Headache month previously presented to the emergency department with headache. This headache came on suddenly, was located in the parietal areas, described as a severe pressure rated 8-10/10, and was associated with nausea, photophobia, and phonophobia. Phenotypically, the headache was migrainous. This headache was very similar to his presentation when the leaking aneurysm was discovered, with the only difference being the lack of a “popping” sensation on this presentation. On detailed history, the patient revealed that he had had a low intensity pressure headache 3-5/10 since the coiling procedure, which he treated with acetaminophen. On physical exam, he appeared uncomfortable holding the top of his head. His blood pressure was 161/79, but otherwise vital signs and examination were within normal limits. He had a computerized tomography (CT) of the head, CT and MR angiography, which showed only post-embolization of the basilar tip saccular aneurysm. Two lumbar punctures did not reveal evidence of intracranial bleed. He was treated for headache with acetaminophen and ibuprofen without significant relief. Opiates and antiemetics were used with minimal effect. Prednisone was initiated and was abandoned after 2 days of inefficacy. Sumatriptan was given twice without relief. Indomethacin 50 mg 3 times daily was initiated with significant relief coming after the third dose, with headache pain being rated 0-2/10. He remained headache-free while taking indomethacin at his 1-week follow-up visit. Headache after endovascular intervention is commonly reported. Here we report 2 cases of post-endovascular coiling-associated headache that were successfully treated with indomethacin. Post-procedure headache following endovascular coiling is reported in 72% of patients.1 The International Classification of Headache Disorders-III beta (ICHD-III beta)2 defines “headache attributed to an intracranial endovascular procedure (6.7.1)” as a new headache following intracranial angioplasty or embolization that develops within seconds of the procedure, is severe, unilateral, and ipsilateral to the procedure, and resolves within 24 hours after the end of the procedure. In Baron et al’s1 series of 372 patients with headache following intracranial neurovascular procedures, including 263 patients with postaneurysmal coiling headache, the headaches often began days to weeks after the procedure and commonly lasted 1 to 6 months or longer. While our 2 patients would not meet ICHD-III diagnostic criteria due to post-aneurysmal coiling rather than angioplasty or embolization, onset of headache at the time of SAH rather than during the procedure, and duration of headache after the procedure, they are very consistent with the large series of patients with headache
697 following intracranial neurovascular procedures presented by Baron et al.1 Since headache following endovascular coiling can be severe and long-lasting, effective therapy is required. Treatment with sumatriptan and dihydroergotamine are mentioned in case series,1 but there are no reports of their efficacy or of alternative therapies. We present 2 patients, one who did not respond to sumatriptan, opiates, or prednisone, and another who did not respond to propranolol, high dose ibuprofen, or nortriptyline, but both had a complete resolution of headache pain with indomethacin. Drew Triplett, DO; Roberto Colon, MD; Kerianne Springer, MD; Glen D. Solomon, MD Department of Internal Medicine, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA
REFERENCES 1. Baron EP, Moskowitz SI, Tepper SJ, et al. Headache following intracranial neuroendovascular procedures. Headache. 2012;52:739-748. 2. Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders – 3 beta. Cephalalgia. 2013;33:629-808.
Trigger Point Injection Reduces the Pain of Idiopathic Intracranial Hypotension The usual causes of head and neck pain include irritation of intracranial structures such as dura, periosteum, cranial nerves, venous sinuses, and meningeal and cerebral arteries and of pericranial structures such as muscle, connective tissue, bone, and nerve.1,2 Myofascial pain caused by trigger points in muscle or tendon is usually the result of local injury from excessive stretching or local trauma or from remote irritation of boney or peripheral neuronal structures external to the meninges, nerves, and blood vessels outside the inner surfaces of the skull and spinal canal.3 Here is a case of idiopathic intracranial hypotension causing myofascial pain which diminished after a trigger point injection. Four weeks before neurologic evaluation a 45-yearold woman developed pain behind the right eye while Conflict of Interest: None. Financial Support: None.
