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Polymyoclonus Resulting from Possible Accidental Subdural Injection of Local Anesthetic

1997; Lippincott Williams & Wilkins; Volume: 84; Issue: 3 Linguagem: Inglês

10.1213/00000539-199703000-00042

1526-7598

Stephen C. Dreskin, Zahid H. Bajwa, Lance J. Lehmann, Carol A. Warfield,

Spine and Intervertebral Disc Pathology

Epidural steroid injections are often used in the treatment of radicular back pain and are effective in the management of cervical and lumbosacral radiculopathy and spinal stenosis. Although considered relatively safe, they are not without risk. The most common complications are transient worsening of pain and postdural puncture headache. Rare but potentially serious complications include bleeding, infection, and unintentional intravenous, intrathecal, or subdural injections. Epidural steroid injections typically involve the injection of a depot steroid diluted in normal saline and/or local anesthetic. If local anesthetic is unintentionally injected intravascularly, agitation, perioral numbness, tinnitus, and even seizures occur almost immediately. Subdural injections are characterized by a high, patchy block of delayed onset often associated with a profound sympathetic block and resultant hypotension. Case Report A 56 -yr-old man who was referred to the Beth Israel Hospital Pain Center complained of severe low back pain and symptoms of neurogenic claudication after walking about 50 yards. The patient had undergone decompressive laminectomies from L3 to L5 for spinal stenosis 4 and 11 mo earlier. His symptoms were not relieved by bed rest, physical therapy, or medication. After discussing possible treatment options, the patient elected to undergo an epidural steroid injection. The procedure was performed with the patient in the seated position without sedation at the L4-5 level with a 17-gauge Touhy needle. At a depth of approximately 5 cm, loss of resistance to saline was noted. After negative aspiration of blood and cerebrospinal fluid (CSF), a 3-mL test dose of 1% lidocaine with epinephrine was administered. Ten minutes later, a mixture of 10 mL of 1 % lidocaine and 120 mg of triamcinolone was injected. The patient did not complain of paresthesias during needle placement or injection. His blood pressure was 130/72 mm Hg on arrival at the recovery room. He was hemodynamically stable and asymptomatic until 20 min later, when he was found to be sedated and had a blood pressure of 57/39 mm Hg. The patient was treated with 1000 mL of lactated Ringer's solution and 30 mg of ephedrine intravenously, which increased his blood pressure to 108/70 mm Hg. The patient was monitored using pulse oxymetry for 2 h after the injection and was not noted to be hypoxic. Five minutes prior to the onset of myoclonus and approximately 30 min after the initial injection, the patient had a patchy sensory level as high as C4, motor weakness as high as C5, 2/5-3/5 strength in his lower extremities, and 3/5-4/5 strength in his upper extremities. The diagnosis of subdural injection was made. Fifteen minutes after the episode of hypotension, the patient developed bilateral myoclonus of his upper extremities, which developed into generalized myoclonus and slurred speech. The episode was observed by a neurologist who confirmed the diagnosis of polymyoclonus. Extremity movements were widespread, brief, jerky, involuntary, asymmetric, and asynchronous and occurred at 15- to 45-s intervals. The patient was treated with a total of 11 mg of intravenous midazolam with progressive improvement and eventual resolution of symptoms 30 min after the myoclonus began. This was followed by a 1-h period in which the patient experienced anxiety and moving legs. Two hours after the injection, the patient was alert and oriented, with normal mental status, language function, and attention. Cranial nerves were intact. There were two to three beats of nonsustained horizontal nystagmus. His motor, sensory, and reflex examination was unchanged from baseline. The patient was admitted to the hospital for observation. Electrocardiograms in the recovery room and upon discharge the following day were unchanged from baseline. Discussion Subdural blockade has occasionally been used as a planned procedure in chronic pain management [1] but more commonly results unintentionally from an attempted epidural anesthetic [2-7]. The subdural space is a potential space located between the dura mater and the arachnoid mater. The boundaries of the subdural space have been demonstrated by myelography, and it has been cannulated using spinaloscopy [4,8,9]. The subdural space begins caudally at the filum terminale at the S1-2 level and extends superiorly into the cranium, spreading around the surfaces of the brain. In contrast, the spinal epidural space ends at the foramen magnum and has no contact with the intracranial epidural space. The subdural space, filled with a minute amount of fluid and trabeculated connective tissue, lies adjacent to the nerve roots and lymphatic vessels of the spinal nerves [10]. Presumed subdural injection of local anesthetic was first described by DeSaram in 1956 [3]. She reported three cases of attempted obstetrical epidural anesthesia with characteristics of both epidural and subarachnoid blockade in which a negative aspiration of blood and CSF was noted prior to injection of local anesthetic. Since that time, there have been several reports describing a constellation of signs and symptoms attributed to subdural injection of local anesthetics [5-7]. Due to capillary effect and the low resistance of the subdural space, subdural placement of local anesthetic appropriate for epidural anesthesia results in extensive spread. Consequently, a high level of sensory, motor, and sympathetic block results. However, due to the trabeculated nature of the subdural space, the onset of motor and sympathetic block is usually delayed with patchy distribution. Sensory blocks are more dense and originate more quickly because the subdural space is enlarged closer to the dorsal sensory nerve roots as they enter the spinal cord, allowing a greater volume of local anesthetic to pool in this area. Lubenow et al. [11] performed a retrospective study of 2182 patients receiving lumbar epidural steroid injections for low back pain and found the incidence of subdural blockade to be 0.8%. Moreover, they state that previous back surgery may predispose patients to accidental subdural injection. This may be due to a thinner epidural and wider subdural space due to scarring, retraction, stenosis, and the marked decrease in epidural fat. Our case report demonstrates many of the characteristics of a subdural block, including timing of onset and resolution of block, negative aspiration for blood or CSF, and the constellation of symptoms described. Moreover, we report a previously undescribed complication of epidural or subdural block: polymyoclonus. As the subdural space ascends into the cranium, it becomes a larger potential space. Therefore, volumes of local anesthetic unintentionally injected subdurally usually only reach the dependent structures in the cranium such as the cerebellum and lower cranial nerves. Polymyoclonus can originate from multiple sites in the central nervous system and is frequently linked to cerebellar dysfunction [12,13]. Due to the dependent anatomical position of the cerebellum and its frequent association with myoclonus, we feel that a local anesthetic, steroid, or preservative effect on the cerebellum was the most likely cause of our patient's polymyoclonus. Polymyoclonus in this setting can also represent lidocaine-, steroid-, or preservative-induced seizure-like activity arising from the spinal cord. Spinal myoclonus is characterized by myoclonic activity spreading up and down the spinal cord through propriospinal pathways. Also known as propriospinal myoclonus, it involves both the upper and lower extremities. Spinal myoclonus has been described in patients after spinal cord trauma and subarachnoid injections of irritating substances during myelography [14]. The action of local anesthetic drugs and intravenous anesthetics such as etomidate on the spinal cord and/or supraspinal system may lead to cortical disinhibition and pyramidal tract inhibition [15]. Hypotension causing cerebral hypoperfusion could also cause polymyoclonus. It seems unlikely in our case because the hypotension was quickly treated, and myoclonus developed after normal blood pressure was restored.