Vinorelbine and ifosfamide for unresectable non-small cell lung cancer

OBJECTIVE: The diagnostic value of cine magnetic resonance imaging (CMRI) that visualizes fluid and tissue movement was evaluated in patients with spinal intradural arachnoid cysts, a rare but increasingly detected cause of spinal cord dysfunction. METHODS: Four patients with thoracic spinal intradural arachnoid cysts were investigated with conventional T1- and T2-weighted and cardiac-gated CMRI. Four normal volunteers also underwent CMRI for comparison. RESULTS: Sagittal T1- and T2-weighted imaging showed lesions as an abnormal widening of the posterior spinal subarachnoid space, but mixed high- and low-signal intensities on T2-weighted imaging suggested cystic lesions. CMRI, using 16 to 20 sagittal gradient echo images during the cardiac cycle of normal volunteers, indicated synchronous signal changes along the subarachnoid space, suggesting a smooth cerebrospinal fluid flow. CMRI of patients detected that the caudal or cranial direction of the high-signal propagation suddenly reversed at some locations (as if rebounding) in an asynchronous fashion along the lesion (asynchronous rebound phenomenon), which was well demonstrated by the closed-loop video mode. Cystectomy revealed that the cysts consisted of multiple lobules and that the asynchronous rebound phenomenon corresponded with some boundaries of cyst lobules. CMRI also visualized dynamic spinal cord compression by the cyst. CONCLUSION: CMRI can demonstrate abnormal fluid flow and spinal cord compression caused by a spinal intradural arachnoid cyst.     

Cervical arachnoid cysts after craniocervical decompression for Chiari II malformations: report of three cases

OBJECTIVE AND IMPORTANCE: We describe three cases in which ventrally situated cervical arachnoid cysts led to spinal cord or cervicomedullary compression after repeat craniocervical decompression for Chiari II malformations. CLINICAL PRESENTATION: All three patients underwent craniocervical decompression when their Chiari malformations became symptomatic. The first patient developed chronic vertiginous spells and headache and was treated with repeated craniocervical decompression procedures during several years. Seven months after undergoing her third decompression procedure, she developed severe dizzy spells, which were determined to be of brain stem origin. The second patient had a small, asymptomatic arachnoid cyst anterior to the brain stem discovered at age 6 years. After undergoing repeat craniocervical decompression for headaches 8 years after undergoing his first procedure, the patient developed severe neck pain and acute quadraparesis. A third patient underwent repeat craniocervical decompression at age 14 years for cranial nerve dysfunction. Postoperatively, he acutely developed paresis of extraocular movements and incoordination of the upper extremities. All three patients were found to have anteriorly situated arachnoid cysts compressing the brain stem and/or cervical spinal cord. INTERVENTION AND TECHNIQUE: Fenestration of the arachnoid cyst or drainage with cystoperitoneal shunting adequately treated acute brain stem or cervical spinal cord compression. All three patients had achieved satisfactory relief from their acute symptoms of neural compression at their follow-up examinations. CONCLUSION: An association between spinal arachnoid cysts and neural tube defects has previously been reported. However, the development of previously undetected spinal arachnoid cysts after craniocervical decompression was unexpected. We hypothesize that extensive craniocervical decompression may alter the cerebrospinal fluid pressure dynamics in such a way that the anterior subarachnoid space, previously compressed, may dilate. Occasionally, because of perimedullary arachnoiditis, the cerebrospinal fluid may become loculated and act as a mass. Direct fenestration or shunting may successfully treat this problem, and less extensive craniocervical decompression may avoid it.     

An unusual spinal intradural arachnoid cyst

Spinal intradural arachnoid cysts are seen most frequently in the thoracic region, particularly near the midline posteriorly. A thoracic intradural arachnoid cyst in this typical location is reported, with the additional unusual finding of herniation of the spinal cord through an anterior defect in the dura matter. The MRI findings are described.     

Improving the nutrition of refugees and displaced people in Africa: workshop in Machakos, Kenya, 5-7 December 1994

We report an unusual post-traumatic spinal cord herniation, which became symptomatic 38 years after the trauma. A 44-year-old man presented with a 2-year history of increasing impotence, neuropathic bladder dysfunction and dissociated sensory loss below the level of T6. At the age of 6 years he had a severe blunt spinal injury with transient paraparesis. MRI revealed right lateral and ventral displacement of the spinal cord at the T5/6 level. The spinal cord was surgically exposed and found to herniate through a ventral defect of the arachnoid membrane and the dura mater. As there were no other events that could have precipitated spinal cord herniation the reported blunt trauma in childhood is the most likely cause for the spinal cord herniation in this patient.     

