Browse

You are looking at 71 - 80 of 101 items for

  • By Author: Tubbs, R. Shane x
  • By Author: Oakes, W. Jerry x
Clear All
Restricted access

R. Shane Tubbs, John C. Wellons III, Jeffrey P. Blount, Paul A. Grabb and W. Jerry Oakes

✓The authors report on three pediatric patients with ventriculoperitoneal (VP) shunts who presented with chronic right shoulder pain. Imaging revealed that the distal peritoneal catheter was positioned between the right hemidiaphragm and liver. Following surgical repositioning of the distal tubing, all patients experienced resolution of their shoulder pain, which has not recurred. Although seemingly rare, referred shoulder pain from a VP shunt should be added to the list of complications seen with this method of cerebrospinal fluid diversion. The clinician who cares for patients with VP shunts may wish to evaluate cases of shoulder pain without obvious neural or musculoskeletal cause by performing imaging of the distal shunt tubing.

Restricted access

R. Shane Tubbs and W. Jerry Oakes

✓Self-mutilation after deafferentation injuries has rarely been reported in humans. The authors report on a 16-year-old girl who was born with a myelomeningocele. In adolescence it was noted that concurrent with her spinal cord becoming symptomatically tethered she began to self-mutilate her digits. A rare manifestation of the tethered spinal cord may be dysesthesias that led to self-mutilation.

Restricted access

R. Shane Tubbs and W. Jerry Oakes

✓Self-mutilation after deafferentation injuries has rarely been reported in humans. The authors report on a 16-year-old girl who was born with a myelomeningocele. In adolescence it was noted that concurrent with her spinal cord becoming symptomatically tethered she began to self-mutilate her digits. A rare manifestation of the tethered spinal cord may be dysesthesias that led to self-mutilation.

Restricted access

R. Shane Tubbs, John C. Wellons III, Jeffrey P. Blount and W. Jerry Oakes

✓The authors present three children born with myelomeningocele and hydrocephalus. Each presented with symptoms/signs of ventriculoperitoneal shunt malfunction. All patients at the time of presentation exhibited significant urinary bladder infections and were appropriately treated for their infection. No patient was found to have an underlying shunt infection. All patients without medically threatening symptoms were carefully observed and noted to have resolution of their shunt dysfunction symptoms/signs following treatment of their urinary bladder infections and thus did not undergo a shunt operation.

Based on the courses of these patients, we believe that significant urinary bladder infection in patients with myelodysplasia in whom a shunt has been placed may often be enough to bring a subclinical shunt malfunction to clinical attention or even to be the cause of temporary distal peritoneal shunt malabsorption. Although the exact mechanism for this dysfunction is unclear, treatment of the bladder infection may address the symptomatic shunt dysfunction in some patients so as to avoid operative intervention. We emphasize, however, that careful observation of these patients should be performed during hospitalization because they often rely on adequate cerebrospinal fluid diversion. Only patients with mild symptomatology should be observed first as the initial line of treatment.

Restricted access

R. Shane Tubbs, John C. Wellons III, Jeffrey P. Blount and W. Jerry Oakes

✓The authors present three children born with myelomeningocele and hydrocephalus. Each presented with symptoms/signs of ventriculoperitoneal shunt malfunction. All patients at the time of presentation exhibited significant urinary bladder infections and were appropriately treated for their infection. No patient was found to have an underlying shunt infection. All patients without medically threatening symptoms were carefully observed and noted to have resolution of their shunt dysfunction symptoms/signs following treatment of their urinary bladder infections and thus did not undergo a shunt operation.

Based on the courses of these patients, we believe that significant urinary bladder infection in patients with myelodysplasia in whom a shunt has been placed may often be enough to bring a subclinical shunt malfunction to clinical attention or even to be the cause of temporary distal peritoneal shunt malabsorption. Although the exact mechanism for this dysfunction is unclear, treatment of the bladder infection may address the symptomatic shunt dysfunction in some patients so as to avoid operative intervention. We emphasize, however, that careful observation of these patients should be performed during hospitalization because they often rely on adequate cerebrospinal fluid diversion. Only patients with mild symptomatology should be observed first as the initial line of treatment.

