the anterior cranial fossa the anterior meningeal artery (branch from the ethmoidal artery) is responsible for blood supply, in the middle cranial fossa the middle meningeal artery and some accessory arteries are responsible for blood supply, the middle meningeal artery is a direct branch from the maxillary artery and enter the cranial cavity through the foramen spinosum and then divides into anterior (which runs usually in vertical direction across the pterion) and posterior (which runs posterosuperiorly) branches, while the accessory meningeal  arteries (which are branches from the maxillary artery) enter the skull through foramen ovale and supply area between the two foramina, and the in posterior cranial fossa the dura mater has numerous blood supply from different possible arteries:


A. posterior meningeal  artery (from the ascending pharyngeal artery through the jugular foramen)
B. meningeal arteries (from the ascending pharyngeal artery through hypoglossal canal)
C. meningeal arteries (from occipital artery through jugular or mastoid foramen)
D. meningeal arteries (from vertebral artery through foramen magnum)


The two layers of dura mater run together throughout most of the skull. Where they separate, the gap between them is called a  dural venous sinus . These sinuses drain blood and  cerebrospinal fluid  (CSF) from the brain and empty into the  internal jugular vein .


Arachnoid villi , which are outgrowths of the  arachnoid mater  (the middle meningeal layer), extend into the dural venous sinuses to drain CSF. These villi act as one-way valves.
 Meningeal veins , which course through the dura mater, and  bridging veins , which drain the underlying neural tissue and puncture the dura mater, empty into these dural sinuses. A rupture of a bridging vein causes a  subdural hematoma .


The supratentorial dura mater membrane is supplied by small meningeal branches of the  trigeminal nerve  (V1, V2 and V3). [ 8 ]  The innervation for the infratentorial dura mater are via upper cervical nerves and the  meningeal branch of the vagus nerve. [ 9 ]


Many medical conditions involve the dura mater. A  subdural hematoma  occurs when there is an abnormal collection of blood between the dura and the arachnoid, usually as a result of torn bridging veins secondary to head trauma. An  epidural hematoma  is a collection of blood between the dura and the inner surface of the skull, and is usually due to  arterial  bleeding.  Intradural procedures, such as removal of a  brain tumour  or treatment of  trigeminal neuralgia  via a  microvascular decompression , require that an incision is made to the dura mater. To achieve a watertight repair and avoid potential post-operative complications, the dura is typically closed with  sutures . If there is a dural deficiency, then a dural substitute may be used to replace this membrane.  Small gaps in the dura can be covered with a  surgical sealant film .


In 2011, researchers discovered a connective tissue bridge from the  rectus capitis posterior major  to the cervical dura mater. Various clinical manifestations may be linked to this anatomical relationship such as  headaches ,  trigeminal neuralgia  and other symptoms that involved the cervical dura. [ 10 ]  The  rectus capitis posterior minor  has a similar attachment. [ 11 ]


The dura-muscular, dura-ligamentous connections in the upper cervical spine and occipital areas may provide anatomic and physiologic answers to the cause of the  cervicogenic headache . This proposal would further explain manipulation's efficacy in the treatment of cervicogenic headache. [ 12 ]


The American Red Cross and some other agencies accepting blood donations consider  dura mater transplants , along with receipt of pituitary-derived growth hormone, a risk factor due to concerns about  Creutzfeldt–Jakob disease . [ 13 ]


Cerebellar tonsillar ectopia, or  Chiari malformation , is a condition that was previously thought to be congenital but can be induced by trauma, particularly whiplash trauma. [ 14 ]  Dural strain may be pulling the cerebellum inferiorly, or skull distortions may be pushing the brain inferiorly.


Dural ectasia  is the enlargement of the dura and is common in connective tissue disorders, such as  Marfan syndrome  and  Ehlers–Danlos syndrome . These conditions are sometimes found in conjunction with Arnold–Chiari malformation.


Spontaneous cerebrospinal fluid leak  is the fluid and pressure loss of spinal fluid due to holes in the dura mater.


The name  dura mater  derives from the Latin for  tough mother (or hard mother) , [ 15 ]  a  loan translation  of Arabic  أم الدماغ الصفيقة  ( umm al-dimāgh al-ṣafīqah ), literally 'thick mother of the brain', matrix of the brain, [ 16 ] [ 17 ]  and is also referred to by the term "pachymeninx" (plural "pachymeninges"). [ 16 ]


Dural tear  is a tear occurring in the  dura mater  of the brain. It is usually caused as a result of trauma or as a complication following surgery. [ 1 ]


In case of head injury, a dural tear is likely in case of a  depressed skull fracture . A  burr hole  is made through the normal skull near the fractured portion, and  Adson's elevator  is introduced. Underlying dura is separated carefully from the overlying depressed bone fragments. The dura that is now visible is carefully examined to exclude any dural tear. [ citation needed ]


The whole extent of the dural tear is exposed by removing the overlying skull. The ragged edges of the tear are excised. However, care should be taken not to excise too much dura as it may increase the chances for spread of infection into the  subarachnoid space . Removing too much dura will also make it difficult to close the tear. If there is not much dural loss, interrupted sutures are made with non-absorbable material. In case of dural loss, the defect is closed using a transplant from fascia lata or pericranium given that there is not much contamination of the dura. In case of contamination, the defect is left alone and a primary suture is performed at a later date.


If dural tear is associated with haemorrhage from dural vessels, they are coagulated using  diathermy . This technique is preferred because the vessels are too small to be picked up by an artery forceps. Large vessels, if present, can be under-run with suture. When the dural tear is associated with a dural sinus hemorrhage, a graft of  pericranium  is used for a small tear and a muscle graft from  temporalis  is used for a large tear. The muscle graft is flattened by hammering before using it for grafting.


