Clinical Reasoning:

Abstract

A 61-year-old woman with a stable traumatic anterior L4 vertebral wedge fracture without spinal canal compromise was referred because of an intense and refractory pain at the level of fracture in spite of maximal medical therapy. MRI scans showed anterior wedging of L4 vertebral body involving the superior endplate with intact posterior wall ( figure 1A). Percutaneous vertebroplasty (PV) was indicated for her high surgical risk. Under general anesthesia, right L4 transpedicular PV was performed under X-ray fluoroscopy using polymethylmethacrylate (PMMA; volume injected 3 cm 3 ; SpinePlex ® ; Kalamazoo, MI).No critical leaks or lesions of the posterior cortex or the lateral recess were identifiable in postprocedure fluoroscopy.Two hours after PV, the patient presented an intense burning pain in both legs, Lhermitte sign, and tactile hypersensitivity associated with low blood pressure (50/30 mm Hg), respiratory rate (8 breaths/ minute), and body temperature (rectal temperature: 35.0°C), together with hypoxemia (SaO 2 : 75%, in room air) and sinus tachycardia (heart rate 141/ minute). The initial symptoms were followed by sustained (35-45 seconds) and almost continuous muscle spasms in bulbar, pharyngolaryngeal, intercostal, paravertebral, and leg muscles, spontaneous and in response to minimal stimuli, stiffness of the body, lockjaw, frothing of the mouth, opisthotonus, bilateral Babinski sign, and generalized hyperreflexia. The patient was fully conscious during these episodes. During severe spasms, there was respiratory arrest. The patient was immediately referred to the neurointensive care unit (NICU). She was intubated and mechanically ventilated.

Ascending Tonic Clonic Seizure Syndrome after Percutaneous Vertebroplasty

“…The release of MMA monomers into bloodstream is a potential cause of adverse general reaction, and several MMA esters show a strychnine-like activity [ 9 ]. As in the case described by Godoy et al [ 10 ], the effect of the MMA monomers on inhibitory neurons could have led to loss of inhibitory function in the spinal cord determining an impairment of the glycine/GABA mediated inhibitory influence of Renshaw cells on motor neurons.…”