Restricted access

R. Shane Tubbs, Cheryl R. Killingsworth, Dennis L. Rollins, William M. Smith, Raymond E. Ideker, John C. Wellons III, Jeffrey P. Blount and W. Jerry Oakes

Object. Vagus nerve stimulation is known to decrease the frequency, duration, and intensity of some types of intracranial seizures in both humans and animals. Although many theories abound concerning the mechanism for this action, the true cause remains speculative. To potentially elucidate a pathway in which vagus nerve stimulation aborts seizure activity, seizures were initiated not in the cerebral cortex but in the spinal cord and then vagus nerve stimulation was performed.

Methods. Ten pigs were anesthetized and placed in the lateral position, and a small laminectomy was performed in the lumbar region. Topical penicillin, a known epileptogenic drug to the cerebral cortex and spinal cord, was applied to the dorsal surface of the exposed cord. With the exception of two animals that were used as controls, once seizure activity was discernible via motor convulsion or increased electrical activity the left vagus nerve, which had been previously isolated in the neck, was stimulated. Following multiple stimulations of the vagus nerve and with seizure activity confirmed, the cord was transected in the midthoracic region and vagus nerve stimulation was performed.

Vagus nerve stimulation resulted in cessation of spinal cord seizure activity in all (87.5%) but one experimented animal. Transection of the spinal cord superior to the site of seizure induction resulted in the ineffectiveness of vagus nerve stimulation to cause cessation of seizure activity in all study animals.

Conclusions. The effects of vagus nerve stimulation on induced spinal cord seizures involve descending spinal pathways. The authors believe that this experiment is the first to demonstrate that spinal cord neuronal hyperactivity can be suppressed by stimulation of a cranial nerve. These data may aid in the development of alternative mechanisms for electrical stimulation in patients with medically intractable seizures. Further studies are now necessary to isolate which specific tracts, nuclei, and neurotransmitters are involved in this process.

Restricted access

R. Shane Tubbs, Cheryl R. Killingsworth, Dennis L. Rollins, William M. Smith, Raymond E. Ideker, John C. Wellons III, Jeffrey P. Blount and W. Jerry Oakes

Object

Vagus nerve stimulation is known to decrease the frequency, duration, and intensity of some types of intracranial seizures in both humans and animals. Although many theories abound concerning the mechanism for this action, the true cause remains speculative. To potentially elucidate a pathway in which vagus nerve stimulation aborts seizure activity, seizures were initiated not in the cerebral cortex but in the spinal cord and then vagus nerve stimulation was performed.

Methods

Ten pigs were anesthetized and placed in the lateral position, and a small laminectomy was performed in the lumbar region. Topical penicillin, a known epileptogenic drug to the cerebral cortex and spinal cord, was applied to the dorsal surface of the exposed cord. With the exception of two animals that were used as controls, once seizure activity was discernible via motor convulsion or increased electrical activity the left vagus nerve, which had been previously isolated in the neck, was stimulated. Following multiple stimulations of the vagus nerve and with seizure activity confirmed, the cord was transected in the midthoracic region and vagus nerve stimulation was performed.

Vagus nerve stimulation resulted in cessation of spinal cord seizure activity in all (87.5%) but one experimented animal. Transection of the spinal cord superior to the site of seizure induction resulted in the ineffectiveness of vagus nerve stimulation to cause cessation of seizure activity in all study animals.

Conclusions

The effects of vagus nerve stimulation on induced spinal cord seizures involve descending spinal pathways. The authors believe that this experiment is the first to demonstrate that spinal cord neuronal hyperactivity can be suppressed by stimulation of a cranial nerve. These data may aid in the development of alternative mechanisms for electrical stimulation in patients with medically intractable seizures. Further studies are now necessary to isolate which specific tracts, nuclei, and neurotransmitters are involved in this process.

Restricted access

R. Shane Tubbs, Bermans J. Iskandar, Alfred A. Bartolucci and W. Jerry Oakes

Object. Although the traditional nomenclature used to describe hindbrain hernias is useful, there are certainly patients in whom these morphological entities do not strictly apply. One such group is composed of patients with the more recently described Chiari 1.5 malformation in which a Chiari I malformation is seen in combination with brainstem herniation through the foramen magnum. In an attempt to elucidate further the best surgical strategy and to refine the descriptive terminology, the authors retrospectively analyzed all cases at their institutions in which this form of hindbrain herniation was diagnosed.

