Clinical Characteristics of Subarachnoid Hemorrhage With or Without Headache

Clinical Characteristics of Subarachnoid Hemorrhage With or Without Headache

Clinical Characteristics of Subarachnoid Hemorrhage With or Without Headache Masaki Naganuma, MD,* Shodo Fujioka, MD,† Yuichiro Inatomi, MD,* Toshiro ...

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Clinical Characteristics of Subarachnoid Hemorrhage With or Without Headache Masaki Naganuma, MD,* Shodo Fujioka, MD,† Yuichiro Inatomi, MD,* Toshiro Yonehara, MD,* Yoichiro Hashimoto, MD,‡ Teruyuki Hirano, MD,x and Makoto Uchino, MDx

Objective: Some patients report the absence of a typical headache at the onset of subarachnoid hemorrhage (SAH). We investigated the clinical backgrounds and characteristics of patients with SAH without headache and compared the findings with those of patients with SAH and headache. Methods: We examined 224 patients retrospectively who underwent intracranial aneurysmal clipping. Patient’s characteristics, Fisher’s computed tomography grade, situation at onset, site of ruptured aneurysm, and symptoms were compared. Subjects were categorized into two groups: headache group and nonheadache group. Results: Eighteen patients (8.0%) did not present with headache. There were no significant differences in terms of age, sex, Fisher’s computed tomography grade, onset time, or site of ruptured aneurysm. Conclusions: The patients without headache have no specific clinical characteristics over patients with common SAH. Key Words: Headache—ruptured aneurysm—subarachnoid hemorrhage. Ó 2008 by National Stroke Association

Subarachnoid hemorrhage (SAH) usually causes a sudden onset of severe headache. However, approximately 2% to 8% of patients with SAH do not experience a headache at onset,1-3 and others report a gradually worsening headache.3,4 Patients with SAH who do not experience a typical headache may be misdiagnosed as having a tension type headache, migraine, common cold, or viral meningitis.4-8 To reduce the risk of re-bleeding from a ruptured aneurysm or vasospasm-induced cerebral ischemia,3,8-11 it is

Departments of *Neurology and †Neurosurgery, Stroke Center, Saiseikai Kumamoto Hospital, Kumamoto City, Japan; ‡Department of Neurology, Kumamoto City Hospital, Kumamoto city, Japan; and xDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto city, Japan. Received December 5, 2007; revision received March 12, 2008; accepted April 7, 2008. Address correspondence to Masaki Naganuma, MD, Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Fujishirodai 5-7-1, Suita City, Osaka 565-8565, Japan. E-mail: [email protected]. 1052-3057/$—see front matter Ó 2008 by National Stroke Association doi:10.1016/j.jstrokecerebrovasdis.2008.04.009

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important to recognize and confirm the diagnosis of SAH as early as possible. Misdiagnosis at the first medical examination has been correlated with an increased risk of re-bleeding, symptom deterioration, and poor outcome.7,8,12 However, making a correct diagnosis of SAHwithout the typical symptoms, especially headache, is difficult. The clinical characteristics of patients with SAH without headache have been poorly investigated.13-16 Therefore, we evaluated the clinical backgrounds and characteristics of patients with SAH without headache and compared the findings with those of patients with SAH and headache.

Materials and Methods Patients who were admitted to our hospital between January 1, 1990, and December 31, 1997, with SAH attributable to a ruptured intracranial saccular aneurysm and who underwent aneurysmal clipping were included in this study. All patients were given a diagnosis of SAH using head computed tomography (CT). The following procedures were used at our institute: (1) patients in neurologic grade I to III (classified according to Hunt and

Journal of Stroke and Cerebrovascular Diseases, Vol. 17, No. 6 (November-December), 2008: pp 334-339

SUBARACHNOID HEMORRHAGE WITHOUT HEADACHE 17

Kosnik ) on admission underwent emergency surgery for aneurysmal clipping; (2) patients in neurologic grade IV and V underwent conservative therapy until their condition improved to grade I to III; (3) patients in grade IV and V with intracerebral hematoma contributing consciousness disturbance underwent emergency surgery for aneurysmal clipping and hematoma evacuation; and (4) patients older than 80 years or having poor predisease ADLs was bedridden or nearly bedridden. We distributed questionnaires that included initial symptoms to the subjects by post in April 1998. The questionnaire detailed time, location, and behavior at onset; initial symptoms; existence of headache; state of headache at onset; and occurrence of symptoms other than headache. We included the patients who answered the questionnaires in this study, but excluded the patients who died, had high-grade unconsciousness, or lost their memory concerning onset at the time of investigation.

