Tarlovcyst and arachnoiditis 

 Home  | Photoalbum  | Contact  





Dr Aldrete & al

Extract from : "Arachnoïditis: the evidence revealed" 
Written by Prof.J.A. Aldrete 
publisher “Editorial Alfil” Mexico City – 2009 
for buying go to : 
J. Antonio Aldrete, MD, MS  
Rhamsis F. Ghaly, MD, FACS 
Previously a subject that has received little attention as a pre-determinant factor in the development of complications in spinal interventions, is now, receiving greater acknowledgement as a cause of certain symptomatology that does not conform to the classical clinical picture of radiculopathy, postural cephalea, or CSF hypotension syndromes. In stead, these not so rare developmental lesions are found incidentally, more readily by the more common use of magnetic resonance that has become the preferred diagnostic tool to determine the nature and the extent of some neurological diseases. 
These cysts are noted when neurological symptoms appear from the compressive effect they may have produced in the skull or in the spine. Formerly, they have been considered just an unexpected finding, but in fact they may contribute to the origin of such symptoms, they may aggravate them or they may be a warning signal that such particular patient may have a minor disruption of the normal cerebrospinal fluid (CSF) circulation or of the blood/ brain barrier that might have triggered a greater production of the CSF volume, a delay in its ascending return and/or an impairment of its absorption that may stagnate within the dural sac enlarging the cysts and even forming new cystic-like cavities. 
Respiratory movements and pulsatil (cardiac) movements may be seen transmitted on the normal dural cover in the cranium or in the spine; also, changes of posture, coughing, sneezing, the Valsalva maneuver and bearing down during defecation may produce displacement of the CSF. Venous obstruction, as produced by the Queckenstedt test (bilateral compression of the jugular veins) increases pressure within the cranium and a corresponding increase displacement of CSF down the spine takes place. Increases of abdominal pressure produce a concomitant elevation of the lumbar spine pressure and so the symptoms related to the neural tube size in relation to the diameter of the vertebral canal, may be exacerbated. 
This clear liquor is produced in the intracranial arachnoid villi located next to the inner layer of the dural wall, precisely in the astrocyte layer of the brain’s capillary endothelium. The rate of production varies according to the inner pressure and pathological conditions, but it has been estimated that it is produced at a rate of 0.4ml/min or about 500ml/day, implying a rate of turn over of about 4 times in 24 hrs. It is glucose rich, but protein poor, as a matter of fact, 60�f the CSF proteins pass through the choroids plexus. The concentration of proteins is greater in the lumbar than in the, thoracic or cervical regions, which in turn have greater concentration of proteins than the cisterna magna or the cerebral ventricles (1). In addition, there are enzymes, substance P, serotonin, ions, tryptophan, buffers (2) (much less than in blood). 
The arachnoid villi, also called Pacchioni’s granulations, are cylindrical structures found within the dural wall, more frequently around the longitudinal venous sinus, the lateral sinus and other major intracranial venous sinuses. They are either round or oval, adhered internally to the pia by a wide base pedicle (Figure 1) with direct contact with the venous sinuses as they appear submerged in them, while the opposite end appears to protrude toward the subarachnoid compartment, including some connective tissue, trabeculae intertwined with other trabeculae coming from the veins but saturated, in the inward space, mostly as a sponge, by CSF. 
They are separated by a thin endothelial membrane within a venous sinus and a thicker endothelial cover or dura matter exposed to the arachnoid (3). It can be assumed that in the normal state, when the subarachnoid pressure increases, the venous sinuses’ pressure decreases; however in pathological conditions, this mechanism may function differently, increasing or decreasing both sides of the blood-brain (B/B) barrier, simultaneously (4). 
It is usually assumed that the venous system is capable to absorb three times the volume of CSF produced daily; however it has been suspected that under certain abnormal situations such as after injections of irritant substances into the CSF (methylene blue, blood, 2-chloroprocaine), a mild reabsorption impairment may take place producing then a “low-pressure communicating hydrocephalus syndrome” superimposed to whatever other condition may be present. 
These may occur in the cranium or in the spine; the most common location for the former are in the cerebello-pontine angle; whereas in the spine, they are most frequently seen at the distal end of the sacral vertebral canal (figure 2) precisely at the termination of the sac, also common at the dorsal aspect of the thoracic spine, usually located in the mid line but may be present at any other location. Another characteristic is the fact that in most cases congenital cysts are extradural whereas acquired cysts are in their majority, located within the dural sac (5). 
