Daniel J. Won

Tethered cord syndrome: overview of diagnosis and treatment

Abstract This article covers the basis of tethered cord syndrome as a stretch-induced spinal cord disorder, including pathophysiology, signs and symptoms, imaging diagnosis, indication for surgical treatment, and surgical procedures. Anomalies that cause mechanical spinal cord tethering are listed, and the surgical untethering technique for each anomaly is described.

Concept of arteriovenous malformation compartments and surgical management

Abstract Cerebral AVMs are known to be a source of intracranial hemorrhages and epileptic seizures. Their natural history indicates approximately 15% mortality and 35% morbidity over a 15-year period. This significant mortality and morbidity mandates a need for satisfactory treatment of this entity, ideally by elimination of AVMs. Microsurgical resection, endovascular embolization and radiosurgery (irradiation) are the three effective modes of treatment currently available. However, no objective criteria have been established for which mode(s) of treatment should be selected for individual patients with AVMs. Considering the complexity of AVMs and variable conditions of individual patients, neurosurgeons, intravascular interventionalists and radiosurgeons must make their own decisions on how to treat each patient based on their experience. In practice, treatment of small AVMs in non-functional areas is favored equally by each of these specialists, while they tend to avoid treatment of large AVMs, particularly those in functional areas of the brain. The authors report the surgical intervention of large AVMs, including those located in functional areas of the hemisphere by special techniques. One can demonstrate AVM compartments by using angiography and with the aid of color Doppler ultrasonography, each compartment can be outlined and dissected individually until all the compartments are isolated without causing any damage to the surrounding brain and the entireAVM is rendered shrunken and then removed. The concept of compartmental treatment of AVMs may be applied in the future to radiosurgery and intravascular embolization of large AVMs.

Symptomatic protocols for adult tethered cord syndrome

Abstract Diagnosis of tethered cord syndrome (TCS) is complicated because anatomical information is not adequate for this task. For example, recent studies have shown that the combination of an elongated cord and a thick filum terminale, demonstrated by MRI or at operation, is no longer an essential feature for the diagnosis of TCS. For TCS diagnosis, emphasis should rather be on its characteristic symptomatology and accentuated by postural changes, since TCS is a functional disorder of the lumbosacral spinal cord. In this report, the authors present the list of signs and symptoms pertinent to TCS in adult and late teenage patients to serve as a diagnostic means.

Adult tethered cord syndrome: relative to spinal cord length and filum thickness

Abstract The adults with tethered cord syndrome (TCS) are divided into two groups: group-1 adult TCS patients with spinal dysraphism; and group-2 patients without dysraphism who develop signs and symptoms in adulthood. A significant number of group-2 patients failed to show elongation of the spinal cord and abnormally thick filum terminale. This paper reports the combinations of the location of the caudal end of the spinal cord and the thickness of the filum terminale in 104 patients with group-2 adult TCS. The caudal end of the spinal cord was found at the L2–3 intervertebral space or above in 37 patients (35.6%) and below L2–3 level in 67 patients (64.4%). The diameter of the filum was <2 mm in 60 patients (57.7%) and ≥2 mm in 44 patients (42.3%). These data clearly indicate that the pre-operative diagnosis of adult TCS must rely primarily on the neurological symptomatology and the specific imaging feature, posterior displacement of the conus and filum that attach the posterior arachnid membrane.

348 Pain Control by Coaptation Procedure C3 and C4 Anterior Rami to Brachial Plexus.

INTRODUCTION Previously, the authors presented the coaptation of C3 and C4 primary rami to one of brachial plexus trunks to regain function from cervical root avulsion-caused paralysis. The purpose of this presentation is 2-fold: (1) discuss specific surgical techniques and (2) discuss control or prevention of intractable pain associated with root avulsion. METHODS (1) The surgical procedure consists of exposure of C3 and C4 anterior rami coaptation to the upper trunk (Erb-Duchenne) or lower trunk (Klumpke), with sural nerve bridge graft, and additionally intercostal nerve coaptation to median and ulnar nerves for flail arm. (2) Of 30 total patients, 23 patients presented with Erb-Duchenne palsy due to C5 and C6 root avulsion, 3 presented with Klumpke palsy due to C8 and T1 avulsion, and 4 presented with C5 through T1 avulsion (a flail arm). These patients are divided into 2 groups according to pain control: Group 1 patients were operated on within 3 months after avulsion, group 2 was treated surgically later than 3 months postinjury. RESULTS (1) The surgical procedure consists of exposure of C3 and C4 anterior rami coaptation to the upper trunk (Erb-Duchenne) or lower trunk (Klumpke), with sural nerve bridge graft, and additionally intercostal nerve coaptation to median and ulnar nerves for flail arm. (2) Of 30 patients, 23 patients presented with Erb-Duchenne palsy due to C5 and C6 root avulsion, 3 presented with Klumpke palsy due to C8 and T1 avulsion, and 4 presented with C5 through T1 avulsion (a flail arm). These patients are divided into 2 groups according to pain control: Group 1 patients were operated on within 3 months after avulsion; group 2 was treated surgically later than 3 months post injury. CONCLUSION Coaptation procedures are effective to control arm and hand pain associated with nerve root avulsion.

Syringomyelia Associated with Tethered Cord Syndrome

The pathogenesis and dynamic pathophysiology of syringomyelia are not fully understood. Pathogenetically, syringomyelia is categorized as either a communicating syrinx (hydromyelia) or a noncommunicating syrinx. The latter category includes those caused by (1) contusion, (2) compression, (3) traction, (4) arachnoiditis, (5) tumors, and (6) ischemia. Syringomyelia located in the lumbosacral cord is likely derived from the same types of pathogenesis. The signs and symptoms of lumbosacral syringomyelia are similar to those of tethered cord syndrome (TCS), caused by the lesion being in the central portion of the spinal cord. Neurological deficits in these disorders are motor and sensory deficits in the lower limbs, incontinence, and musculoskeletal deformities. Syringomyelia associated with TCS is a unique combination and difficult to correlate because TCS is a metabolic functional disorder and syringomyelia is an anatomic functional criterion. The authors divided a series of syrinx patients into three groups: (1) those with lumbosacral syringomyelia associated with tethered spinal cord, in which the spinal cord is anchored by an inelastic filum; (2) those with low thoracic and lumbar syringomyelia associated with TCS, in which a lipoma, lipomyelomeningocele, or meningocele manque is the mechanical cause of tethering; and (3) those with a syrinx in the lower thoracic and lumbosacral cord without evidence of a tethered cord. The syrinxes in the patients in all three groups were considered to be isolated from the fourth ventricle cord. The authors’ observations include: (1) The incidence of lumbosacral syrinx in tethered spinal cord patients is much lower than that in TCS patients; (2) The group 1 patients have milder neurological symptomatology than do the group 2 patients. The degree of improvement in the neurological conditions and physical activities are much greater in group 1 than in group 2 patients; (3) Group 3 patients tend to have more serious neurological deficits associated with hydrocephalus and severe musculoskeletal deformities. Based on these facts, the authors postulate that syrinxes should be drained in cases in which the signs and symptoms suggest that the neurological deficits are more significant than those for TCS alone.