If dural tear is associated with a brain injury, wide exposure of the wound is done to examine the extent of brain damage. All devitalized brain tissues are removed along with extravasated blood, foreign bodies and pieces of bone. All devitalized tissue and foreign bodies are removed by a combination of irrigation and suction.


Following dural repair, skull deficit is treated by using moulded tantalum plates or acrylic inlays, three to six months after the head injury. [ 2 ]


Eloquent cortex  is a name used by  neurologists  for areas of  cortex  that—if removed—will result in loss of  sensory  processing or linguistic ability, or  paralysis . The most common areas of eloquent cortex are in the left  temporal  and  frontal lobes  for  speech  and  language , bilateral  occipital lobes  for  vision , bilateral  parietal lobes  for  sensation , and bilateral  motor cortex  for movement.


Neuroimaging  techniques such as  magnetic resonance imaging ,  electroencephalography , or  magnetoencephalography  are especially useful non-invasive tools to locate eloquent cortices. [ 1 ]  Much higher spatial and temporal resolution maps of cortical activity can be achieved with a technique called  electrocorticography , however this requires placement of  subdural  electrodes on the surface of the brain and this must be done during surgery.


Endovascular coiling  is an  endovascular  treatment for  intracranial aneurysms  and  bleeding  throughout the body. The procedure reduces blood circulation to an aneurysm or blood vessel through the implantation of detachable platinum wires, with the clinician inserting one or more into the blood vessel or aneurysm until it is determined that blood flow is no longer occurring within the space. It is one of two main treatments for cerebral  aneurysms, the other being  surgical clipping .


Endovascular coiling is typically used to treat  cerebral aneurysms . The main goal is prevention of rupture in unruptured aneurysms, and prevention of rebleeding in ruptured aneurysms by limiting blood circulation to the aneurysm space. Clinically, packing density is recommended to be 20-30% or more of the aneurysm's volume, typically requiring deployment of multiple wires. [ 1 ]  Higher volumes may be difficult due to the delicate nature of the aneurysm; intraoperative rupture rates are as high as 7.6% for this procedure. [ 2 ]  In ruptured aneurysms, coiling is performed quickly after rupture because of the high risk of rebleeding within the first few weeks after initial rupture. The patients most suitable for endovascular coiling are those with aneurysms with a small neck size (preferably <4 mm), luminal diameter <25 mm and those that are distinct from the parent vessel. [ 3 ]  Larger aneurysms are subject to compaction of coils, due to both looser packing densities (more coils are needed) and increased blood flow. Coil compaction renders them unsuitable as they are incapable of stemming blood flow. [ 4 ]  However, technological advances have made coiling of many other aneurysms possible as well.


A number of studies have questioned the efficacy of endovascular coiling over the more traditional surgical clipping. Most concerns involve the chance of later bleeds or other recanalization. [ 5 ] [ 6 ] [ 7 ]  Due to its less invasive nature, endovascular coiling usually presents faster recovery times than surgical clipping, with one study finding a significant decrease in probability of death or dependency compared to a neurosurgical population. [ 8 ]  Complication rates for coiling as well are generally found to be lower than microsurgery (11.7% and 17.6% for coiling and microsurgery, respectively). Despite this, intraoperative rupture rates for coiling have been documented as being as high as 7.6%. [ 2 ]  Clinical results are found to be similar at a two-month and one year follow-up between coiling and neurosurgery. [ 9 ]


Reported recurrence rates are quite varied, with rates between 20 and 50% of aneurysms recurring within one year of coiling, and with the recurrence rate increasing with time. [ 2 ] [ 10 ]  These results are similar to those previously reported by other endovascular groups. [ 11 ]  Other studies have questioned whether new matrix coils work better than bare platinum coils. [ 12 ]


The  International Subarachnoid Aneurysm Trial  tested the efficacy of endovascular coiling against the traditional micro-surgical clipping. The study initially found very favorable results for coiling, however its results and methodology were criticized. Since the study's release in 2002, and again in 2005, some studies have found higher recurrence rates with coiling, while others have concluded that there is no clear consensus between which procedure is preferred. [ 13 ]


Risks of endovascular coiling include  stroke , aneurysm rupture during the procedure and aneurysm recurrence and rupture after the procedure. [ 3 ]  Additionally in some patients coiling may not be successful. In general, coiling is only performed when the risk of aneurysm rupture is higher than the risks of the procedure itself.


Similar to patients who experience neurosurgical procedures, coiling results in an increase in resting energy expenditure, albeit at a slightly reduced rate than their neurosurgery counterpart. This can lead to malnutrition if steps are not taken to compensate for the increased metabolic rate. [ 14 ]


The treatment works by promoting blood clotting ( thrombosis ) in the aneurysm, eventually sealing it from the blood flow. This is accomplished by decreasing the amount of blood flow going into the aneurysm, increasing the residence time of the blood (thereby lowering the velocity) in the aneurysm space and reducing the  wall shear stress  of the aneurysm wall. This change in the blood flow, or  hemodynamics , is ultimately dependent on several factors, including:


While these factors are crucial to the success of the procedure, thrombosis ultimately is dependent on biological processes, with the coiling only providing the appropriate conditions for the process to occur, and hopefully closing the aneurysm.


