Background:Type I Arnold–Chiari malformation (ACM) has an adult onset and consists of a downward displacement of the cerebellar tonsils and the medulla through the foramen magnum. There is paucity of literature on the anesthetic management during pregnancy of residual ACM Type I, with cervical xyphosis and persistent syringomyelia.Case Description:A 34-year-old woman with surgically corrected ACM Type I presented for Cesarean delivery. A recent MRI demonstrated worsening of cervical xyphosis after several laminectomies and residual syringomyelia besides syringopleural shunt. Awake fiberoptic intubation was performed under generous topical anesthesia to minimize head and neck movement during endotracheal intubation. We used a multimodal general anesthesia without neuromuscular blockade. The neck was maintained in a neutral position. Following delivery, the patient completely recovered in post-anesthesia care unit (PACU), with no headache and no exacerbation or worsening of neurological function.Conclusions:The present case demonstrates that patients with partially corrected ACM, syringomyelia, cervical kyphosis, and difficult intubation undergoing Cesarean delivery require an interdisciplinary team approach, diligent preparation, and skilled physicians.

Spinal epidural hematoma (SEH) is rare and not without serious sequelae. We report a patient who developed Brown-Séquard syndrome from SEH after fluoroscopic-guided cervical steroid injection and favorable response to methylprednisolone (MP). A 56-year-old man reported immediate sharp shooting pain to the upper extremities on introduction of epidural toughy needle. A total of 5 mL of 0.2% ropivacaine and 120 mg methylprednisolone acetate suspension was administered at the C6-7 interspace. Within half an hour, a neurologic deficit occurred at C7-8 and right Brown-Séquard syndrome developed. Once SEH was suspected (3 hours after onset of neurologic deficit), a protocol of high-dose MP intravenous infusion was initiated. Immediate incomplete recovery of motor, sensory, and sphincteric functions was noted within 30 minutes of infusion. Emergency spinal C6-T2 bilateral decompressive laminectomies and evacuation SEH were performed within an expected delay (10 hours from the onset of neurologic deficit). Fluoroscopic guidance does not take the place of adherence to meticulous technique. An unexplained neurologic deficit after invasive spinal procedures should raise the concern for SEH. Early recognition and emergent evacuation remain the mainstay management for SEH. This case suggests some neuroprotection from MP in cases of cervicothoracic cord compression secondary to traumatic SEH. When potential risks for SEH exist, it is advisable not to administer local anesthetic so as not to interfere with neurologic assessment and delaying the diagnosis.

A long-standing case of severe dysesthesia due to a supraclavicular glomus tumor is presented. Chronic pain caused by a subcutaneous glomus (non-chemodectoma) tumor is rare and usually misdiagnosed. The supraclavicular location, presentation, and coincidence of trauma history are unique in this case. A 62-year-old male complained of 20 years of intractable right shoulder and supraclavicular region pain, which started 6 months after a fall. The pain was unrelieved by repeated and extensive physical therapy, chiropractic manipulation, local steroid injections, and two shoulder operations. The cause of the condition remained undiagnosed and obscure. Local surgical exploration revealed a subcutaneous grayish mass with pathologically proven glomus tumor. Immediate alleviation of the pain and tenderness followed complete resection of the mass. The patient remained free of pain at a 2-year follow-up. Subcutaneous glomus (non-chemodectoma) tumors can occur in unusual sites, and should be considered in chronic regional pain syndromes. Immediate cure is generally achieved by local resection. Pertinent literature is reviewed.

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Nitric oxide contributes to basal vascular tone but is not a major contributor to the mechanism of hypercapnia-induced cerebral vasodilation, except in cortex, in primates.

Profound hypothermia with circulatory arrest is an important surgical adjuvant that allows protected cessation of cerebral blood flow for a brief period. In seven patients undergoing this procedure, continuous spectroscopic measurement of cerebral hemoglobin oxygen saturation was performed. Circulatory arrest at 18 degrees C was associated with a significant progressive desaturation (p < 0.01) of residual cerebral hemoglobin. Arrest time varied based on operative complexity (range 10 to 65 minutes), and a negative linear correlation between arrest time (y) and oxygen saturation (x) was noted (y = -0.87 x + 64). Five patients whose saturation remained above 35% had no neurological injury attributable to hypoxia. One patient (Hunt and Hess Grade 0) whose saturation fell below 35% had evidence of a global hypoxic injury at postmortem examination. Spectroscopically measured cerebral hemoglobin saturation (cerebral oximetry) may be used to monitor metabolic activity during circulatory arrest. Although the clinical utility of such monitoring cannot be established at this time, the potential may exist to prolong the safe duration of induced circulatory arrest for cerebral protection.

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