Clinical Characteristics The clinical characteristics of the eligible patients were reviewed retrospectively according to their medical chart and questionnaires. We investigated the following clinical characteristics and the initial symptoms obtained from the questionnaire and medical records: age, sex, onset time (which was estimated in 4-hour increments at 12-4am, 4-8am, 8am-12pm, 12-16pm, 4-8pm, and 8pm12am), Fisher’s CT grade18 on admission, site of ruptured aneurysm, location at onset (home, indoor except home, and outdoor), behavior at onset (normal activity and heavy activity), having headache or not, character of headache, and other symptoms. We defined sudden-onset and severe headache as typical, and a headache other than the typical headache, which was mainly a feeling of squeezing, as an atypical headache. The timing of initial symptom onset, which was the most crucial point in this study, was determined as the time when the patient initially felt strange before admission. Fisher’s CT grade was determined by two neurosurgeons on admission. Brain angiography was performed to determine the site of the ruptured aneurysm.

Statistical Analysis We categorized the patients with SAH into two groups. Patients with typical and atypical headache during their hospital days before intracranial aneurysmal clipping were included in the SAH with headache group. Typical headache is a sudden-onset, severe headache. Atypical headache is a gradual-onset, nonsevere headache, described as squeezing, throbbing, or similar to a cold. The nonheadache group consisted of patients who did not experience headache during the hospital days before intracranial aneurysmal clipping. Patients who did not report headache as their initial symptom were also

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classified into the headache group if they had severe headache after admission. We compared the two groups statistically by age, sex, and head CT findings, and analyzed onset time, location, behavior, and site of ruptured aneurysm at onset. Comparisons were made using the Chi-square test, Fisher’s exact test, Cramer’s V:Fisher CT grade test, or MannWhitney U test when appropriate. We considered that P less than .05 was statistically significant. Software (StatView, Version 5.0, SAS Institute Inc, Cary, NC), was used for analyses.

Results In all, 532 patients underwent intracranial aneurysmal clipping for ruptured aneurysms in our hospital between January 1, 1990, and December 31, 1997. We distributed questionnaires to all of these patients who were alive at discharge. According to our inclusion criteria, 224 patients (42.1%) were examined in this study (Fig 1). Of the 160 subjects who reported headache at onset, 136 presented with sudden-onset severe headache and 24 presented with atypical headache. Of the 24 patients with atypical headache, 9 presented later with severe headache. Of the 160 subjects, the site of aneurysm was the internal carotid artery in 48, anterior cerebral artery in 58, middle cerebral artery in 49, and vertebral-basilar artery in 5. The Fisher’s CT grade was 1 in 8 patients, 2 in 60 patients, 3 in 73 patients, 4 in 14 patients, and unknown in 5 patients. A total of 46 subjects reported headache that occurred after admission. These subjects did not present with headache at onset, and presented subsequently with typical headache. Their initial symptoms included feeling sleepy, feeling cut at the cerebral artery, feeling something flowing in the occipital region of the head, feeling something bursting in the head, feeling a loss of consciousness, not feeling well, slight nausea, vertigo, and dizziness. The site of aneurysm in these patients was internal carotid artery in 16 patients, anterior cerebral artery in 14 patients, middle cerebral artery in 15 patients, and vertebral-basilar artery in 1 patient. The Fisher’s CT grade was 1 in 0 patients, 2 in 13 patients, 3 in 29 patients, 4 in 3 patients, and unknown in 1 patient. Therefore, 206 patients (92.0%) with headache from onset to operation were included in the headache group, and 18 patients (8.0%) without headache before operation were included in the nonheadache group.

Clinical Characteristics Table 1 shows the clinical characteristics of the nonheadache group. In the nonheadache group, the mean age was 59.9 years, and 3 patients (16.7%) were male. Each patient showed various symptoms at onset, and most patients reported that their first symptom occurred during nonexertional daily activity. The median Fisher’s

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336 Figure 1.

532 cases of SAH had surgery

replied to questionnaire

Flow chart of inclusion of patients.