A case of idiopathic spinal cord herniation

The authors experienced a case of idiopathic spinal cord herniation with duplicated dura mater. A 63-year-old woman presented right dominant slowly progressive spastic paraplegia and dissociated sensory disturbance. Magnetic resonance imaging (MRI) demonstrated an enlarged dorsal arachnoid space associated with an apparently focally narrowed thoracic cord. The cord was kinked towards the anterior and closely applied to vertebral body at the level of Th3-4. Computed tomographic myelography (CTM) revealed homogeneous filling at dorsal arachnoid space immediately after injection and no defects. At operation multilocular arachnoid cyst and duplicated dura mater was respectively observed dorsally, and ventrally. From defected area of the inner layer, a ventral part of the spinal cord was incarcerated between the two dural layers. After rejection of arachnoid cyst and inner layer was performed, the patient recovered neurologically. Idiopathic spinal cord herniation is a rare disease that shows slowly progressive myelopathy at middle age. The herniations were observed at ventral thoracic cord in all reported cases. The mechanism of this disease is still uncertain. But at least three successive factors seem to be necessary for formation of herniation, 1) abnormal structure of the dura mater such as defect, diverticulum and duplication; 2) adhesion between the cord and the destructive dura mater, and 3) continuous cerebrospinal fluid (CSF) pressure pushing the cord outward from subdural space. In the thoracic spine, mobility is limited compared with the cervical and lumbar spine, and because of physiological curvature the cord situates rather ventrally. For these reasons the incidence of adhesion might be higher at ventral thoracic spine. Although neuroradiological imagings especially MRI and CTM were useful, operative findings were necessary for definitive diagnosis in many reported cases. Considering the effectiveness of surgical treatment, study of the ventral side of the cord should be important to avoid misdiagnosis.     

Subarachnoid hemorrhage secondary to spinal arteriovenous malformation and aneurysm. Report of a case and review of the literature

A patient with recurrent subarachnoid hemorrhage was seen initially with intermittent signs and symptoms of intracranial and spinal cord dysfunction. Myelography and spinal angiography revealed an arteriovenous malformation (AVM) and aneurysm of the spinal cord. Extensive investigation failed to reveal any intracranial lesion. The relationship of subarachnoid hemorrhage at a spinal level to the development of remote neurological abnormalities is discussed, and previous reports of aneurysms associated with spinal AVM are reviewed.     

Spontaneous thoracic spinal cord herniation. A case report

STUDY DESIGN: This is a case report. OBJECTIVE: To focus attention on spontaneous spinal cord herniation as a rare cause of myelopathy that can be diagnosed preoperatively and can be corrected surgically. SUMMARY OF BACKGROUND DATA: A 34-year-old woman presented with spastic paraparesis. Magnetic resonance imaging scan of the thoracic spine revealed anterior displacement and tethering of the cord at T6-T7 and a dorsal intradural arachnoid cyst. Excision of the cyst was performed without improvement in symptomatology. During reoperation the thoracic spinal cord hernia was discovered and was reduced intradurally. METHODS: The authors describe the clinical, radiographic, and surgical findings of this patient and review the findings from other reported cases. They discuss the proposed theories for the pathophysiology of the cord herniation and the surgical management. RESULTS: The patient had idiopathic thoracic spinal cord herniation as there was no history of previous spine surgery or injury. The authors believe that the cord herniated through a congenital dural defect, which resulted in the development of a pseudoarachnoid cyst dorsally to the hernia. The patient improved after intradural reduction of the hernia and closure of the dural defect. CONCLUSION: Idiopathic spinal cord herniation should be recognized as a cause of progressive myelopathy that can be managed successfully with microsurgical techniques.     

