Background— Clinical observations of migraine headache symptoms in patients with a patent foramen ovale (PFO), both of which conditions are highly prevalent, have raised the question of a possible pathophysiological relationship. We sought to evaluate the assumption of an association between migraine headaches and the presence of PFO by use of a large case-control study. Methods and Results— We conducted a case-control study to assess the prevalence of PFO in subjects with and without migraine. Case subjects were those with a history of migraine (diagnosed by neurologists at a specialty academic headache clinic). Control subjects were healthy volunteers without migraine 1:1 matched on the basis of age and sex with case subjects. Presence of PFO was determined by transthoracic echocardiogram with second harmonic imaging and transcranial Doppler ultrasonography during a standardized procedure of infused agitated saline contrast with or without Valsalva maneuver and a review of the results by experts blinded to case-control status. PFO was considered present if both studies were positive. Odds ratios were calculated with conditional logistic regression in the matched cohort (n=288). In the matched analysis, the prevalence of PFO was similar in case and control subjects (26.4% versus 25.7%; odds ratio 1.04, 95% confidence interval 0.62 to 1.74, P =0.90). There was no difference in PFO prevalence in those with migraine with aura and those without (26.8% versus 26.1%; odds ratio 1.03, 95% confidence interval 0.48 to 2.21, P =0.93). Conclusions— We found no association between migraine headaches and the presence of PFO in this large case-control study.
The alteration of extracranial blood flow in conjunction with clinical signs of autonomic nervous system dysfunction have led to various explanations concerning the pathophysiology of migraine headache. Reflex sympathetic dystrophy, a painful disorder of the sympathetic nervous system, can be treated by blocking the sympathetic nerves located in the stellate ganglion, resulting in vasodilation, ptosis, miosis, and anhydrosis. In theory, these changes could trigger a migraine headache attack secondary to autonomic dysfunction reflecting an imbalance between sympathetic and parasympathetic nervous systems. This may be especially true in a patient with a previous history of meningitis that may have resulted in a disorder of cerebrovescular regulation. We report a 56‐year‐old man with no previous history of migraine who developed migraine with aura after a stellate ganglion block. Those episodic headaches occurred with decreasing frequency end severity for over 6 months, with eventual complete resolution. This interesting phenomenon has not been reported in the English literature and may help to better understand the pathophysiology of migraine.
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.
Chronic pain is a well-known and troublesome complication following thoracotomy. Approximately 50% of patients experience some type of chronic post-thoracotomy pain syndrome (PTPS) even 2 years after thoracic surgery.1 Persistent pain after thoracotomy may indicate either a possible recurrence or progression of malignancy. However, a few patients have intense, sharp, shooting and burning pain, consistent with neuropathic pain located in the distribution of an intercostal nerve (intercostal neuralgia). This is not related to the malignancy, and can be due to nerve entrapment, neuroma formation, or persistent nerve irritation.
Various centrally acting pharmacologic therapies are used to treat neuropathic pain, including antidepressants and anticonvulsants, in addition to opioid and nonopioid analgesics. Anticonvulsants that are reported to decrease neuropathic pain include phenytoin, carbamazepine, sodium valproate, and gabapentin.2-4 However, many patients either do not receive optimal pain relief or are unable to continue with these medications because of adverse effects.
Topiramate …
Herpes zoster (shingles) is a localized infection that begins in the dorsal root ganglla of the cranial or spinal nerves and spreads as a rash over the corresponding dermatome. It usually is caused by reactivation of latent varicella-zoster virus remaining from childhood chicken pox. Postherpetic neuralgia (PHN) is a chronic neuropathic pain syndrome that occurs as a complication of shingles, most commonly in older persons. Acute zoster and PHN can be severe conditions associated with impaired sleep, decreased appetite, depression, anxiety disorder, and diminished libido. Management of zoster-related pain should begin as soon as possible after the onset of symptoms. Combination therapy--including antiviral, antidepressant, corticosteroid, opioid, and topical agents--provides the most effective analgesia.
Tricyclic antidepressants (TCA) have been shown to provide analgesia for a variety of neuropathic and headache pain syndromes regardless of the presence of depression. There is a high incidence of depression in patients with chronic pain, thereby making tricyclic antidepressants particularly suitable for chronic pain patients. We wanted to study patterns of use of tricyclic antidepressants in our Pain Management Center (Beth Israel Hospital, Boston, MA, U.S.A.) primarily to answer four questions: (1) What percentage of all patients were treated with tricyclic antidepressants? (2) How many patients were treated with each antidepressant, and what was the dose range used for individual antidepressants? (3) Were tricyclic antidepressants beneficial for chronic pain, and was that response dependent on a particular dose? (4) Did patients receive an adequate TCA trial, and what factors led to the discontinuation of a TCA trial?A total of 1,145 pain clinic patient charts were reviewed in alphabetical sequence. A total of 282 patients were identified as being treated with tricyclic antidepressants. Data were obtained from these 282 charts regarding the patient's age, diagnosis, tricyclic antidepressant use and dose, other pain treatments, response to treatment, and side effects. The existing diagnosis of depression was documented if possible. Tricyclic antidepressant doses were defined as low doses when the equivalent of 50 mg or less of amitriptyline was used, and as full doses when the equivalent of at least 150 mg of amitriptyline was used. Response to treatment was noted as mild, moderate, or marked improvement. Patients reporting mild improvement were considered nonresponders.Of 1,145 patients, 282 were treated with tricyclic antidepressants. A total of 205 (73%) of the patients were treated with low doses and only 34 (12%) with full doses. The remaining 43 (15%) received intermediate doses. Amitriptyline was the most commonly used drug (58%). Amitriptyline and doxepin appeared to be more effective than other tricyclic antidepressants. The rate of response to our treatment among the 31 patients with a coexisting diagnosis of depression was similar to the patients without documented depression. In patients with tricyclic antidepressants as the only treatment, there was only a trend toward greater response with full dose. In terms of side effects causing dose limitation or discontinuation of the drug, clomipramine, amitriptyline, and doxepin appeared to be worse than imipramine, desipramine, and nortriptyline.Tricyclic antidepressants were used in 25% of patients referred to a multidisciplinary pain center and were commonly used in low to intermediate doses, even in situations in which there were neither side effects nor optimal clinical response.