698 shopping. This searing pain traveled to the back of the skull and resolved almost immediately upon lying down.Within 3 minutes of arising, the pain reached 7-9/10 severity on the visual analog scale. Complete blood count (CBC), estimated sedimentation rate, C-reactive protein, and Lyme titers were normal. Chiropractic treatment originally improved and then, at later sessions, worsened the headache. Two short courses of prednisone produced only temporary relief. She had no other symptoms. In the sixth week of her illness, the examination was normal except for tenderness over the right trochlea and semispinalis capitis. Pressing on these areas reproduced her entire headache. Trigger point injection of the right semispinalis capitis with 2 cc of 1% lidocaine reduced her pain from 7/10 to 2/10 within 3 minutes.4 She had almost no headache for the next 3 days, even when upright, but 5/10 intensity pain returned. A second semispinalis capitis trigger point injection gave good relief for 3 days, even though the patient was only minimally tender in the area, before 5/10 intensity pain returned. The magnetic resonance imaging of the brain demonstrated supratemporal, falx, tentorial, and internal auditory canal region dural thickening which diffusely enhanced after gadolinium infusion. When headaches did not fully resolve after 7 days of flat bed rest, she underwent a lumbar blood patch. She had a reduction in headache immediately after the procedure and complete resolution of pain within 24 hours. She had no further cephalic tenderness. Myofascial pain and intracranial disease are wellknown causes of headache, but this may be the first medical report showing an intracranial lesion can cause a myofascial trigger point. The assumed cause of positional headache in idiopathic intracranial hypotension is traction of the meninges or of dilated blood vessels at the base of the brain from the effects of gravity or from a dural tear.5,6 In the patient described, an intracranial process may have induced a secondary trigger point which, in turn, caused much of her headache. Treating the myofascial trigger point significantly reduced the pain which otherwise would have been ascribed to the intracranial processes of idiopathic intracranial hypotension. This case shows that not all headaches from intracranial disease are a direct result of the intracranial process. Resolution of the patient’s pain and physical findings with elimination of idiopathic intracranial hypotension indicates the patient’s myofascial pain was a secondary result of her intracranial process. Trigger point injection provided temporary relief, but the headache returned because the underlying cause of the headache persisted.
May 2015 Most clinicians do not examine the muscles and ligaments of the head and neck (the myofascial exam) of headache patients. Even in cases similar to this one, as in occipital nerve blockade for post-dural puncture headache, no anatomic information on the source or nidus of the pain can be derived because there is no information on the specific location of tenderness and on the specific target of the procedure.7,8 Once found, local tender areas, causing referral of pain replication the patient’s discomfort, respond quickly to local anesthetic (trigger point) injection. This case shows that peripheral treatment of an intracranial disease may provide significant temporary relief. Clinicians should perform a myofascial exam on all patients with headache irrespective of the putative cause of the headache. We may find that acute stroke and other intracranial processes may cause discomfort which can be alleviated by trigger point injections or other treatments for myofascial pain.9 The myofascial exam of patients with headaches associated with acute and other intracranial diseases may lead to a better understanding of the causes of these headaches.10 Michael R. Sorrell, MD Department of Neurology, Tufts University School of Medicine, Boston, MA; Springfield Neurology Associates, Springfield, MA, USA
REFERENCES 1. Dalessio DJ. Pain-sensitive structures within the cranium. In: Dalessio DJ, ed. Wolff’s Headache and Other Head Pain, 4th edn. New York: Oxford University Press; 1980:2455. 2. Graff-Redford SB. Myofascial pain: Diagnosis and management. Curr Pain Headache Rep. 2004;8:463-467. 3. Simons DG, Travell JG, Simons LS. Head and neck pain. In: Simons DG, Simons LS, eds. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol 1, 2nd edn. Baltimore, MD: Lippincott Williams & Wilkins; 1999:239-483. 4. Robbins MS, Kuruvilla D, Blumenfeld AH, et al. Trigger point injections for headache disorders: Expert consensus methodology and narrative review. Headache. 2014;54: 1441-1459. 5. Ferrante E, Savino A, Sances G, Nappi G. Spontaneous intracranial hypotension syndrome: Report of 12 cases. Headache. 2004;44:615-622. 6. Schievink WI, Dodick DW, Mokri B, Silberstein S, Bouser MG, Goadsby PJ. Diagnostic criteria for headache due to spontaneous intracranial hypotension: A perspective. Headache. 2011;51:1442-1444.