229 cases

no

yes initially severe deficit or lost memory (answered questionnaire incorrectly)

79 cases yes

no 224 eligible cases

headache occurring at onset 160 cases

no headache at onset 64 cases

headache occurred after admission 46 cases SAH with headache 206 cases

no headache during total course 18 cases SAH without headache 18 cases

CT grade was 2. Table 2 shows the clinical features of the two groups. In the headache group, the mean age was 57.6 years, and the median Fisher’s CT grade was 3. The headache and nonheadache groups showed no significant difference statistically in age, sex, Fisher’s CT grade, and site of ruptured aneurysm.

Situation at Onset Table 3 shows the time, location, and behavior at onset of each group. Regarding the time at onset, the time period of 4 to 8pm was the most frequent in the headache group, and the time period of 12 to 4pm was the most frequent in the nonheadache groups. However, no statistical difference was observed between the two groups. The main location where the first symptom occurred was at home in both groups. The specific location at home in headache group was the living room in 24.3%, bed in 10.2%, washroom in 13.6%, bathtub in 9.7%, and kitchen in 7.8%. In the nonheadache group, the specific location at home was the living room in 27.8%, bed in 5.6%, washroom in 16.7%, bathtub in 5.6%, and kitchen in 11.1%. In regard to the behavior at onset, heavy activity including strenuous work, heavy labor, and sexual intercourse was less frequent than normal activity including normal daily activity, light labor, urination or evacuation, and rest in each group. There were no significant differences in the location or behavior at onset between the groups.

Discussion Our results demonstrate that SAH presented with symptoms other than headache at onset in 64 patients (28.6%), and 18 patients (8%) never experienced headache

during the hospital days before surgery. There were no significant differences in age, sex, Fisher’s CT grade, site of ruptured aneurysm, onset time, and the location or the behavior at onset between the two groups. In our investigation, 8.0% of the patients with SAH did not experience headache. A few previous investigations1-3 showed that between 2% to 8% of patients with SAH do not experience headache. Walton1 investigated the patients with SAH who were admitted to their hospital during a 10-year period, and reported that 2% of patients with SAH did not experience headache. Graf and Nibbelink2 investigated patients with SAH who had an aneurysm in the anterior portion of the circle of Willis and had undergone an operative procedure, and reported that 8% of patients with SAH did not experience headache. Adams et al3 investigated patients with SAH who were misdiagnosed initially, and found that 3% of the patients with SAH did not present with headache. Our subjects and results were similar to the results of the study by Graf and Nibbelink.2 According to these results, in patients with SAH who have surgery, approximately 8% are without headache. No significant clinical differences were observed between the headache and nonheadache groups in our investigation. The reason for no differences in the clinical characteristics may include: (1) small number of subjects enrolled in the study; and (2) no information of clinical characteristics such as diabetes mellitus, use of analgesic agents, and other clinical background. In regard to behavior at onset, previous studies19,20 revealed that SAH often occurs during normal activity. Our study was consistent with previous studies in both the headache and nonheadache group. None of the subjects in the nonheadache group had an aneurysm in the vertebral-basilar artery,

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Table 1. Initial symptom, situation of onset, Fisher’s computed tomography classification, and location of aneurysm

Patients

Age, y Sex

Symptom at onset

Place at onset

Onset time

Behavior at onset Nonexertional daily activity Nonexertional daily activity Nonexertional daily activity Nonexertional daily activity Nonexertional daily activity Strenuous work Nonexertional daily activity Nonexertional daily activity Nonexertional daily activity Nonexertional daily activity Unknown Unknown Nonexertional daily activity Unknown Light working Strenuous work

1

63

F

Unusual feeling in neck

Outdoor

6 AM

2

52

F

Feeling sickness

Home living

12 AM

3

58

F

Feeling sickness

Home living

7 PM

4

69

F

Generalized weakness

Home bathtub

12 AM

5

65

F

Feeling dazed

Home kitchen

1 PM

6 7

61 60

M F

8

55

M

9

60

M Feeling pushed from back

10

59

F

11 12 13

62 55 67

14 15 16

Gradual pain of shoulder Indoor except home Gradual pain of neck Home washroom Generalized weakness

4 PM 9 PM

Home living

12 AM

Home kitchen

8 AM

Feeling pushed from back

Outdoor

4 PM

F F F

Loss of consciousness Visual disturbance Crash sound in head

Home living Unknown Home bed

11 AM Unknown 8 AM

54 51 49

F F F

Home washroom Indoor except home Indoor except home

12 AM 8 PM 6 PM

17

74

F

Feeling sickness Crash sound in head Burning feel in back of head Loss of consciousness