Endovascular coiling is usually performed by an  interventional neuroradiologist  or neurosurgeon with the patient under general anaesthesia. The whole procedure is performed under  fluoroscopic imaging  guidance. A guiding catheter is inserted through the femoral artery and advanced to a site close to the aneurysm after which angiography is performed to localize and assess the aneurysm. After this, a microcatheter is navigated into the aneurysm.


The treatment uses detachable coils made of platinum that are inserted into the aneurysm using the microcatheter. A variety of coils are available, including Guglielmi Detachable Coils (GDC) which are platinum, Matrix coils which are coated with a biopolymer, and hydrogel coated coils. Coils are also available in a variety of diameters, lengths, and cross sections. [ 16 ]  A coil is first inserted along the aneurysm wall to create a frame, with the core then being filled with more coils. [ 17 ]  A series of progressively smaller coils may also be used. Success is determined by injecting a contrast dye into parent artery and qualitatively determining if dye is flowing into the aneurysm space during fluoroscopy. If no flow is observed, the procedure is considered completed. [ 2 ]  In the case of wide-necked aneurysms a  stent  may be used. [ 18 ]


Endovascular coiling was a developed through the synthesis of a number of innovations that took place between 1970 and 1990 in the field of electronics, neurosurgery, and  interventional radiology . [ 4 ]  While the procedure itself has been and continues to be compared to surgical clipping, the development of the concept and procedure has resulted in it becoming the gold standard at many centers. [ 4 ]


The first documented technique of using metal coils to induce thrombosis was accomplished by Mullan in 1974. Copper coils were inserted into a giant aneurysm through externally puncturing the aneurysm wall via craniotomy. Five patients died, with ten having satisfactory process. [ 19 ]  It did not gain popularity due to the specialized equipment required, in addition to the technique being unsuitable for many types of aneurysms. [ 4 ]  Later, in 1980, similar techniques were developed by Alksne and Smith using iron suspended in  methyl methacrylate  in a limited set of patients. There were no deaths in 22 consecutive cases with low morbidity. [ 20 ]  This technique also did not gain traction due to advances in clipping. [ 4 ]


As a means of avoiding invasive methods, early endovascular interventions involved the usage of detachable and nondetachable  balloon catheters  to occlude the aneurysm while preserving the  parent artery . [ 21 ]  Despite the innovative approach, the aneurysms were often found to adapt to the shape of the balloon itself resulting in higher incidents of aneurysm rupture. This procedure was deemed "uncontrollable" due to its high morbidity and mortality rate, but it demonstrated that the endovascular approach was feasible for many aneurysms. [ 4 ]  Endovascular coils would later be used in 1989 by Hilal et al., but these were short, stiff coils that offered no control, preventing dense packing of the aneurysm. [ 22 ]  Controllable microguidewire systems were later used. [ 4 ]


In 1983 the use of electrically induced thrombosis for intracranial aneurysms was described for the first time. [ 23 ]  A stainless steel electrode  supplied a positive current to the aneurysm to stimulate electrothrombosis. Minimal occlusion was achieved, but the researchers discovered that the erosion of the electrode due to  electrolysis  would be useful as a detachment system. [ 4 ]  Detachable coils were constructed from a platinum coil soldered to a stainless steel delivery wire, first described in 1991 by Guglielmi et al. [ 3 ]  When combined with a controllable microguide wire system, multiple coils could be inserted to fully pack an aneurysm. [ 4 ]


Given the complexity of modeling the vasculature, much research has been devoted towards modeling the hemodynamics of an aneurysm before and after an intervention. Techniques such as  particle image velocimetry  (PIV) and  computational fluid dynamics / finite element analysis  (CFD/FEA) have yielded results that have influenced the direction of research, but no model to date has been able to account for all factors present. [ 2 ] [ 24 ] [ 25 ]  Advantages of the  in-silico  research method include flexibility of selecting variables, but one comparative study has found that simulations tend to over-emphasis results compared to PIV, and are more beneficial for trends than exact values. [ 25 ]


Medical images, particularly  CT angiography , can be used to generate 3D reconstructions of patient specific anatomy. When combined with CFD/FEA, hemodynamics can be estimated in patient specific simulations, giving the clinician greater predictive tools for surgical planning and outcome evaluation to best promote thrombus formation. [ 26 ] [ 27 ]  However, most computer models use many assumptions for simplicity, including rigid walls (non-elastic) for vasculature, substituting a porous medium in place of physical coil representations, and  navier-stokes  for fluid behavior. However, new predictive models are being developed as computational power increases, including algorithms for simulations of coil behavior in-vivo. [ 16 ]


An  external ventricular drain  ( EVD ), also known as a  ventriculostomy  or  extraventricular drain , is a device used in  neurosurgery  to treat  hydrocephalus  and relieve elevated  intracranial pressure  when the normal flow of  cerebrospinal fluid  (CSF) inside the  brain  is obstructed. An EVD is a flexible plastic catheter placed by a  neurosurgeon  or  neurointensivist  and managed by  intensive care unit  (ICU) physicians and nurses. The purpose of external ventricular drainage is to divert fluid from the ventricles of the brain and allow for monitoring of  intracranial pressure . An EVD must be placed in a center with full neurosurgical capabilities, because immediate neurosurgical intervention can be needed if a complication of EVD placement, such as bleeding, is encountered.