Headache 7. Akin Takmaz S, Unal Kantekin C, Kaymak C, Bas¸ar H. Treatment of post-dural puncture headache with bilateral greater occipital nerve block. Headache. 2010;50:869-872. 8. Niraj G, Kelkar A, Girotra V. Greater occipital nerve block for postdural puncture headache (PDPH): a prospective audit of a modified guideline for the management of
699 PDPH and review of the literature. J Clin Anesth. 2014;26:539-544. 9. Vestergaard K, Andersen G, Nielsen MI, Jensen TS. Headache in stroke. Stroke. 1993;11:1621-1624. 10. Sorrell MR. The physical examination of migraine. Curr Pain Headache Rep. 2006;10:350-354.
697 following intracranial neurovascular procedures presented by Baron et al.1 Since headache following endovascular coiling can be severe and long-lasting, effective therapy is required. Treatment with sumatriptan and dihydroergotamine are mentioned in case series,1 but there are no reports of their efficacy or of alternative therapies. We present 2 patients, one who did not respond to sumatriptan, opiates, or prednisone, and another who did not respond to propranolol, high dose ibuprofen, or nortriptyline, but both had a complete resolution of headache pain with indomethacin. Drew Triplett, DO; Roberto Colon, MD; Kerianne Springer, MD; Glen D. Solomon, MD Department of Internal Medicine, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA
REFERENCES 1. Baron EP, Moskowitz SI, Tepper SJ, et al. Headache following intracranial neuroendovascular procedures. Headache. 2012;52:739-748. 2. Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders – 3 beta. Cephalalgia. 2013;33:629-808.
Trigger Point Injection Reduces the Pain of Idiopathic Intracranial Hypotension The usual causes of head and neck pain include irritation of intracranial structures such as dura, periosteum, cranial nerves, venous sinuses, and meningeal and cerebral arteries and of pericranial structures such as muscle, connective tissue, bone, and nerve.1,2 Myofascial pain caused by trigger points in muscle or tendon is usually the result of local injury from excessive stretching or local trauma or from remote irritation of boney or peripheral neuronal structures external to the meninges, nerves, and blood vessels outside the inner surfaces of the skull and spinal canal.3 Here is a case of idiopathic intracranial hypotension causing myofascial pain which diminished after a trigger point injection. Four weeks before neurologic evaluation a 45-yearold woman developed pain behind the right eye while Conflict of Interest: None. Financial Support: None.
698 shopping. This searing pain traveled to the back of the skull and resolved almost immediately upon lying down.Within 3 minutes of arising, the pain reached 7-9/10 severity on the visual analog scale. Complete blood count (CBC), estimated sedimentation rate, C-reactive protein, and Lyme titers were normal. Chiropractic treatment originally improved and then, at later sessions, worsened the headache. Two short courses of prednisone produced only temporary relief. She had no other symptoms. In the sixth week of her illness, the examination was normal except for tenderness over the right trochlea and semispinalis capitis. Pressing on these areas reproduced her entire headache. Trigger point injection of the right semispinalis capitis with 2 cc of 1% lidocaine reduced her pain from 7/10 to 2/10 within 3 minutes.4 She had almost no headache for the next 3 days, even when upright, but 5/10 intensity pain returned. A second semispinalis capitis trigger point injection gave good relief for 3 days, even though the patient was only minimally tender in the area, before 5/10 intensity pain returned. The magnetic resonance imaging of the brain demonstrated supratemporal, falx, tentorial, and internal auditory canal region dural thickening which diffusely enhanced after gadolinium infusion. When headaches did not fully resolve after 7 days of flat bed rest, she underwent a lumbar blood patch. She had a reduction in headache immediately after the procedure and complete resolution of pain within 24 hours. She had no further cephalic tenderness. Myofascial pain and intracranial disease are wellknown causes of headache, but this may be the first medical report showing an intracranial lesion can cause a myofascial trigger point. The assumed cause of positional headache in idiopathic intracranial hypotension is traction of the meninges or of dilated blood vessels at the base of the brain from the effects of gravity or from a dural tear.5,6 In the patient described, an intracranial process may have induced a secondary trigger point which, in turn, caused much of her headache. Treating the myofascial trigger point significantly reduced the pain which otherwise would have been ascribed to the intracranial processes of idiopathic intracranial hypotension. This case shows that not all headaches from intracranial disease are a direct result of the intracranial process. Resolution of the patient’s pain and physical findings with elimination of idiopathic intracranial hypotension indicates the patient’s myofascial pain was a secondary result of her intracranial process. Trigger point injection provided temporary relief, but the headache returned because the underlying cause of the headache persisted.