Home living

12 AM

18

64

F

Crash sound in head

Home washroom

7 AM

Nonexertional daily activity Urinating or evacuating

Fisher’s Site of CT grade aneurysm 1

Acom

1

MC

3

Acom

2

ICW

3

Acom

2 2

Ant chor ICPC

2

Acom

3

ICPC

3

ICPC

3 1 2

Acom ICPC MC

3 2 3

ICPC MC Acom

3

MC

2

ICPC

Abbreviations: Acom, anterior communicating artery; Ant chor, anterior choroidal artery; CT, computed tomography; F, female; ICPC, internal carotid artery posterior communicating artery; ICW, internal carotid artery wall; M, male; MC, middle cerebral artery.

Table 2. Demographic characteristics of patients with subarachnoid hemorrhage with or without headache

Age, y, mean (range) Male Fisher’s CT grade 1 2 3 4 Unknown Site of ruptured aneurysm Anterior cerebral artery Middle cerebral artery Internal carotid artery Vertebral-basilar artery Abbreviation: CT, computed tomography.

Headache group n 5 206

Nonheadache group n 5 18

P value

57.6 (21-82) 66 (32.0%)

59.9 (49-74) 3 (16.7%)

.361 .115 .101

8 (3.9%) 73 (35.4%) 102 (49.5%) 17 (8.3%) 6 (2.9%)

3 (16.7%) 7 (38.9%) 8 (44.4%) 0 (0%) 0 (0%)

72 (35.0%) 64 (31.1%) 64 (31.1%) 6 (2.9%)

6 (33.3%) 4 (22.2%) 8 (44.4%) 0 (0%)

.092

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Table 3. Demographic characteristics of patients with subarachnoid hemorrhage with or without headache

Time 12-4am 4-8am 8-12pm 12-4pm 4-8pm 8-12am Unknown Place at onset Home Indoor except home Outdoor Unknown Behavior at onset Normal activity Heavy activity Unknown

Headache group n 5 206 (%)

Nonheadache group n 5 18 (%)

13 (6.3) 32 (15.5) 37 (18.0) 27 (13.1) 49 (23.8) 28 (13.6) 20 (9.7)

0 (0) 2 (11.1) 3 (16.7) 6 (33.3) 4 (22.2) 2 (11.1) 1 (5.6)

135 (65.5) 27 (13.1) 41 (19.9) 3 (1.5)

12 (66.7) 3 (16.7) 2 (11.1) 1 (5.6)

185 (89.8) 14 (6.8) 7 (3.4)

13 (72.2) 2 (11.1) 3 (16.7)

P value .169

.061

.371

but this may reflect the small number of subjects in the nonheadache group. We addressed the initial symptoms, even though the initial symptoms of the nonheadache group may not be distinctive. The initial symptoms were ‘‘crash sound in the head’’ in 3 patients, generalized weakness in two patients, loss of consciousness in two patients, and visual disturbance in 1 patient. These symptoms were usually considered as general malaise, but these symptoms were consistent with cerebrovascular disease. However, the reported symptoms of ‘‘feeling sickness’’ in 3 patients, ‘‘feeling pushed from the back’’ in two patients, and ‘‘gradual pain of the neck or shoulder,’’ ‘‘unusual feeling in the back,’’ ‘‘burning feel in the back of the head,’’ and ‘‘feeling dazed’’ were considered to be general malaise. A few previous reports investigated symptoms when not accompanied by headache. Hauerberg et al13 investigated the symptom of a warning leak, and 4 of those patients reported no headache. Two patients had loss of consciousness and nausea/vomiting, one patient had loss of consciousness and nuchal rigidity/pain, and one patient had nuchal rigidity. However, these 4 patients were presented in the figure legend, and had no further reference. A few case studies14-16 reported atypical symptoms of SAH without headache. One case report14 examined a patient without initial headache who presented a variety of electrocardiogram changes. In another case,15 a patient had posterior neck pain and malaise at first, and another patient16 had lumbago and neck pain. The characteristics of first symptom of SAH without headache varied, therefore, we could not identify a distinctive feature of the onset symptom. Previous studies reported that 15% to 51% of SAH cases were misdiagnosed during the first medical examinations when the symptoms were slight.3,5,7,8,12,20,21 Patients with