EVDs are a short-term solution to hydrocephalus, and if the underlying hydrocephalus does not eventually resolve, it may be necessary to convert the EVD to a  cerebral shunt , which is a fully internalized, long-term treatment for hydrocephalus. [ 1 ]


The EVD catheter is most frequently placed by way of a twist-drill craniostomy placed at  Kocher's point , a location in the  frontal bone  of the skull, with the goal of placing the catheter tip in the frontal horn of the  lateral ventricle  or in the  third ventricle . [ 2 ] [ 3 ]  The catheter is typically inserted on the right side of the brain, but in some cases a left-sided approach is used, and in other situations catheters are needed on both sides. [ 3 ]  EVDs can be used to monitor intracranial pressure in patients with  traumatic brain injury  (TBI), [ 4 ]   subarachnoid hemorrhage  (SAH), [ 5 ]   intracerebral hemorrhage  (ICH), or other brain abnormalities that lead to increased CSF build-up. In draining the ventricle, the EVD can also remove blood products from the ventricular spaces. This is important because blood is an irritant to brain tissue and can cause complications such as  vasospasm .


The EVD is leveled to a common reference point that corresponds to the skull base, usually the  tragus  or  external auditory meatus . The EVD is set to drain into a closed, graduated burette at a height corresponding to a particular pressure level, as prescribed by a healthcare professional, usually a  neurosurgeon  or  neurointensivist . Leveling the EVD to a set pressure level is the basis for  cerebrospinal fluid  (CSF) drainage;  hydrostatic pressure  dictates CSF drainage. The fluid column pressure must be greater than the weight of the CSF in the system before drainage occurs. It is therefore important that family members and visitors understand the patient's head of bed position cannot be changed without assistance. [ 6 ]


An example of a healthcare provider order regarding an EVD is: set EVD to drain CSF for ICP > 15 mm Hg, check and record cerebrospinal fluid drainage and  intracranial pressure  at least hourly. Continuous CSF drainage is associated with a higher risk of complications. [ 7 ]  The  cerebral perfusion pressure  (CPP) can be calculated from data obtained from the EVD and systemic blood pressure. In order to calculate the CPP the  intracranial pressure  and  mean arterial pressure  (MAP) must be available. [ 6 ]


C
 P
 P
 =
 M
 A
 P
 −
 I
 C
 P

 {\displaystyle CPP=MAP-ICP}


Other areas that should be monitored are: signs and symptoms of intracranial hypertension, looking for any leaks in the EVD system to prevent infection from entering the brain, and changes in the amount and color of the CSF. A sudden increase in hourly output of CSF may indicate intracranial hypertension, bloody CSF may indicate recurrent aneurysm rupture, and cloudy CSF may indicate brain infection. [ 8 ]


EVD placement is an invasive procedure. It is associated with several potential complications:


Bleeding can occur along the EVD insertion tract or in the several layers of the meninges that prohibit passage into the brain. If drilling or dural puncture is not successful, the surgeon may dissect away dura and create a secondary bleed known as an epidural or subdural hemorrhage. Bleeding from EVD placement can be life-threatening and can require neurosurgical intervention in some cases. The risk of hemorrhage with EVD placement is increased if the patient suffers from  coagulopathy .


Mechanical complications from EVD placement can be categorized into:


Malplacement of the EVD tube into the brain tissue instead of ventricles can occur in 10 to 40% of the cases. Therefore, computed tomography (CT), ultrasound, endoscopy, and stereotactic neuronavigation are used to minimize placement errors of EVD tubes. [ 8 ]


Obstruction/occlusion of EVD commonly due to fibrinous/clot like material or kinking of the tube. The brain can swell due to pressure build up in the ventricles and permanent brain damage can occur. Physicians or nurses may have to adjust or flush these small diameter catheters to manage medical tube obstructions and occlusions at the intensive-care bedside. [ 9 ]


After EVD placement, the drain is tunneled subcutaneously and secured with  surgical sutures  and/or  surgical staples . However, it is possible for the EVD to dislodge or migrate. This will cause the tip of the drain to migrate away from its intended position and provide inaccurate ICP measurement or lead to occlusion of the drain.


The EVD is a foreign body inserted into the brain, and as such it represents a potential portal for serious infection. Historically, the rate of infections associated with EVDs has been very high, ranging from 5% to > 20%. [ 10 ] [ 11 ]  Infections associated with EVDs can progress to become a severe form of brain infection known as  ventriculitis . Protocols designed to reduce the rate of EVD infections have been successful, applying  infection control  'bundle' approaches to reduce the rate of infection to well less than 1%. [ 12 ] [ 13 ] [ 14 ]


Although neurological deficits from passing the EVD catheter across the brain are uncommon, there can be an association of a patient's poor neurological status with EVD malplacement. [ 15 ]  In one report, the EVD was inserted too deeply into the fourth ventricle; the authors hypothesized that the patient's coma was due to irritation of the  recticular activating system . The patient's level of consciousness improved after the EVD was adjusted. [ 15 ]


Facetectomy  is a  surgical procedure  which involves  decompression  of a  spinal nerve root . For example, it can be performed in severely resistant cases of  cervical rhizalgia , where the cervical nerve roots within the  intervertebral foramina  are decompressed. [ 1 ]


Failed Back Syndrome  ( abbreviated  as  FBS )  is a  condition  characterized by  chronic pain  following  back surgeries . [ 1 ] [ 2 ]  The term "post-laminectomy syndrome" is sometimes used by doctors to indicate the same condition as failed back syndrome. [ 3 ]  Many factors can contribute to the onset or development of FBS, including residual or recurrent  spinal disc herniation , persistent  post-operative  pressure on a  spinal nerve , altered joint mobility,  joint hypermobility  with instability, scar tissue ( fibrosis ),  depression ,  anxiety ,  sleeplessness ,  spinal  muscular  deconditioning  and  Cutibacterium acnes  infection. [ 4 ]   An individual may be predisposed to the development of FBS due to  systemic disorders  such as  diabetes ,  autoimmune disease  and  peripheral blood vessels (vascular) disease .