Methods. The authors reviewed the database for all patients in whom Chiari 1.5 malformation had been diagnosed. Each patient had undergone a posterior fossa decompressive surgery. Magnetic resonance images were evaluated for the extent of caudal descent of the brainstem, amount of tonsillar ectopia, inclination of the odontoid process, and any brain or brainstem abnormalities. Clinical presentations and postoperative results were correlated to the aforementioned radiological findings.

Twenty-two patients were identified. The obex was a mean 14.4 mm inferior to the foramen magnum, and the medulla exhibited a flattened appearance in the midsagittal plane in all patients. Syringomyelia was documented in 50% of the cases. The cerebellar tonsils were found to lie at C-1 and C-2 in nine and 13 patients, respectively. The mean angulation of the odontoid process was 84.4°. No abnormalities or caudal descent of the midbrain or pons was identified. Eighteen patients experienced resolution of preoperative symptoms. Persistence of syringomyelia prompted a second posterior fossa operation secondary to progressive scoliosis in 13.6% of the patients.

Conclusions. No single sign or symptom was found to be peculiar to the Chiari 1.5 malformation, although all patients in whom this diagnosis was established had undergone a posterior fossa decompressive surgery. A significant number (13.6%) of patients required repeated operation for persistent syringomyelia. Neurosurgeons may wish to consider that many patients may not respond as well to posterior fossa decompressive surgery especially if syringomyelia is present.

Restricted access

R. Shane Tubbs, Daniel Webb, Matthew D. Smyth and W. Jerry Oakes

Object. The authors hypothesized that children with preoperative Chiari I malformation and an absent gag reflex may harbor pharyngeal musculature atrophy identifiable on magnetic resonance (MR) imaging.

Methods. Thirty patients with preoperative Chiari I malformation and a functioning gag reflex, five patients with preoperative Chiari I malformation and complete absence of gag reflex, and 50 control individuals underwent radiological measurement of the posterior pharyngeal wall thickness.

The thickness of the posterior pharyngeal wall in age-matched controls was significantly thinner (p < 0.0001) than that in patients with Chiari I malformation and no functioning gag reflex. Additionally, in patients with hindbrain herniation and absent gag reflex, the posterior pharyngeal wall thicknesses were comparable to or thinner than those in age-matched controls. A general decrease in the thickness of the posterior pharyngeal wall was found in control individuals who were older compared with patients with Chiari I malformation and a preserved gag reflex in whom the prevertebral soft tissues were found to increase in thickness with age.

Analysis of these data showed that in children with a nonfunctioning gag reflex the prevertebral soft tissue, composed primarily of the superior constrictor muscle, is statistically thinner compared with that in age-matched controls and age-matched children with Chiari I malformation and a functioning gag reflex. The authors theorize that the discrepancy between this measurement in controls and patients with hindbrain herniation is due to the thickening of the craniocervical ligaments that is known to occur in this clinical entity.

Conclusions. The finding that prevertebral soft tissue thickens with age in patients with Chiari I malformation and functioning gag reflex alone may aid in the interpretation of soft-tissue injury following cervical spine injuries in this group.

Restricted access

R. Shane Tubbs, Matthew D. Smyth, John C. Wellons III and W. Jerry Oakes

Object. The literature contains scant data regarding variations in anatomy at the level of the foramen of Magendie in patients with Chiari I malformation and syringomyelia.

Methods. Based on their operative experience and hospital data, the authors detailed the incidence of arachnoid veils found in juxtaposition to the foramen of Magendie in patients with hindbrain herniation. Additionally, radiological studies were retrospectively reviewed in cases in which such an anomaly was noted intraoperatively.

Of 140 patients with Chiari I malformation who underwent decompressive surgery, an associated syrinx was demonstrated in 80 (57%). The foramen of Magendie was obstructed by an arachnoid veil in 10 (12.5%) of these patients; once the lesion was punctured, the cerebrospinal fluid drained freely from this median aperture. On retrospective review of imaging studies, none of these anomalous structures was evident. In all patients with an arachnoid veil and syringomyelia resolution of syringomyelia was revealed on postoperative imaging.

Conclusions. In the absence of a clear pathophysiology of syrinx production, the authors would recommend that patients with syringomyelia and Chiari I malformation undergo duraplasty so that, if present, these veils can be fenestrated.