Thoracic arachnoid cyst presenting incomplete features of Brown-Séquard syndrome: a case report

Spinal intradural arachnoid cyst presenting incomplete features of Brown-Séquard syndrome is very rare. Only 6 cases have been reported. We report one in a thoracic lesion. A 42-year-old man noticed thermohypesthesia in his right leg, and monoparesis in his left leg. On admission, he presented incomplete features of Brown-Séquard syndrome below the Th7 level. MRI showed the spinal cord to be displaced antero-laterally to the right at Th6-7 level. Myelography and CT myelography failed to show the cyst wall, but an arachnoid cyst was totally removed with T5-8 osteoplastic laminotomy. Sensory disturbance has not changed postoperatively, but motor weakness in his left leg recovered within one month after the operation. No cystic lesion has been detected by MRI during the ten months since the operation. We investigated all seven cases in the literature including our case which showed incomplete features of Brown-Séquard syndrome. As regards to the location of the cyst, all cases were at the mid-thoracic level. And four cases were at the midline. These results suggest that the mechanism of Brown-Séquard syndrome associated with spinal arachnoid cyst may be related not only to the laterality of the lesion but also to the asymmetrical circulation in the watershed area.     

Spinal aneurysmal cyst with medullary compression. Apropos of a case with preoperative embolization

The authors report the case of a vertebral aneurysmal bone cyst, at the thoracic level, with spinal cord compression. 16 months after operation, the initial neurological signs reappeared. Selective angiography pointed out a good picture, through not specific, of the lesion; the embolisation, then performed, provided considerable relief for the complete removal of the important vascular bone formation. The diagnostic, therapeutic and pathogenic problems of the vertebral aneurysmal bone cysts are discussed.     

Adult opossums (Didelphis virginiana) demonstrate near normal locomotion after spinal cord transection as neonates

When the thoracic spinal cord of the North American opossum (Didelphis virginiana) is transected on postnatal day (PD) 5, the site of injury becomes bridged by histologically recognizable spinal cord and axons which form major long tracts grow through the lesion. In the present study we asked whether opossums lesioned on PD5 have normal use of the hindlimbs as adults and, if so, whether that use is dependent upon axons which grow through the lesion site. The thoracic spinal cord was transected on PD5 and 6 months later, hindlimb function was evaluated using the Basso, Beattie, and Bresnahan (BBB) locomotor scale. All animals supported their weight with the hindlimbs and used their hindlimbs normally during overground locomotion. In some cases, the spinal cord was retransected at the original lesion site or just caudal to it 6 months after the original transection and paralysis of the hindlimbs ensued. Surprisingly, however, these animals gradually recovered some ability to support their weight and to step with the hindlimbs. Similar recovery was not seen in animals transected only as adults. In order to verify that descending axons which grew through the lesion during development were still present in the adult animal, opossums subjected to transection of the thoracic cord on PD5 were reoperated and Fast blue was injected several segments caudal to the lesion. In all cases, neurons were labeled rostral to the lesion in each of the spinal and supraspinal nuclei labeled by comparable injections in unlesioned, age-matched controls. The results of orthograde tracing studies indicated that axons which grew through the lesion innervated areas that were appropriate for them.     

Paramesencephalic arachnoid cysts

The term "paramesencephalic" is proposed to describe the location of a general class of arachnoid cysts observed in four patients. These cysts, which appear to arise within the subarachnoid space, are characterized by a lack of communication with the ventricular system. Usually, the arachnoid tissue is normal, and the cyst fluid resembles cerebrospinal fluid both macroscopically and microscopically. Hydrocephalus is variably accompanied by localizing signs. Problems may be encountered in the diagnosis of suprasellar (case 4), parapineal (case 3), incisural (case 1), and interpeduncular (cases 2 and 4) arachnoid cysts. Early surgical exploration is strongly recommended.     

A study of adenosine treatment in experimental acute spinal cord injury. Effect on arachidonic acid metabolites

STUDY DESIGN: A prospective, randomized, blinded experimental trauma study. STUDY OBJECTIVE: The effect of adenosine on arachidonic acid metabolites and lipid peroxidation was investigated in induced spinal cord injury. SUMMARY OF BACKGROUND DATA: Effects of adenosine in ischemia-reperfusion models have been studied, but no studies of adenosine's effect on direct trauma to the spinal cord have been reported. METHODS: Thirty-seven adult Wistar albino rats were randomly divided into four groups and underwent laminectomy. Group 1 underwent a sham operation. Group 2 received an intravenous adenosine infusion of 100 micrograms/kg per minute for 30 minutes. In Group 3, a standard spinal cord trauma of 50 g.cm strength was established at the lower thoracic level with a "weight-drop" technique, and Group 4 received an infusion of adenosine (100 micrograms/kg per minute) for 30 minutes after the trauma. RESULTS: Tissue prostaglandin E2 activity was significantly higher in adenosine-treated trauma groups when compared with that in other groups (P < 0.0001). The difference in tissue leukotriene C4 activity between control and trauma groups was significant (P < 0.05). Adenosine infusion after trauma limited the increases in lipid peroxidation, with the difference approaching significance at P = 0.06. The structure of myelin was well preserved in the adenosine-treated trauma group. However, the changes were irreversible in severely damaged areas. CONCLUSION: After acute spinal cord trauma, intravenous adenosine infusion of 100 micrograms/kg per minute could attenuate progression to secondary injury, but adenosine alone was not effective yet.     