Arachnoid cysts are usually, clinically silent, in the first four decades of life. They may be found incidentally at a radiological study or whenever circumstances (trauma, illness) indicate such a study. The symptoms derived from the presence of theses cystic structures are usually mild or not very apparent, as the vertebral canal and the adjacent structures have gradually accommodated to their presence. However, they may become clinically evident at the fourth or fifth decade of life when degenerative changes in the spine may indicate a radiological examination and then the cysts are discovered. However, any prior event such as dural punctures, spinal anesthesia or trauma, whenever the circulation of CSF is altered (i.e. subsequent CSF leak), or if a sudden increase of the intradural pressure takes place (hematoma, epidural blood patches, tumors, etc.) then the clinical manifestations may appear to become magnified (6). Attempts to remove them may elicit recurrence, within months, under greater pressure. Of interest was the report by de Seze et al (6a) obtained from retrospective questionnaires sent to rehabilitation centers in France only to find that spinal arachnoid cysts were present in two out of 12 patients that developed severe, long-lasting complications of the nerve root and spinal cord after central neuraxial blockades. 
Aldrete et al (6b) reported one patient with chronic headaches that received a spinal anesthetic and developed PDPH. After receiving an epidural blood patch the headache changed to being relieved by standing up and worsening in the supine position. An MRI of the brain showed “subclinical hydrocephalus, that persisted for four years. 
The arachnoid cysts are the most commonly found intraspinal cysts; they usually have a single layered arachnoid cell lining without epithelium or cilia, their fluid is colorless and undistinguishable from CSF. There is the possibility that they have a direct communication with the dural sac and although a communicating duct is seldom shown, standing MRI with contrast ought to complement the usual work up on these patients, in order to find a communicating channel with the dural sac. Detailed studies performed by Santamarta et al (7) have not only shown such linkage but have proposed that symptoms vary as there is usually a “slit-valve” mechanism that may explain the delay and periodicity of symptoms seen in many of these patients. Further attempts to excise or to drain such cystic-like structures usually results in recurrence and may trigger further scarring in and around the dural sac with tethering of the nerve roots ( figure 3) and/or the spinal cord within (figure 4). If patients with a silent sacral arachnoid cyst receive caudal epidural blocks or catheters they run the risk of a dural puncture at the level of the cyst that may precipitate a major alteration of the CSF migration (7a) and a serious CSF leak. 
In cases of progressive cyst enlargement, patients usually have a paretic gait, a positive Romberg test with non-lateralized instability, lower extremity weakness and not uncommonly somatognosia mostly in the more involved foot; occasionally, in the pre-radiological era they were mistaken for tumors (7, 8). In contrast to other space occupying lesions within the vertebral canal, these patients surprisingly exhibit, hyperreflexia of the patellar and Achilles tendon locations. 
These clinical features vary from the so called Tarlov cysts (9) which also consist of sacral perineural arachnoid cysts arising from the neural tube, but appearing more lateral; they should not be confused with cystic dilatation arising from the cuffs accompanying the early exit of the nerve roots from the dural sac. Tarlov cysts are usually lateral to the dural sac (figure 5), within the sacral canal, but should not be confused with other cyst-like extensions of the dural sac. As shown in Figure 6, on occasion, they may be larger than the dural sac at the sacral level. An schematic drawing shows the difference between a pseudomeningocele and a Tarlov cyst in reference to the normal morphology of the nerve root sheath and its accompanying dural cuff (Figure 7) appearing sometimes parallel to the dural sac or to one side of it, at the most dependant and distal end of the meningeal sac (10). A communicating duct may or may not be demonstrable at MRI with contrast or in a CAT scan post myelogram (11). Attempts to treat these headaches by epidural blood patches are not only futile, but hazardous, as another incidental dural entry may occur. 
An unusual congenital cyst is the entero-dorsal, enterogenous or entero-neural cyst, that consists of a persistent communication between the neuroenteric canal and the primitive endoderm from early gestation that may be manifested by pressure or moderate pain sensation in the mid thoracic region, sometimes elicited by swallowing or by moderate trauma to the thoracic spine. At radiological exam, they are most commonly found in the ventral cervico-thoracic and thoracic canal and may be occasionally associated with duplication of the GI tract and also with dysraphic bony abnormalities of the vertebral bodies. The lining of these cysts contain ciliated secreting columnar epithelium that can secrete mucin which is phatognomonic of these cysts (12). Attempts to drain them by fenestration or by performing a microsurgical excision are indeed difficult because of their location and hazardous because of the delicate adjacent structures; besides these attempts are frequently followed by worse clinical symptoms derived from the fibrosis and scarring that eventually developed.  