May 2015 Most clinicians do not examine the muscles and ligaments of the head and neck (the myofascial exam) of headache patients. Even in cases similar to this one, as in occipital nerve blockade for post-dural puncture headache, no anatomic information on the source or nidus of the pain can be derived because there is no information on the specific location of tenderness and on the specific target of the procedure.7,8 Once found, local tender areas, causing referral of pain replication the patient’s discomfort, respond quickly to local anesthetic (trigger point) injection. This case shows that peripheral treatment of an intracranial disease may provide significant temporary relief. Clinicians should perform a myofascial exam on all patients with headache irrespective of the putative cause of the headache. We may find that acute stroke and other intracranial processes may cause discomfort which can be alleviated by trigger point injections or other treatments for myofascial pain.9 The myofascial exam of patients with headaches associated with acute and other intracranial diseases may lead to a better understanding of the causes of these headaches.10 Michael R. Sorrell, MD Department of Neurology, Tufts University School of Medicine, Boston, MA; Springfield Neurology Associates, Springfield, MA, USA
REFERENCES 1. Dalessio DJ. Pain-sensitive structures within the cranium. In: Dalessio DJ, ed. Wolff’s Headache and Other Head Pain, 4th edn. New York: Oxford University Press; 1980:2455. 2. Graff-Redford SB. Myofascial pain: Diagnosis and management. Curr Pain Headache Rep. 2004;8:463-467. 3. Simons DG, Travell JG, Simons LS. Head and neck pain. In: Simons DG, Simons LS, eds. Myofascial Pain and Dysfunction: The Trigger Point Manual, Vol 1, 2nd edn. Baltimore, MD: Lippincott Williams & Wilkins; 1999:239-483. 4. Robbins MS, Kuruvilla D, Blumenfeld AH, et al. Trigger point injections for headache disorders: Expert consensus methodology and narrative review. Headache. 2014;54: 1441-1459. 5. Ferrante E, Savino A, Sances G, Nappi G. Spontaneous intracranial hypotension syndrome: Report of 12 cases. Headache. 2004;44:615-622. 6. Schievink WI, Dodick DW, Mokri B, Silberstein S, Bouser MG, Goadsby PJ. Diagnostic criteria for headache due to spontaneous intracranial hypotension: A perspective. Headache. 2011;51:1442-1444.
Headache 7. Akin Takmaz S, Unal Kantekin C, Kaymak C, Bas¸ar H. Treatment of post-dural puncture headache with bilateral greater occipital nerve block. Headache. 2010;50:869-872. 8. Niraj G, Kelkar A, Girotra V. Greater occipital nerve block for postdural puncture headache (PDPH): a prospective audit of a modified guideline for the management of
699 PDPH and review of the literature. J Clin Anesth. 2014;26:539-544. 9. Vestergaard K, Andersen G, Nielsen MI, Jensen TS. Headache in stroke. Stroke. 1993;11:1621-1624. 10. Sorrell MR. The physical examination of migraine. Curr Pain Headache Rep. 2006;10:350-354.