atypical symptoms may be given an incorrect diagnosis and have a poor outcome. The results of our investigation showed that some of patients with SAH may have an onset with sudden symptoms, but not headache. Therefore, we suggest that a CT scan be performed in patients with sudden symptoms associated with the brain. Our findings, however, do not provide any suggestions as to which symptoms closely indicate the existence of SAH, because all of the subjects in our investigation were given the diagnosis of SAH correctly. Additional information as to the sudden symptoms related to SAH and others is needed. Our study has the following limitations: (1) our investigation is a retrospective study; (2) we were unable to obtain a completed questionnaire from approximately half of the patients; (3) we excluded patients who lacked this information because of the severity of their medical condition or death; (4) we did not analyze the contribution of risk factors, such as hypertension, smoking, and excessive drinking22,23; and (5) the number of subjects in the nonheadache group was small. In summary, 8% of patients with SAH who underwent aneurysmal clipping did not present headache, and the first symptoms of these patients were of general malaise. There were no unique clinical features of patients with SAH without headache compared with patients with SAH and headache.

References 1. Walton JN. Subarachnoid hemorrhage. Edinburgh: E&S Livingstone Ltd, 1956. p. 48-64. 2. Graf CJ, Nibbelink DW. Cooperative study of intracranial aneurysms and subarachnoid hemorrhage: Report on a randomized treatment study III. Stroke 1974;5:559-601.

SUBARACHNOID HEMORRHAGE WITHOUT HEADACHE 3. Adams HP Jr, Jergenson DD, Kassell NF, et al. Pitfalls in the recognition of subarachnoid hemorrhage. JAMA 1980;244:794-796. 4. Brust JC. Subarachnoid hemorrhage: Early detection and diagnosis. Hosp Pract 1982;17:73-80. 5. Kassell NF, Kongable GL, Torner JC, et al. Delay in referral of patients with ruptured aneurysms to neurosurgical attention. Stroke 1985;16:587-590. 6. Seymour JJ, Moscati RM, Jehle DV. Response of headaches to nonnarcotic analgesics resulting in missed intracranial hemorrhage. Am J Emerg Med 1995;13:43-45. 7. Mayer PL, Awad IA, Todor R, et al. Misdiagnosis of symptomatic cerebral aneurysm: Prevalence and correlation with outcome at four institutions. Stroke 1996; 27:1558-1563. 8. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000; 342:29-36. 9. Kassell NF, Peerless SJ, Durward QJ, et al. Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery 1982;11:337-343. 10. Kassell NF, Torner JC, Haley C, et al. The international cooperative study on the timing of aneurysm surgery. J Neurosurg 1990;73:18-36. 11. Schievink WI. Intracaranial aneurysms. N Engl J Med 1997;336:28-40. 12. Bassi P, Bandera R, Loiero M, et al. Warning signs in subarachnoid hemorrhage: A cooperative study. Acta Neurol Scand 1991;84:277-281.

339 13. Hauerberg J, Andersen BB, Eskesen V, et al. Importance of the recognition of a warning leak as a sign of a ruptured intracranial aneurysm. Acta Neurol Scand 1991;83:61-64. 14. Asplin BR, White RD. Subarachnoid hemorrhage: Atypical presentation associated with rapidly changing cardiac arrhythmias. Am J Emerg Med 1994;12:370-373. 15. Schattner A. Pain in the neck. Lancet 1996;348:411-412. 16. Weissman MN. Atypical presentation of subarachnoid hemorrhage: Case report and review of the literature. WMJ 2002;101:47-50. 17. Hunt WE, Kosnik EJ. Timing and perioperative care in intracranial aneurysm surgery. Clin Neurosurg 1974; 21:79-89. 18. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980; 6:1-9. 19. O’Hare TH. Subarachnoid hemorrhage. J Emerg Med 1987;5:135-148. 20. Fontanarosa PB. Recognition of subarachnoid hemorrhage. Ann Emerg Med 1989;18:1199-1205. 21. Neil-Dwyer G, Lang D. ‘‘Brain attack’’–aneurysmal subarachnoid hemorrhage: Death due to delayed diagnosis. J R Coll Physicians Lond 1997;31:49-52. 22. Mayberg MR, Batjer HH, Dacey R, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage. Stroke 1994;25:2315-2328. 23. Sankai T, Iso H, Shimamoto T, et al. Prospective study on alcohol intake and risk of subarachnoid hemorrhage among Japanese men and women. Alcohol Clin Exp Res 2000;24:386-389.