In general, if the cysts give indication to grow or they become highly symptomatic, cyst-to-subarachnoid, cyst-to-pleura or cyst-to-peritoneum shunts have been advocated to divert the cystic fluid, with some success. The laparoscopic implantation of the distal portion of the catheter has simplified this procedure and has reduced the frequency of episodes of dysfunction Although they may require repeat revisions (13).  
Ependymal cysts are more frequently noted in children around the ventral aspect of the cervical spinal cord; they may have a ciliated cuboidal or columnar epithelium lining. They manifest as an occupying mass lesion with slow rate of growth  
In some instances, dermal sinus tracts present in childhood as skin findings with associated neurological deficits or infection. These dermal sinus are an uncommon form of dysraphism more frequently found in the lumbosacral region but occasionally in the neck as well. On the corresponding skin area, pigmentation changes (Figure 8), erythema, sinus ostea, skin tags and subcutaneous masses may be found. Ackerman and Menezes (12) suggested that before surgical exploration, complete radiological and electrophysiological testing is advised, because during surgical exploration, bifid spinous processes, tethered spinal cords and/or clumped spinal roots may be found, ensuing in neurological deficits persisting for life, in many of these patients. 
Some of these truly cystic entities ought to be differentiated from pseudocysts that develop after surgical intradural interventions which appear to form from the adherence of nerve roots to each other, to the spinal cord which seem to be cystic-like in sagittal views (Figure 3 and 4). But in fact they are misrepresentations of pseudo cavities by the loculation of CSF created by plastered roots to the internal wall of the sac, to other roots or by the so called phenomenon of “tethering” (figure 3 and 4) common in the thoracic spinal cord and adhesion of the lumbar nerve roots to the dural sac. They should not be diagnosed as cysts (figure 9), since they in reality do not form a completely closed cavity (14). 
Most arachnoid (sacral) and entero-neural cysts, if asymptomatic, are best left alone, but should be followed up for any signs of enlargement or compromise of the adjacent neural structures; in the former case, caudal punctures are contraindicated. Although, a lumbar epidural or subarachnoid block may be feasible (6a, 7a), however, the risk of an incidental dural puncture on the former with possibility of CSF leaks in both instances may destabilize an otherwise normal CSF flow. Though not very common, the seriousness of this complication does not warrant their indication, as their consequences may be organ function threatening. 
A most interesting issue is the possible genetic link of arachnoid cysts found in a sister and a brother (15) suggesting that relatives of these patients ought to have a genetic profile and a neurological work-up done. The incidence of this abnormality remains undetermined, as of this date. 
These usually congenital lesions may be defined as “a hernial protrusion of the meninges through a defect of the skull or of the osseous structures of the spinal column”; then, by definition, “intraspinal meningocele” or an “occult meningocele” are misnomers as they appear in the medical literature. The majority of true meningoceles are usually associated with failure of development of the vertebral arch. Isolated cases may be seen in patients with neurofibromatosis, Marfan’s syndrome, Ehlers-Danlos syndrome and a few other connective tissue disorders or in chondro-oseus dysplasias. Discovery of some of these lesions by radiologic studies justifies to perform a complete neurological examination on these patients. 
A variety of cystic and cystic-like formations may develop intradural from a number of causes. Although occasionally it is not easy to determine the etiology, in most instances there are previous antecedents (tuberculosis, spinal taps, spinal operations (Figure 9), incidental dural punctures (Figure 10), cephaleas, etc) that may offer clues as to the possible origin of the cysts (16, 17). Rarely do intradural cysts occur spontaneously. 
Several theories have been advanced as to the pathophysiology of these lesions most of them related to an impaired circulation and distribution of the CSF within the dural sac, being: 
a) The acute meningeal inflammatory process, after some time gives way to scarring and adhesions with subsequent vessel constriction, cord ischemia and local softening leading to cavity formation (figure 10). 
b) The arachnoiditic process is of such magnitude that partial or near total obstruction of the dural sac takes place with considerable impairment of the CSF flow inducing central canal dilatation, followed by ischemia, myelomalacia approaching the appearance of a syrinx but with the nerve roots evident around the spinal cord as shown in figure 10a. 
c) Less common are cavities may be created within the spinal cord parenchyma as demonstrated in figure 12 with enhancement of the spinal nerve roots and the cord, due to intramedullary injury (from needle puncture and catheter cannulation). 