Common symptoms of Failed Back Surgery Syndrome (FBS) include diffuse, dull, and aching pain in the back or legs, often accompanied by abnormal sensations such as sharp, pricking, or stabbing pain in the extremities. [ 5 ]  Patients may also experience pain at a different level from the location originally treated, along with an inability to fully recuperate and restricted mobility. Sharp, stabbing pain in the back, numbness, back spasms, or pain radiating from the lower back into the legs are frequently reported. In addition to physical discomfort, FBS can lead to psychological symptoms such as anxiety, depression, and  insomnia . Some individuals may develop a dependence on pain medication due to  chronic pain . [ 6 ]


The number of  spinal surgeries  varies around the world. The  United States  and the  Netherlands  report the highest number of spinal surgeries, while the  United Kingdom  and  Sweden  report the fewest. Recently, there have been calls for more aggressive surgical treatment in  Europe . Success rates of spinal surgery vary for many reasons. [ 7 ] [ 8 ] [ 9 ]


Patients who have undergone one or more operations on the  lumbar spine  and continue to experience pain afterwards can be divided into two groups.


In 1992, Turner  et al.  published a survey of 74 journal articles which reported the results after decompression for  spinal stenosis .  Good to excellent results were on average reported by 64% of the patients.  There was, however, a wide variation in outcomes reported.  There was a better result in patients who had a degenerative  spondylolisthesis . [ 13 ]  A similarly designed study by Mardjekto et al. found that a concomitant spinal  arthrodesis  (fusion) had a greater success rate. [ 14 ]  Herron and Trippi evaluated 24 patients, all with degenerative  spondylolisthesis  treated with  laminectomy  alone.  At follow-up varying between 18 and 71 months after surgery, 20 out of the 24 patients reported a good result. [ 15 ]   Epstein  reported on 290 patients treated over a 25-year period.  Excellent results were obtained in 69% and good results in 13%. [ 16 ]   These optimistic reports do not correlate with "return to competitive employment" rates, which for the most part are dismal in most spinal surgery series. [ citation needed ]


In the past two decades there has been a dramatic increase in  fusion surgery  in the U.S.: in 2001 over 122,000 lumbar fusions were performed, a 22% increase from 1990 in fusions per 100,000 population, increasing to an estimate of 250,000 in 2003, and 500,000 in 2006. [ 17 ] [ 18 ] [ 19 ]  In 2003, the national bill for the hardware for fusion alone was estimated to have soared to $2.5 billion a year. [ 18 ] [ 20 ]
For patients with continued  pain after surgery  which is not due to the above complications or conditions,  interventional pain physicians  speak of the need to identify the "pain generator" i.e. the anatomical structure responsible for the patient's pain. To be effective, the surgeon must operate on the correct  anatomic structure , but is often not possible to determine the source of the pain. [ 21 ] [ 22 ]  The reason for this is that many patients with  chronic pain  often have disc bulges at multiple spinal levels and the physical examination and imaging studies are unable to pinpoint the source of pain. [ 21 ]  In addition,  spinal fusion  itself, particularly if more than one spinal level is operated on, may result in "adjacent segment degeneration". [ 23 ]   This is thought to occur because the fused segments may result in increased  torsional  and  stress forces  being transmitted to the  intervertebral discs  located above and below the fused  vertebrae . [ 23 ]  This pathology is one reason behind the development of artificial discs as a possible alternative to fusion surgery.  But fusion surgeons argue that  spinal fusion  is more time-tested, and artificial discs contain metal hardware that is unlikely to last as long as biological material without shattering and leaving metal fragments in the spinal canal. These represent different  schools of thought . (See discussion on disc replacement infra.) [ citation needed ]


Another highly relevant consideration is the increasing recognition of the importance of " chemical radiculitis " in the generation of  back pain . [ 24 ]   A primary focus of surgery is to remove "pressure" or reduce mechanical compression on a  neural  element: either the  spinal cord , or a  nerve root . But it is increasingly recognized that  back pain , rather than being solely due to compression, may instead entirely be due to chemical  inflammation of the nerve root.   It has been known for several decades that disc herniations result in a massive inflammation of the associated nerve root. [ 24 ] [ 25 ] [ 26 ] [ 27 ]  In the past five years increasing evidence has pointed to a specific inflammatory mediator of this pain. [ 28 ] [ 29 ]   This inflammatory molecule, called  tumor necrosis factor-alpha  (TNF), is released not only by the herniated or protruding disc, but also in cases of disc tear (annular tear), by facet joints, and in  spinal stenosis . [ 24 ] [ 30 ] [ 31 ] [ 32 ]  In addition to causing pain and inflammation, TNF may also contribute to  disc degeneration . [ 33 ]  If the cause of the pain is not compression, but rather is inflammation mediated by TNF, then this may well explain why surgery might not relieve the pain, and might even exacerbate it, resulting in FBS.