Spinal cord evoked potentials and edema in the pathophysiology of rat spinal cord injury. Involvement of nitric oxide

The possibility that nitric oxide is somehow involved in the early bioelectrical disturbances following spinal cord injury in relation to the later pathophysiology of the spinal cord was examined in a rat model of spinal cord trauma. A focal trauma to the rat spinal cord was produced by an incision of the right dorsal horn of the T 10-11 segments under urethane anaesthesia. The spinal cord evoked potentials (SCEP) were recorded using epidural electrodes placed over the T9 and T12 segments of the cord following supramaximal stimulation of the right tibial and sural nerves in the hind leg. Trauma to the spinal cord significantly attenuated the SCEP amplitude (about 60%) immediately after injury which persisted up to 1 h. However, a significant increase in SCEP latency was seen at the end of 5 h after trauma. These spinal cord segments exhibited profound upregulation of neuronal nitric oxide synthase (NOS) immunoreactivity, and the development of edema and cell injury. Pretreatment with a serotonin synthesis inhibitor drug p-chlorophenylalanine (p-CPA) or an anxiolytic drug diazepam significantly attenuated the decrease in SCEP amplitude, upregulation of NOS, edema and cell injury. On the other hand, no significant reduction in SCEP amplitude, NOS immunolabelling, edema or cell changes were seen after injury in rats pretreated with L-NAME. These observations suggest that nitric oxide is somehow involved in the early disturbances of SCEP and contribute to the later pathophysiology of spinal cord injury.     

Cerebrospinal fluid pressure changes in response to coughing

CSF pressure recordings have been taken from the lumbar region and the cisterna magna of 16 patients during coughing in the sitting position. Isolated coughs of low amplitude have been studied. The lumbar pressure waves occur sooner and lower. Thus there is a phase during which the lumbar pressure exceeds the cisternal, followed by one in which the cisternal exceeds the lumbar. These phenomena may be conveniently displayed on a differential trace. The phase during which the cisternal pressure exceeds the lumbar may be protracted. It is suggested that Froin's syndrome, central subarachnoid pouches and syringobulbia may be associated with upward pressure waves. Cough headache, the filling stages of communicating syringomyelia and tonsillar herniation may be associated with valve-like blockage at the foramen magnum which produces craniospinal pressure dissociation by interfering with downward or rebound pulsation. Decompensation of hydrocephalus after birth may be related to pulsation in association with crying; also after removal of a meningocele sac decompensation may be related to the effects of similar pulsation modified by changes in capacitance following operation. The cord destruction of syringomyelia, and the mechanisms which fill spinal subarachnoid cysts may be related to pressure waves directed both upwards and downwards. The merits and limitations of cough impulse as a clinical test for spinal blockage are discussed, and the suggestion is made that after further evaluation they may provide a more sensitive indication of spinal blockage than Queckenstedt's test.     

A physiologic assessment of intrathecal amitriptyline in sheep

BACKGROUND: Intrathecal injection of amitriptyline enhances antinociception from intravenous morphine and reduces neuropathic pain behavior in animals. This study represents part of a preclinical assessment of intrathecal amitriptyline to determine its safety for use in humans. METHODS: Low thoracic intrathecal, femoral, and pulmonary arterial catheters were inserted in 18 adult ewes, followed 96 h later by intrathecal injection of saline or 5 mg amitriptyline and by determination of spinal cord blood flow, hemodynamic variables, behavioral changes, cerebrospinal fluid concentrations of catecholamines and amitriptyline, and spinal tissue concentrations of amitriptyline. In six other ewes, low thoracic intrathecal and femoral arterial catheters were inserted and blood pressure and heart rate were measured after intrathecal injection of saline or 0.25, 1, or 5 mg amitriptyline. Four other ewes received cervical intrathecal injection of 5 and 10 mg amitriptyline, and antinociception was determined. RESULTS: Thoracic intrathecal injection of amitriptyline produced dose-dependent sedation but did not significantly affect spinal cord blood flow or hemodynamic variables. Spinal cord tissue concentrations of amitriptyline were 100 times greater in tissue near the tip of the thoracic intrathecal catheter compared with cervical cord tissue. Cerebrospinal fluid concentrations of catecholamines did not significantly change after amitriptyline was administered. Cervical intrathecal injection of 5 mg amitriptyline produced mild antinociception, whereas 10 mg produced intense sedation and, in one sheep, seizures and death. CONCLUSIONS: Although other preclinical toxicity studies are necessary before introducing intrathecal amitriptyline for use in humans, this study did not reveal dangerous changes in blood pressure or spinal cord blood flow from this agent.     