These events may be the cause of not only primary cephaleas, but also pressure sensation in the lumbar spine or the neck region, both not necessarily related to other causes of back pain or headache, respectively. Dysesthesia may be present, with or without cauda equina syndrome with transverse myelitis-like syndrome. Diagnostic interventions such as dural puncture, differential spinals or discography going astray may further exacerbate the symptoms and complicate the possible therapeutic measures. 
Previous spinal invasion have been noted to produce tuberculous meningitis and arachnoid cysts (17). Undiagnosed cases of neurocysticercosis may present as space-occupying lesions from good size subarachnoid cysts appearing as intradural extramedullary masses with meningeal reaction at imaging studies; their origin may be confirmed by positive immunodiagnostic tests (18, 18a). For specific details, readers are advised to see chapter-------. 
When lipid base contrast media was used, lumbar myelography was also known to produce cystic lesions (19, 20, 20a) that could be found either intracranially or within the spinal leptomeninges. 
Nogues et al (21) reported one case of a subarachnoid cyst and an intradural extramedullary spinal lesion in a patient that had undergone lumbar epidural anesthesia complicated by a “total spinal”, one year earlier. A second patient had prolonged sensory block after epidural anesthesia; six years later, a subarachnoid cyst (from C7 to T6 and a syrinx from T9 downwards) were found at MRI with “mild descent of cerebellar tonsils”. The third patient that had epidural anesthesia, developed unsteady gait, urinary dysfunction and legs weakness. She was found to have hyperreflexia and bilateral clonus; at MRI a cystic collection with multiple septa were noted from T1 to T10 and a tethered cord. An intramedullary cyst was also seen from T10 to T12. Dense arachnoiditis was found in the thoracic and lumbar regions requiring a lumbo-peritoneal shunt. All patients had a gradually deteriorating course thereafter. In every case, substantial doses of lidocaine 2�ere used as anesthetic. The authors postulated that the intrathecal injection of an epidural dose of the local anesthetics might have produced cord ischemia in case #1 and in case #2, the presence of Chiari I syndrome could have contributed to the formation of syringomyelia and in patient #3 the extensive resection of the lesions probably caused the progressive neuro deficit that followed. In every instance, alteration of the CSF normal flow was suspected. 
Sklar et al (22) reported eight patients with acquired intradural arachnoid abnormalities supposedly caused by epidural anesthesia; at MRI examination subarachnoid cysts were found in six of them with irregular surface noted in seven of them. Associated intramedullary cysts and myelomalacia were seen in two cases. The authors attributed the cystic arachnoiditis occurring in these patients to a previous epidural anesthetic given to them presumptively, but not proven, due to preservatives contained in the local anesthetics used. One other case was caused by an epidural infection that followed the epidural anesthetic. 
Similarly, Sghirlanzoni et al (23), reported several cases of intrathecal cysts that supposedly followed the administration of epidural anesthesia; data on the local anesthetics used, dosages and details on technical difficulty were not described. 
In a different view, Taniguchi et al (24) reported the occurrence of an arachnoid cyst that developed after repair of ruptured vertebral aneurysm in which in addition to successful clipping, fibrin glue was applied to the suture line to achieve a “water tight dural closure” that could not be obtained otherwise; also bone dust, bone chips and fibrin glue were used to close the bone defect. Gait abnormalities, loss of balance and sensory loss on both feet were noted and the radiological studies showed a spinal arachnoid cyst and spinal arachnoiditis. Similar findings were described by Shah et al, who reported a patient that had had a myelogram 28 years earlier.  
Other foreign materials have been used in attempts to seal dural defects or reinforce weak suture lines, among them polyglactin 910 (25), Silastic (25a), polaxamer 407 (26), Adcon-L (27) , but all of them have produced occasional subsequent cyst formation, arachnoiditis and fibrosis. 
Other mechanism is the dilatation of the dural and arachnoidal sheets with proliferation of the “root arachnoidea” caused by loculation of the CSF as its exit into extradural space and is impeded by intrathecal proliferation of the arachnoid, and extradural connective and fibrous tissues, where the laminectomy was done (Figure 10), extending to just above the dorsal ganglion, as noted by Rexed (28) who describes them as acting as a funnel, loculating CSF (Figure 9, 10a), clinically represented as mild, but persistent radiculopathy. 
Of 15 798 patients examined by the author, for low back pain, from 1989 to 2008, six cases of asymptomatic arachnoid cysts, located in the sacral canal (29), were found at radiological examination ( Figure 2). No action was taken except to inform the patients and warn them about any intraspinal intervention especially the caudal approach to epidural anesthesia and dural punctures including spinal anesthesia. 
In the same lapse of time, from the same group, 38 adult patients with acquired arachnoid cysts have been seen, their medical records were reviewed, a physical exam was conducted with a complete review of all the imaging and electrophysiological studies available (29a). In 24 patients, more than one cyst was noted, usually with location in more than one segment of the spine. In 21 instances, spinal surgery was the initial procedure, whereas in seven patients the primary procedure was steroid epidural injection with evidence of unexpected dural puncture, two received epidural anesthesia, five more had undergone spinal anesthesia and three others sustained paraspinal pain-relief procedures. The data obtained from such reviews is shown in Table 1.  
Cranial (2) Spinal Anesthesia Ventric-Pleural Shunt x 1 * 
Cervical (1) Paraesthesia in cervical  
Intramedullary Surgical excision Yes 
Steroid injection Cervical-pleural shunt no 
Thoracic (12) Tumors, granulomas, epidural anesthesia, surgery Surgical excision Yes 
Thorac-pleura shunt No 
Lumbar (18) ISEI, surgery 
Epidural Anesthesia Surgical excision-failed Yes 
Lumbar-peritonial shunt No 
Multiple (24) Laminectomies, Fusions Repeated operations Intrathecal infusion pumps Yes 
Fibrin glue, ADL-40, Floseal Reoperation  
Thrombin, Methylene blue  
Local Anesthetic , ISEI  
*one patient developed facial nerve palsy after placement of the ventricular shunt catheter over the VII cranial nerve nucleus Figures 11 and 12) 
High dosages, large volumes and/or high concentrations 
ISEI=Incidental intrathecal Steroid Injection  
Most treatments were unsuccessful.  
It must be clarified, that in patients with lumbar arachnoiditis, the abnormal position and clumping of the nerve roots at the beginning of the cauda equina may resemble cystic cavities in sagittal views (figure 13) and also occasionally in axial views (figure 14). However at surgical exploration these cystic cavities are not found, but just the agglomeration of the nerve roots and their aberrant adherence to the internal wall of the dural sac, which, in rare instances, may loculate cerebrospinal fluid, giving the false appearance of cavitary cysts but in fact are pseudocysts ( figures 15 and 16) circumscribed by the very adjoining, affected nerve roots. 
“Imaging mirages” may also appear in cases of stenosis of a non-operated symptomatic spine demonstrating certain compression of the cauda equina, especially at the levels of the L3 and L4 vertebrae where Larsen and Smith (30) found the vertebral canal to be narrower, more so at the L3-L4 disc level. The lumbar sagittal diameters were noted not to be different between adult men and women irrespective of the presence or absence of stenosis. Essentially, these authors felt that the dural sac acts as a “thin walled liquid filled container”, exercising minimal tension on its wall. In these cases, patients usually have a magnification of their symptoms not justified in their radiological findings; moreover, any interventional procedure within the lumbar spine has high probability of incidental dural puncture, CSF leaks, dural tears and considerable reduction in the improvement resultant from any invasive or operative procedure performed in the lumbar spine. 
The opposite may occur when two interventions are done in adjacent interspaces, leaving a cystic-like round dilatation in between two narrow points.  
Currently, most of these cases follow surgical procedures or interventional procedures within and around the spine (6, 31) with subsequent extradural scarring and fibrosis eventually forming a dural dilatation, a dural ectasia or gradually a progressive radial enlargement of the sac (32), sometimes doubling the diameter (figure 16). Scintillography has allowed to take another view of pseudocysts that appear to be created by adjacent constrictions, leaving one small central round receptacle with CSF, but clearly demonstrating the narrow points above and below it (Figure 17). Attempts to treat arachnoiditis cysts surgically are justified only when a) spinal cord or nerve roots are severely compromised (32), b) to avoid loosing sphicter function or, c) motor activity of the lower extremities. When any of these instances occurs a decompressive procedure might need to be done; otherwise reappearance of fibrosis and scarring would offset whatever initial gain was obtained. 
A recently published review of neurological complications after central neuraxial blockade (32) noted that of nine patients that had this complication, two had spinal arachnoid cysts. Attempts to drain them, or to perform invasive procedures in the spine that may penetrate the dural sac may have deleterious consequences (6a, 7a, 33, 34), therefore any interventional or surgical procedure is discouraged, unless absolutely necessary. 
In their majority, extradural but intraspinal cysts are usually congenital; they are asymptomatic during childhood and adolescence but they may be discovered as imaging studies are obtained in the process of diagnosis of degenerative pathology. Puncture or removal may be hazardous and serious sequelae may follow the alteration of the normal flow of the cerebrospinal fluid.  
The discovery of intradural cysts implies a serious complication from whatever procedure preceded the finding. This diagnosis requires a complete work up to identify the cause, the size, the possible location of another cyst anywhere in the neuroaxis. Derivation of excessive CSF to an adjacent low pressure cavity such as the pleura or the peritoneum seems to be the least harmful approach rather than to attempt to surgically excise them. Extradural cysts, if not causing pressure on any neurological or vascular structure may be best left alone and be followed periodically. Unsuspected cystic lesions within the spine such as Tarlov cysts may expand the dural sac and may well displace the spinal cord and/or the nerve roots. Above all, a well planned diagnostic strategy using various imaging studies and changing the position of the patient to determine if the cord and nerve roots are affixed to the dural sac wall, repeated neurological examinations will provide progress or the lack of it as the patient is closely observed. The careful and not too long diagnostic process is best followed by an objective decision for treatment of these conditions. Interventions invading the spine, especially the dural would be best avoided, unless absolutely indicated.  
1. Bernards CL: The spinal meninges and their role in spinal drug movement. In Spinal Drug Delivery. T L Yaksh (ed). Elsevier Science BV, Amsterdam. 1999:pp.133-75.  
2. Weber ML, Aldrete JA, O’Higgins JW: Tensoes de gases, pH nos texidios e no liquido intersticial: Revisao de metodologia, normais e anormais. Rev Bras Anest 1972:22:102-9.  
3. Testut L, Latarjet A: Anatomia Humana. Vol III. Salvat Editores SA. Barcelona. 1976:pp. 19-52. 
4. Drayer BP, Schnechel DE, Bydder GM et al: Radiographic quantitation of reversible blood-brain barrier disruption in-vivo. Radiology 1982:143:85-9. 
5. Mailleux P, Dooms G, Coulier B et al: Lumbar arachnoid cysts: two unusual cases. J Belge Radiol 1992:75:119-23. 
6. Wang MY, Allan DO, Levi MD, Green BA: Intradural spinal arachnoid cysts in adults. Surg Neurol 2003:60:49-51. 
6a. de Sèze M-P, Sztark F, Janvier G, et al: Severe and long-lasting complications of the nerve root and spinal cord after central neuraxial blockade. Anesth Analg 2007;104:975-979. 
6b.Aldrete JA, Reza Medina M, Daud O, et al: Exacerbation of pre existing neurological deficits by neuraxial anesthesia: report of seven cases. J Clin Anesth 2005:17:304-13. 
7. Santamarta D, Aguas J, Ferrer E: The natural history of arachnoid cysts: endoscopic and cine-mode MRI evidence of a slit-valve mechanism. Minim Invasive Neurosurg 1995:38:133-7. 
7a. Lacassie HJ, Jaklitsch P, Njaa M et al: Sacral cyst and choice of anesthesia technique for cesarean section. Anesthesiology 2005:103:Suppl A-139. 
8. Stookey B: Adhesive spinal arachnoiditis, simulating spinal cord tumor. Arch Neurol Psych 1927:17:151-3. 
9. Tarlov IM: Sacral nerve root cysts. Another cause of sciatica or cauda equina syndrome. CC Thomas, Springield, IL. 1953. 
10. Ceccittini M, Florio L: Cystic spinal arachnoiditis: Diagnostic problems in differentiation from intradural spinal neoplasms. Arch Putti Chir Organi :1967:22:64-77. 
11. Borgerson, Varry PS: Extradural psudocysts. Acta Orthopedica Scand 1973:44:12-20. 
12. Ackerman LL, Menezes AH: Spinal congenital dermal sinuses: a 30 year experience. Pediatrics 2003:112:641-7. 
13. Bani A, Telker D, Hesler W et al: Minimally invasive implantation of the peritoneal catheter in V-P shunt placement for hydrocephalus. J Neurosurgery 20006:105:869-72. 
14. Vloeberghs M, Herregodts P, Stadnik T et al: Spinal arachnoiditis mimicking a spinal cord tumor: a case report and review of the literature. Surg Neurol 1992:37:211-5. 
15. Wilson WG, Deponte KE, McIlhenny J et al: Arachnoid cysts in a brother and sister. J Med Genet 1988:43:57-64. 
16. Quinones-Hinojosa A, Nader Sanai BS, Fischbein N et al; Extensive intradural arachnoid cyst of the lumbar spine canal. Surg Neurol 2003:60:57-59. 
17. Van Paesschen W, Van de Kerchove M, Appel B et al: Arachnoiditis ossificans and an arachnoid cyst after cranial tuberculous meningitis. Neurology 1990:40: 714-6. 
18. Blagoveshchenskaia NS: Subarachnoid cysts from cysticercosis. Neurochirurgie 1988:34:280-5. 
18a.Soto-Hernandez JL, Gomez-Llata Andrade S, Rojas-Echeverri LA, et al: Subarachnoid hemorrhage secondary to a ruptured inflammatory aneurysm: a possible manifestation of neurocysticercosis: case report. Neurosurgery 1996:38:197-9. 
19. Motta G Alvisi C: Adhesive, cystic leptomeningitis of the cerebellopontine angle. Rev Otoneurooftalmol 1968:43:17-6. 
20. Kriss TC, Kriss VM: Symptomatic spinal intradural arachnoid cyst development after lumbar myelography. Case report and review of literature. Spine 1997:22:568-72. 
20a.Gnanalingham KK, Joshi SM, Sabin I: Thoracic arachnoiditis, arachnoid cyst and syrinx formation secondary to myelography with Myodil, 30 years previously. Euro Spine J 2006:15:661-3. 
21. Nogues LA, Merello M, Leiguarda R et al: Subarachnoid and intramedullary cysts secondary to epidural anesthesia for gynecological surgery. Eur Neurol 1992:32:99-101. 
22. Sklar EM, Quencer RM, Green BA et al: Complications of epidural anesthesia: MR appearance of abnormalities. Radiology 1991:181:549-54. 
23. Sghirlanzoni A, Marazzi R, Pareyson D et al: Epidural anesthesia and spinal arachnoiditis. Anaesthesia 1989: 44:317-21. 
24. Taniguchi Y S, Suzuki R, Okadaa M et al: Spinal arachnoiditic cysts developing after surgical treatment of a ruptured vertebral artery aneurysm. A possible complication of topical use of fibrin glue. J Neurosurg 1996:84:526-9. 
24a.Shah J, Patkar D, Parmar H et al: Arachnoiditis associated with arachnoid cyst formation and cord tethering following myelography: MRI features. Australian Radiology 2001:45:236-9. 
25. Nessbaum CE, Maurer PK, McDonald JV: Vicryl (polyglactin 910) mesh as a dural substitute in the presence of pia-arachnoid injury. J Neurosurg 1989:71:124-7. 
25a.Lazar ML, Bland JE: Microsurgical intradural lysis and Silastic dural patch  
grafting in lumbar adhesive arachnoiditis. Neurosurgery 1979:5:771-2. 
26. Reigel DH, Bazmi B, Shih SR et al: A pilot investigation of poloxamer 407 for the prevention of meningeal adhesions in the rabbit. Pediatr Neurosurg 1993:19:250-5. 
27. Robertson JT, Maier K, Anderson RW et al: Prevention of epidural fibrosis with Adcon-L in presence of a durotomy during disc surgery: Experiences with a pre-clinical model. Neurol Res 1999:Suppl:61-6. 
28. Rexed B: Arachnoidal proliferations with cyst formation in human spinal nerve roots at their entry into the intervertebral foramina. Acta Radiologica 1947:36:414-21.  
29. Aldrete JA, Ramirez-Bermejo A, Godinez N: unpublished data. 
29a.Aldrete JA, Year Nadal J, Goyenechea F: unpublished data. 
30. Larsen JL, Smith D: Size of the subarachnoid space in stenosis of the lumbar canal. Acta Radiologica Diagnosis 1980:21:627-31. 
31. Johnstone J, Matheny J: Microscopic lysis of adhesive arachnoiditis. Spine 1978:8:36-9. 
32. Howieson J, Norrel HA, Wilson CB: Expansion of the subarachnoid space in the lumbosacral region. Radiology 1968:90:988-92. 
33. Tseng SH, Lin SM: Surgical treatment of thoracic arachnoiditis with multiple subarachnoid cysts caused by epidural anesthesia. Clin Neurol Neurosurg 1997:99:256-8. 
34. Lolge S, Chawla A, Shah J, et al: MRI of spinal intradural arachnoid cyst formation following tuberculous meningitis. Br J Rad 2004:77:920:681-4. 
Adler R, Lenz G: Neurological complaints after unsuccessful spinal anaesthesia as a manifestation of incipient syringomyelia. Eur J Anaesthesiol 1998;15:103-5. 
1. Histologic section of an arachnoid villi protruding through the arachnoid into the subarachnoid space; the vessels providing blood are at the base. The apex appears deviated. x 40. 
2. MRI of the lumbar spine (sagittal view) showing an arachnoid cyst at the S2 level (large arrow), The posterior epidural spaces (small triangles) are gradually smaller, until one is barely perceived at L5-S1. 
3. Axial view of the lumbar spine MRI demonstrating tethering of the lumbar nerve roots from the right wall of the dural sac, to its left wall (small white arrow head. A protruding intervertebral disc, responsible for this anomaly is shown at T12-L1 level (white 1 depicts vertebra L1). 
4. Sagittal view of a thoracic spine MRI showing a tethered spinal cord leaving a posterior intrathecal space giving the false impression of a cyst (white arrow). 
5. A Tarlov Cyst is shown at the S2 level in this sagittal view of the lumbar spine that exhibits thickened and adhered nerve roots from L3 to S1. The L4-L5 intervertebral disc is protruding 
6. Axial view of the S1 vertebra showing a left Tarlov Cyst (TC) displacing the dural sac (D) toward the left. The S1 nerve roots are depicted (S1). 
7. Schematic representation of the arachnoid and dura extending as it covers to early portion of the cuff. The position of the Tarlov cyst allows CSF to enter the bulging cuff but no leak exists. In a pseudomeningocele the false sac surrounds the dura-arachnoid unit, note the defect of the dura-arachnoid unit that allow the CSF to leak and the pseudosac to form.  
8. Midline congenital discoloration of the skin indicating a possible neural tube defect. 
9. Sagittal view of an MRI of the lumbar spine with thicker nerve rotos displaced anteriorly and evenly simulating a cyst (black arrows) behind the L4 and L5 vertebrae, where a laminectomy had been done.  
10. Axial view of an MRI depicting what appears to be an abnormal spinal cord with a filling defect on the right lateral section ((white arrow). 
10a. Post myelogram CAT scan of L3 vertebra, with nerve roots clumped and adhered to the dural sac wall. The central cavity gives the impression of being a cyst. There is fibrosis in the posterior left region of the vertebral canal around the sac and evidence of a midline incision. 
11. Lateral views of an MRI of the skull showing signs of hypertensive hydrocephalus with a wider than usual dural to cerebrum space, an enlarged ventricle (V) and a distended 3rd ventricle (white asterisk). A portion of a catheter is seen in the lower frame. 
12. MRI of the brain showing the draining shunt catheter on the floor of the ventricle, that was apparently over the nucleus of the VII cranial nerve resulting in facial paralysis. 
13. Sagittal view of MRI of the lumbar and lower thoracic spine displaying a small cyst (white arrow) within the lumbar expansion of the thoracic cord. 
14. Axial view of an MRI of L5 vertebra showing a dilatation of the dural cuff around the left L5 nerve. 
15. Sagittal view of an MRI of the lumbar spine showing tethering of the spinal cord (large black arrow), a pseudocyst is shown posterior to the L2-L3 disc, limited by a transverse pseudocyst like wall (vertical black arrow) with nerve roots descending from it. At least two irregular shaped pseudocysts are seen in the subarachnoid space from L4 to S1. 
16. Lumbar spine MRI shows in a sagittal view a constricted dural sac (long arrow) at the L4-L5 level with distal dilatation (short arrow) suggesting a pseudocyst.  
17. Scintillogram of the lumbar spinal dural sac showing a funnel like constriction (large white arrow) appearing at the site of a lumbar laminectomy that had been repeated three times, attempting to drain intrathecal cysts. The right renal pelvis is shown (white arrow head). 

(c) Tarlov-aracEuropeInformation - Made with the help of
Last modified on 1.11.2010
- Already 699 visits on this website!