A 2005 review by Cohen concluded, 'The SI joint is a real yet underappreciated pain generator in an estimated 15% to 25% of patients with axial LBP'. [ 34 ]  Studies by Ha, et al., show that the incidence of SI joint degeneration in post-lumbar fusion surgery is 75% at 5 years post-surgery, based on imaging. [ 35 ]  Studies by DePalma and Liliang, et al., demonstrate that 40–61% of post-lumbar fusion patients were symptomatic for  SI joint dysfunction  based on diagnostic blocks. [ 36 ] [ 37 ]


Recent studies have shown that  cigarette smokers  will routinely fail all spinal surgery, if the goal of that surgery is the decrease of pain and impairment.  Many surgeons consider smoking to be an absolute  contraindication  to spinal surgery.   Nicotine  appears to interfere with bone metabolism through induced  calcitonin  resistance and decreased  osteoblastic  function.  It may also restrict small blood vessel diameter leading to increased scar formation. [ 38 ] [ 39 ] [ 40 ] [ 41 ] [ 42 ] [ 43 ] [ 44 ] [ excessive citations ]


There is an association between  cigarette smoking ,  back pain  and  chronic pain syndromes  of all types. [ 45 ] [ 46 ] [ 39 ] [ 47 ] [ 48 ]


In a report of 426 spinal surgery patients in  Denmark , smoking was shown to have a negative effect on fusion and overall patient satisfaction, but no measurable influence on the functional outcome. [ 49 ]


There is a validation of the hypothetical assumption that postoperative  smoking cessation  helps to reverse the impact of cigarette smoking on outcome after spinal fusion.  If patients cease cigarette smoking in the immediate post operative period, there is a positive impact on success. [ 50 ]


Regular  smoking in adolescence  was associated with low back pain in  young adults . Pack-years of smoking showed an exposure-response relationship among girls. [ 51 ]


A recent study suggested that cigarette smoking adversely affects serum  hydrocodone  levels. Prescribing physicians should be aware that in some cigarette smokers, serum hydrocodone levels might not be detectable. [ 52 ]


In a study from Denmark reviewing many reports in the literature, it was concluded that smoking should be considered a weak risk indicator and not a cause of low back pain. In a multitude of  epidemiologic  studies, an association between smoking and low back pain has been reported, but variations in approach and study results make this literature difficult to reconcile. [ 53 ]  In a massive study of 3482 patients undergoing lumbar spine surgery from the National Spine Network, co-morbidities of (1) smoking, (2) compensation, (3) self reported poor overall health and (4) pre-existing psychological factors were predictive in a high risk of failure. Followup was carried out at 3 months and one year after surgery. Pre-operative depressive disorders tended not to do well. [ 54 ]


Smoking has been shown to increase the incidence of post operative infection as well as decrease fusion rates. One study showed 90% of post operative infections occurred in smokers, as well as  myonecrosis  (muscle destruction) around the  wound . [ 55 ] [ 56 ]


Before the advent of CT scanning, the pathology in failed back syndrome was difficult to understand.  Computerized tomography  in conjunction with  metrizamide   myelography  in the late 1960s and 1970s allowed direct observation of the mechanisms involved in post operative failures. Six distinct pathological conditions were identified: [ citation needed ]


Removal of a disc at one level can lead to  disc herniation  at a different level at a later time.  Even the most complete  surgical excision  of the disc still leaves 30–40% of the disc, which cannot be safely removed. This retained disc can re-herniate sometime after surgery. Virtually every major structure in the abdomen and the posterior  retroperitoneal space  has been injured, at some point, by removing discs using posterior  laminectomy / discectomy  surgical procedures. The most prominent of these is a laceration of the  left internal iliac vein , which lies in close proximity to the anterior portion of the disc. [ 57 ] [ 58 ]  In some studies, recurrent pain in the same radicular pattern or a different pattern can be as high as 50% after disc surgery. [ 59 ] [ 60 ]    Many observers have noted that the most common cause of a failed back syndrome (FBS) is caused from recurrent disc herniation at the same level originally operated. A rapid removal in a second surgery can be curative. The clinical picture of a recurrent disc herniation usually involves a significant pain-free interval.  However, physical findings may be lacking, and a good history is necessary. [ 61 ] [ 62 ] [ 63 ] [ 64 ]  The time period for the emergence of new symptoms can be short or long.  Diagnostic signs  such as the  straight leg raise  test may be negative even if real  pathology  is present. [ 60 ] [ 65 ]  The presence of a  positive myelogram  may represent a new disc herniation, but can also be indicative of a post operative scarring situation simply mimicking a new disc. Newer  MRI  imaging techniques have clarified this dilemma somewhat. [ 61 ] [ 62 ] [ 66 ] [ 67 ] [ 68 ]  Conversely, a recurrent disc can be difficult to detect in the presence of post op scarring.  Myelography  is inadequate to completely evaluate the patient for recurrent disc disease, and  CT  or MRI scanning is necessary.  Measurement of  tissue density  can be helpful. [ 11 ] [ 66 ] [ 69 ] [ 70 ] [ 71 ]


Even though the complications of  laminectomy  for disc herniation can be significant, a recent series of studies involving thousands of patients published under auspices of  Dartmouth Medical School  concluded at four-year follow-up that those who underwent surgery for a lumbar disc herniation achieved greater improvement than nonoperatively treated patients in all primary and secondary outcomes except work status. [ 72 ]


Spinal stenosis  can be a late complication after  laminectomy  for disc herniation or when surgery was performed for the primary pathological condition of  spinal stenosis . [ 11 ] [ 73 ] [ 74 ]  In the Maine Study, among patients with  lumbar spinal stenosis  completing 8- to 10-year follow-up, low back pain relief, predominant symptom improvement, and satisfaction with the current state were similar in patients initially treated surgically or non-surgically. However, leg pain relief and greater back-related functional status continued to favor those initially receiving surgical treatment. [ 75 ]