Spinal cord compression by catheter granulomas in high-dose intrathecal morphine therapy: case report

OBJECTIVE AND IMPORTANCE: The use of chronic intrathecal morphine for the treatment of intractable, nonmalignant pain is becoming more prevalent. A rare but devastating complication of this therapy is the development of spinal cord compression secondary to the formation of intrathecal granulomas. CLINICAL PRESENTATION: We report three cases of intrathecal granuloma formation in the thoracic subarachnoid space, associated with intrathecal morphine pumps. These three patients were receiving high doses of morphine to control their pain (25 mg/d, 28 mg/d, and 45 mg/d, respectively) when they presented with signs and symptoms of thoracic spinal cord compression. Myelography and postmyelographic computed tomography of the spine revealed masses causing spinal cord compression. INTERVENTION: Two patients underwent thoracic laminectomies for resection of these masses, and the other patient had the intrathecal catheter removed. A pathological examination revealed sterile granulomas in the resected masses. CONCLUSION: Intrathecal granulomas are likely to occur with increasing frequency as the use of chronic intrathecal morphine delivery increases in patients with nonmalignant pain. The cause of intrathecal granulomas is unknown, although it is likely that morphine plays a major role in their formation. We think that those patients receiving high doses of morphine are at greater risk for developing this complication.     

Subacute combined degeneration of the spinal cord: MR findings

The authors present the initial and follow-up MR findings in a patient with subacute combined degeneration of the spinal cord, a complication of vitamin B12 deficiency, and a rare cause of demyelination of the dorsal and lateral columns of the spinal cord. Initial study showed high intensity in the dorsal columns of the cervical and thoracic spinal cord on T2-weighted image. Five months after treatment, the abnormal signal intensity was noted to have decreased.     

Large arachnoid cysts at the cranial base

Two infants who presented with macrocephaly had very large noncommunicating cysts at the cranial base that were displacing the brain. Only one of the patients was hydrocephalic; he eventually underwent ventriculoperitoneal shunting after craniotomy and attempted internal drainage of the cyst. The other infant had a cystoperitoneal shunt. Both have done well after 4 and 6 years of follow-up, respectively. These large arachnoid cysts are bilateral lesions with the potential for severe surgical complications and a questionable possibility of cure. The authors recommend systematic radiological investigation to decide the appropriate therapy, including an analysis of the patency of the subarachnoid pathways with radionuclide cisternography and cystography. Simple cystoperitoneal shunting may be the appropriate therapy for most of these large lesions. (Neurosurgery, 6: 76--81, 1980).     

Supratentorial arachnoid cyst and associated subdural hematoma: neuroradiologic studies

CT and MR images of 8 patients with supratentorial arachnoid cyst complicated by subdural hematoma were studied and compared with those of 8 patients who developed nontraumatic subdural hematoma without arachnoid cyst. Of the 8 patients with supratentorial arachnoid cyst, CT and MR disclosed temporal bulging and/or thinning of the temporal squama in all 6 patients with middle fossa arachnoid cysts, and the thinning of the calvaria was evident in another patient with a convexity cyst. Calvarial thinning at the site corresponding to interhemispheric arachnoid cyst was clearly depicted on coronal MR images. In contrast, none of the 8 young patients with nontraumatic subdural hematoma without arachnoid cyst had abnormal calvaria. Temporal bulging and thinning of the overlying calvaria were identified as diagnostic CT and MR features of arachnoid cyst with complicating intracystic and subdural hemorrhage. Radiologists should be aware of this association and should evaluate the bony structure carefully.