A large study of  spinal stenosis  from Finland found the  prognostic factors  for ability to work after surgery were ability to work before surgery, age under 50 years, and no prior back surgery. The very long-term outcome (mean follow-up time of 12.4 years) was excellent-to-good in 68% of patients (59% women and 73% men). Furthermore, in the longitudinal follow-up, the result improved between 1985  and 1991. No special complications were manifested during this very long-term follow-up time. The patients with total or subtotal block in preoperative  myelography  achieved the best result.  Furthermore, patients with block stenosis improved their result significantly in the longitudinal follow-up. The postoperative stenosis seen in  computed tomography  (CT)  scans  was observed in 65% of 90 patients, and it was severe in 23 patients (25%). However, this successful or unsuccessful  surgical decompression  did not correlate with patients' subjective  disability , walking capacity or  severity of pain . Previous back surgery had a strong worsening effect on surgical results. This effect was very clear in patients with total block in the preoperative  myelography . The surgical result of a patient with previous back surgery was similar to that of a patient without previous back surgery when the time interval between the last two operations was more than 18 months. [ 76 ]


Post-operative MRI findings of  stenosis  are probably of limited value compared to symptoms experienced by patients. Patients' perception of improvement had a much stronger correlation with long-term surgical outcome than structural findings seen on post-operation  magnetic resonance imaging . Degenerative findings had a greater effect on patients' walking capacity than stenotic findings. [ 77 ] [ 78 ]


Postoperative radiologic stenosis was very common in patients operated on for  lumbar spinal stenosis , but this did not correlate with  clinical outcome . The clinician must be cautious when reconciling clinical symptoms and signs with postoperative  computed tomography  findings in patients operated on for lumbar spinal stenosis. [ 79 ]


A study from  Georgetown University  reported on one-hundred patients who had undergone  decompressive surgery  for lumbar stenosis between 1980 and 1985.  Four patients with post-fusion stenosis were included. A 5-year follow-up period was achieved in 88 patients. The mean age was 67 years, and 80% were over 60 years of age. There was a high incidence of coexisting medical diseases, but the principal disability was lumbar stenosis with neurological involvement.  Initially there was a high incidence of success, but recurrence of neurological involvement and persistence of low-back pain led to an increasing number of failures. By 5 years this number had reached 27% of the available population pool, suggesting that the failure rate could reach 50% within the projected  life expectancies  of most patients. Of the 26 failures, 16 were secondary to renewed neurological involvement, which occurred at new levels of stenosis in eight and recurrence of stenosis at operative levels in eight. Reoperation was successful in 12 of these 16 patients, but two required a third operation. The incidence of  spondylolisthesis  at 5 years was higher in the surgical failures (12 of 26 patients) than in the surgical successes (16 of 64). Spondylolisthetic  stenosis  tended to recur within a few years following decompression.  Because of  age and associated illnesses , fusion may be difficult to achieve in this group. [ 80 ]


A small minority of lumbar surgical patients will develop a post operative infection. In most cases, this is a bad complication and does not bode well for eventual improvement or future employability.  Reports from the surgical literature indicate an infection rate anywhere from 0% to almost 12%. [ 81 ] [ 82 ] [ 83 ] [ 84 ] [ 85 ] [ 86 ] [ 87 ] [ 88 ] [ 89 ] [ 90 ] [ 91 ] [ 92 ] [ 93 ] [ 94 ] [ 95 ] [ 96 ] [ excessive citations ]  The  incidence of infection  tends to increase as the complexity of the procedure and operating time increase.  Usage of  metal implants  (instrumentation) tends to increase the risk of infection.  Factors associated with an increased infection include  diabetes mellitus ,  obesity ,  malnutrition ,  smoking , previous infection,  rheumatoid arthritis , and  immunodeficiency . [ 97 ] [ 98 ] [ 99 ] [ 100 ] [ 101 ] [ 102 ] [ excessive citations ]  Previous wound infection should be considered as a contraindication to any further spinal surgery, since the likelihood of improving such patients with more surgery is small. [ 103 ] [ 104 ] [ 105 ] [ 106 ] [ 107 ] [ 108 ]   Antimicrobial prophylaxis  reduces the rate of surgical site infection in lumbar spine surgery, but a great deal of variation exists regarding its use. In a Japanese study, utilizing the  Centers for Disease Control  recommendations for antibiotic prophylaxis, an overall rate of 0.7% infection was noted, with a single dose antibiotic group having 0.4% infection rate and multiple dosage antibiotic infection rate of 0.8%. The authors had previously used  prophylactic antibiotics  for 5 to 7 postoperative days. Based on the  Centers for Disease Control and Prevention  (CDC) guideline, their antibiotic prophylaxis was changed to the day of surgery only. It was concluded there was no statistical difference in the rate of infection between the two different antibiotic protocols. Based on the  CDC  guideline, a single dose of prophylactic antibiotic was proven to be efficacious for the prevention of infection in  lumbar spine  surgeries. [ 109 ]


Epidural scarring following a  laminectomy  for disc excision is a common feature when re-operating for recurrent  sciatica  or  radiculopathy . [ 61 ]  When the scarring is associated with a  disc herniation  and/or recurrent  spinal stenosis , it is relatively common, occurring in more than 60% of cases. For a time, it was theorized that placing a  fat graft  over the dural could prevent post operative scarring.  However, initial enthusiasm has waned in recent years. [ 110 ] [ 111 ] [ 112 ] [ 113 ] [ 114 ]  In an extensive  laminectomy  involving 2 or more  vertebra , post operative scarring is the norm.  It is most often seen around the  L5  and  S1 nerve roots . [ 115 ] [ 116 ] [ 117 ]


Fibrous scarring can also be a complication within the  subarachnoid  space.  It is notoriously difficult to detect and evaluate.  Prior to the development of  magnetic resonance imaging , the only way to ascertain the presence of  arachnoiditis  was by opening the  dura . In the days of  CT  scanning and  Pantopaque  and later,  Metrizamide   myelography , the presence of  arachnoiditis  could be speculated based on  radiographic  findings.  Often,  myelography  prior to the introduction of  Metrizamide  was the cause of  arachnoiditis .   It can also be caused by the long term pressure brought about with either a severe  disc herniation  or  spinal stenosis . [ 62 ] [ 61 ] [ 118 ] [ 119 ] [ 64 ]   The presence of both  epidural scarring  and  arachnoiditis  in the same patient are probably quite common.  Arachnoiditis  is a broad term denoting  inflammation of the meninges  and  subarachnoid  space. A variety of causes exist, including infectious,  inflammatory , and  neoplastic  processes. Infectious causes include  bacterial ,  viral ,  fungal , and  parasitic   agents .  Noninfectious inflammatory processes  include surgery, intrathecal hemorrhage, and the administration of  intrathecal  (inside the  dural canal ) agents such as myelographic contrast media,  anesthetics  (e.g.  chloroprocaine ), and  steroids  (e.g. Depo-Medrol, Kenalog). Lately iatrogenic arachnoiditis has been attributed to misplaced  Epidural Steroid Injection therapy  when accidentally administered intrathecally. The preservatives and suspension agents found in all steroid injectates, which aren't indicated for epidural administration by the  U.S. Food & Drug Administration  (FDA) due to reports of severe adverse events including  arachnoiditis ,  paralysis  and  death , have now been directly linked to the onset of the disease following the initial stage of  chemical meningitis . [ 120 ] [ 121 ] [ 122 ] [ 123 ]
 Neoplasia  includes the  hematogenous spread  of  systemic tumors , such as  breast  and  lung carcinoma ,  melanoma , and  non-Hodgkin lymphoma . Neoplasia also includes direct seeding of the  cerebrospinal fluid  (CSF) from primary central nervous system (CNS) tumors such as  glioblastoma multiforme ,  medulloblastoma ,  ependymoma , and  choroid plexus carcinoma . Strictly speaking, the most common cause of  arachnoiditis  in failed back syndrome is not infectious or from cancer.  It is due to non-specific scarring secondary to the surgery or the underlying pathology. [ 124 ] [ 125 ] [ 126 ] [ 127 ] [ 128 ] [ 129 ] [ 130 ] [ 131 ]


Laceration  of a  nerve root , or damage from  cautery  or  traction  can lead to  chronic pain , however this can be difficult to determine. Chronic compression of the nerve root by a persistent agent such as  disc , bone ( osteophyte ) or  scarring  can also permanently damage the nerve root.  Epidural scarring  caused by the initial  pathology  or occurring after the surgery can also contribute to  nerve damage .  In one study of failed back patients, the presence of pathology was noted to be at the same site as the level of surgery performed in 57% of cases. The remaining cases developed pathology at a different level, or on the opposite side, but at the same level as the surgery was performed. In theory, all failed back patients have some sort of nerve injury or damage which leads to a  persistence of symptoms  after a reasonable  healing time . [ 59 ] [ 60 ] [ 132 ]


Failed back syndrome (FBS) is a well-recognized complication of surgery of the lumbar spine. It can result in chronic pain and disability, often with disastrous emotional and financial consequences to the patient. Many patients have traditionally been classified as "spinal cripples" and are consigned to a life of long-term narcotic treatment with little chance of recovery.  Despite extensive work in recent years, FBS remains a challenging and costly disorder. [ 133 ]


The treatments of post-laminectomy syndrome include  physical therapy ,  microcurrent electrical neuromuscular stimulator , [ 134 ]  minor nerve blocks,  transcutaneous electrical nerve stimulation  (TENS),  behavioral medicine ,  non-steroidal anti-inflammatory  (NSAID) medications,  membrane stabilizers ,  antidepressants ,  spinal cord stimulation , and  intrathecal   morphine   pump . Use of  epidural steroid injections  may be minimally helpful in some cases. The targeted  anatomic  use of a potent anti-inflammatory  anti-TNF   therapeutics  is being investigated.


A study of chronic pain patients from the  University of Wisconsin  found that  methadone  is most widely known for its use in the treatment of  opioid  dependence, but  methadone  also provides effective  analgesia .  Patients who experience inadequate pain relief or intolerable side effects with other opioids or who suffer from neuropathic pain may benefit from a transition to methadone as their  analgesic  agent. Adverse effects, particularly respiratory depression and death, make a fundamental knowledge of  methadone 's pharmacological properties essential to the provider considering  methadone  as  analgesic  therapy for a patient with chronic pain. [ 135 ]


Patients who have  sciatic  pain (pain in the back, radiating down the buttock to the leg) and clear clinical findings of an identifiable  radicular  nerve loss caused by a herniated disc will have a better post operative course than those who simply have low back pain. If a specific disc herniation causing pressure on a nerve root cannot be identified, the results of surgery are likely to be disappointing. Patients involved in worker's compensation, tort litigation or other compensation systems tend to fare more poorly after surgery. Surgery for spinal stenosis usually has a good outcome, if the surgery is done in an extensive manner, and done within the first year or so of the appearance of symptoms. [ 11 ] [ 60 ] [ 136 ] [ 137 ] [ 138 ]


Oaklander and North define the Failed Back Syndrome as a chronic pain patient after one or more surgical procedure to the spine.  They delineated these characteristics of the relation between the patient and the surgeon: