Cause Of Thunderclap Headache Research Articles

Etiology and characteristics of non-aneurysmal thunderclap headache presenting to an acute setting

ObjectivesTo describe the characteristics and causes of non-aneurysmal thunderclap headache (TCH) and compare serious from benign underlying causes. MethodsRetrospective cohort study of consecutive adult patients with TCH presenting to a tertiary care academic medical center between 2010 and 2020. Aneurysmal subarachnoid hemorrhage cases were excluded. Cases were categorized into serious or benign; serious TCH was defined as any condition in which delayed diagnosis and treatment could result in neurological disability or death. Risk factors for serious TCH were analyzed. We adhere to standardized guidelines for reporting observational studies. ResultsA total of 932 patients presented with TCH. After exclusion of 393 patients with aneurysmal-type subarachnoid hemorrhage, 539 were included in the analysis. One-half (n = 275, 51.0 %) had a serious cause. Median age was 51 years, 69.0 % were female. Most frequent diagnoses were intracranial hemorrhage (n = 102, 18.9 %), reversible cerebral vasoconstriction syndrome (n = 97, 18.0 %), and idiopathic TCH (n = 102, 38.6 %). A multivariable logistic regression model for prediction of serious TCH included age, hypertension, migraines, recurrent TCH, level of consciousness and other clinical exam findings, and achieved an AUROC of 0.732. This score had a sensitivity of 79.9 % (95 % CI 73.5–83.5 %) for the identification of serious TCH. A 0.5-point increase in the risk score was associated with a 73 % increase in the odds of serious TCH (odds ratio 1.73, 95 % CI 1.53–1.95, p < 0.001). ConclusionOur study describes the relative frequency of presentation and etiologies among patients with TCH This score can aide clinicians in recognising patients with potentially serious cause of TCH, for whom additional imaging and neurological consultation is necessary.

Ketamine Induced RCVS (P3-12.008)

<h3>Objective:</h3> To present a case of RCVS induced by ketamine infusions compounded with triptan and NSAID usage. <h3>Background:</h3> A 47 yo female with a history of depression and migraines presented with a persistent headache for 3 days. On the day of presentation, the patient reported the “worst headache of her life”. The headache was “sharp and squeezing”, frontal and retro-orbital in location, radiating to the back of her head, and exasperated by laying flat. The patient reported taking multiple high-dose NSAIDs along with sumatriptan. She had completed a 3-week course of ketamine infusions (75 mg twice weekly for depression) with last infusion 2 days prior to presentation. She was also on a chronic SSRI for depression. Patient denied any alcohol or current recreational drug use, but did report a history of opioid dependency. Initial CT head demonstrated a moderate-sized right frontal lobe subarachnoid and a small subarachnoid in the right posterior parietal lobe. CTA of head and neck demonstrated vasospasm of the left supraclinoid ICA, left M1 segment, and basilar artery. The location, radiographic appearance, and temporal course was consistent with RCVS. CT Angiogram was negative for any luminal irregularity, focal stenosis, or narrowing. MRI brain with contrast redemonstrated the subarachnoid hemorrhage without evidence of a vasculitic process. Lab work-up was negative for ANA, C4, C3, Sjogren’s Antibodies, RF, Anti-DNAs Ab. CRP and ESR were mildly elevated suggesting mild inflammation. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> The etiology of the headache and subarachnoid hemorrhage was suspected to be medication induced RCVS in the setting of concomitant use of sumatriptan, SSRI, and high doses of ketamine. <h3>Conclusions:</h3> Although a rare phenomena, RCVS is a concerning cause of thunderclap headache that should be recognized. RCVS is not a common occurrence with ketamine usage but clinicians should be aware is this possible adverse effect. <b>Disclosure:</b> Dr. Mufti has nothing to disclose. Dr. Canlas has nothing to disclose. Dr. Ritenuti has nothing to disclose.

Spontaneous pneumorrachia: a rare cause of thunderclap headache

Objective To present a rare cause of thunderclap headache Case presentation Female patient, 39 years old, was admitted to the emergency department of a private hospital in the city of São Paulo, after a sudden and explosive headache followed by two episodes of syncope and motor deficit in the left upper limb. Neurological examination showed weakness of the left upper limb without sensitive impairment. She had previous history of bipolar affective disorder, chronic anemia, and overweight with previous bariatric surgery. The patient was submitted to computed tomography (CT), arterial angiotomography of the skull and cervical neck, which showed rare small gaseous foci in the perivertebral soft tissues and extradural site on the left side in the craniovertebral transition, near the foramen magnum. Small foci of pneumocephalus were found in the posterior fossa, near the left sphenopetrous fissure. Electroneuromyography (ENMG) of four limbs and brain and cervical magnetic resonance imaging (MRI) were performed 48 hours after initial CT scan. ENMG was normal and MRI showed no more expression of the changes described on CT. She was treated with analgesia and was discharged with full reversion of initial symptoms. Conclusion Spontaneous pneumorrhachia is rare disease and is characterized by the presence of air in the spinal canal, both in the intradural and extradural compartments. It is usually benign with spontaneous resolution. Our patient was included in a stroke investigation protocol, due to the thunderclap headache and focal motor deficit. CT revealed the diagnosis. The cervical CT that was performed in the context of cervical CT angiography of the stroke protocol allowed the correct diagnosis. Key-words: Thunderclap headache, Spontaneous Pneumorrhachia, Cervical Computed Tomography Angiography.

Spontaneous bleeding of an arachnoid cyst: a rare cause of thunderclap headache

Introduction A thunderclap headache is a severe headache that starts suddenly and may be a sign of a condition that can be life threatening. Objective To present a case of a rare cause of thunderclap headache. Case presentation A 37-year-old female patient was admitted in the neurological emergence service of a private hospital in the city of São Paulo. She had sudden, explosive, and pulsatile headache, with photophobia and phonophobia. The neurological examination had no focal signs. She had deep vein thrombosis in 2014 in the past and since then she has been irregularly using Warfarin. She underwent CT and MRI of the skull that showed enlargement of the bilateral retrovermian and retrocerebellar cerebrospinal fluid space, with thin membranes/septations inside, and heterogeneous content, with deposition of hemoglobin degradation products. Such findings are consistent with a retrovermian arachnoid cyst with hemorrhagic content. The INR was 1. Conservative and symptomatic treatment was started, and control CT was performed on the second day of hospitalization, demonstrating almost complete reabsorption of hematic material. The patient was discharged after 2 days of hospitalization with complete headache improvement. Conclusion Arachnoid cysts are collections of fluid located between the meningeal membranes. They are congenital and are formed due to a valve defect in the arachnoid membranes leading to a collection of cerebrospinal fluid (CSF) in its interior. Most arachnoid cysts are an incidental finding. About 1 to 2% of the population has an arachnoid cyst and symptoms appear when the cyst increases in size or bleeds. Our patient had a are complication of and arachnoid cyst not related with the use of anticoagulant. Keywords: Thunderclap headache, Arachnoid Cyst Bleeding, Arachnoid Cyst.

Differentiation between Call Fleming syndrome and nervous system vasculitis

IntroductionCall Fleming syndrome is a reversible cerebral vasoconstriction syndrome of idiopathic etiology that causes thunderclap headache. It is a condition with a good prognosis, but clinically and radiologically similar to other diseases, such as nervous system vasculitis. Objectives To bring clinical, radiological and laboratorial aspects of Call Fleming Syndrome and nervous system vasculitis and provide the differentiation of both. MethodologyThe research is an integrative review, carried out in June 2022, using the SciElo and Pubmed databases. From the keywords: Call-Fleming syndrome) AND (Diagnosis), (Case report), (Radiology), the clinical, laboratorial and radiological profile of the Call-Fleming Syndrome was traced while the keywords (Nervous System) AND (Vasculitis) AND (Diagnosis), (Case report), (Radiology) were used to CNS vasculitis. Then, from case reports, radiology articles and laboratory analyses, the diseases in question were compared in terms of similarities and differences. ResultsBoth pathologies are similar from a clinical point of view: they are frequent causes of thunderclap headache, a sudden and severe headache that reaches its maximum intensity within 1 minute. Some patients with Call-Fleming Syndrome may present several neurological deficits, the more frequents in case reports are hemiparesis, hemianopia, and loss of balance. The disease has a limited course that lasts from 1 to 3 months, however, its main complications are hemorrhages and cerebral infarction. The age group affected in the reported cases ranges from 10 to 76 years and there is a slight predominance of cases in women. (To see the complete abstract, please, check out the pdf).

Bruns' syndrome as a cause of thunderclap headache in intraventricular cysticercosis

Neurocysticercosis is an infection caused by the larval stage of the tapeworm Taenia solium. The clinical manifestations depend on load, type, size, location, stage of development of the cysticerci, and the host's immune response against the parasite. An intraventricular cysticercus can produce Bruns syndrome, which can manifest as a thunderclap headache. Here we present an unusual case.

Editors' Note: Pearls &amp; Oy-sters: Isolated Oculomotor Nerve Palsy due to Pituitary Apoplexy Missed on CT Scan

Dr. Marzoughi and colleagues highlight the importance of personal visualization of neuroimaging and pursuit of advanced diagnostic testing in patients with severe headache and suspected intracranial lesions. In their case of an elderly gentleman with thunderclap headache and third nerve palsy, dedicated MRI with thin cuts through the sella identified pituitary apoplexy as the cause of the patient's symptoms. The fact that this patient exhibited brisk pupillary reactivity to light is somewhat atypical for a compressive third nerve palsy, as Professor Pollak comments. However, the authors indicate that the patient was anisocoric at presentation, with more pronounced asymmetry in bright light, meaning the ipsilateral parasympathetic pathway was dysfunctional. Furthermore, the pupillary fibers may be in a less vulnerable position in the cavernous sinus than in the subarachnoid space. Dr. Zhang et al. comment on other differential diagnoses for sudden, severe headache and cranial nerve palsies, which would include aneurysmal subarachnoid hemorrhage. In the absence of radiographic confirmation of a pituitary lesion—or other cause of thunderclap headache and cranial neuropathy (e.g., cavernous sinus thrombosis)—the clinician should pursue an occult aneurysm and/or subarachnoid hemorrhage as the cause of this patient's symptoms. Susceptibility-weighted and FLAIR MRI, conventional angiography, and lumbar puncture to evaluate for xanthochromia may be useful diagnostic tools when the cause of headache and cranial neuropathy(ies) remains elusive. Dr. Marzoughi and colleagues highlight the importance of personal visualization of neuroimaging and pursuit of advanced diagnostic testing in patients with severe headache and suspected intracranial lesions. In their case of an elderly gentleman with thunderclap headache and third nerve palsy, dedicated MRI with thin cuts through the sella identified pituitary apoplexy as the cause of the patient's symptoms. The fact that this patient exhibited brisk pupillary reactivity to light is somewhat atypical for a compressive third nerve palsy, as Professor Pollak comments. However, the authors indicate that the patient was anisocoric at presentation, with more pronounced asymmetry in bright light, meaning the ipsilateral parasympathetic pathway was dysfunctional. Furthermore, the pupillary fibers may be in a less vulnerable position in the cavernous sinus than in the subarachnoid space. Dr. Zhang et al. comment on other differential diagnoses for sudden, severe headache and cranial nerve palsies, which would include aneurysmal subarachnoid hemorrhage. In the absence of radiographic confirmation of a pituitary lesion—or other cause of thunderclap headache and cranial neuropathy (e.g., cavernous sinus thrombosis)—the clinician should pursue an occult aneurysm and/or subarachnoid hemorrhage as the cause of this patient's symptoms. Susceptibility-weighted and FLAIR MRI, conventional angiography, and lumbar puncture to evaluate for xanthochromia may be useful diagnostic tools when the cause of headache and cranial neuropathy(ies) remains elusive.

Severe abrupt (thunderclap) non-traumatic headache at the pediatric emergency department - a retrospective study.

Adult abrupt severe non-traumatic headache (thunderclap) is often related to serious underlying etiologies such as subarachnoid hemorrhage. However, data are sparse regarding thunderclap headache in the pediatric population. The aim of the study was to evaluate the prevalence, characteristics and causes of thunderclap headache in the pediatric and adolescent population, aged 6-18 years, presenting to a pediatric emergency department. The electronic database of a tertiary care pediatric emergency department was searched for children presenting with acute headache during 2016-2018. Headache severity was defined by pain scales, either a visual analogue scale or by the Faces Pain Scale-Revised. Thunderclap headache was diagnosed in 19/2290 (0.8%) of the included patients, all of them with a pain score of 10/10. All the patients had a benign course. Primary headache was diagnosed in 15/19 (78.9%), six patients had migraine and eight were diagnosed with primary thunderclap headache. Four of the 19 patients were diagnosed with secondary headache: three with infectious causes and one with malignant hypertension. Thunderclap headache is rare among children and adolescents presenting to the emergency department. This headache is generally of a primary origin. Extensive evaluation is still needed to rule out severe diagnosis problems.

Management of thunderclap headache in the emergency room: A retrospective cohort study

Introduction The evaluation of red flags is crucial for the accurate the diagnosis of headache disorders, especially for thunderclap headache. We analysed if secondary headache disorders were adequately ruled out in patients that presented to the emergency room with thunderclap headache. Methods In this retrospective cohort study, we screened all patients that visited the emergency room for headache, including those that described thunderclap headache. We measured the frequency with which secondary causes were not adequately ruled out. We analysed the order of the exams, the final diagnosis, and the time elapsed between arrival, initial request for imaging, and the completion of the imaging. Results We screened 2132 patients, and 42 (1.9%) fulfilled eligibility criteria. Mean age was 43.1 ± 17.1 years, and 57% of patients were female. For 22 (52.4%) patients, the work-up was incomplete. Vascular study was missing in 16 (38.1%) patients, cerebrospinal fluid evaluation in nine (21.4%), and magnetic resonance imaging in seven (16.7%), with multiple assessments missing in six (14.3%). There were ten different combinations in which the exams were performed, with the most frequent being the second exam’s cerebral spinal fluid evaluation in 18 (52.9%) and the computed tomography angiogram in 10 (29.4%). A secondary cause of thunderclap headache was found in 16 (38.1%) patients, and four (9.5%) had a primary headache diagnosis after an adequate and complete study. Conclusions Thunderclap onset was described in one of every 50 patients that visited the emergency room for headache. More than half of these patients were not adequately managed. More than a third of thunderclap headache patients had a secondary cause.

An unusual cause of thunderclap headache after eating the hottest pepper in the world – “The Carolina Reaper”

A 34-year-old man with no significant medical history presented to the emergency room (ER) after an episode of thunderclap headache. His symptoms began with dry heaves but no vomiting immediately...

The Typical Thunderclap Headache of Reversible Cerebral Vasoconstriction Syndrome and its Various Triggers

During the last 10 years, reversible cerebral vasoconstriction syndrome (RCVS) has emerged as the most frequent cause of thunderclap headache (TCH) in patients without aneurysmal subarachnoid hemorrhage, and as the most frequent cause of recurrent TCHs. The typical TCHs of RCVS are multiple, recurring over a few days to weeks, excruciating, short-lived, and brought up by exertion, sexual activities, emotion, Valsalva maneuvers, or bathing, among other triggers. All these triggers induce sympathetic activation. In a minority of cases with RCVS, TCH heralds stroke and rarely death. Early diagnosis of RCVS in patients who present with isolated headache enables proper management and might reduce the risk of eventual stroke. This review describes the characteristics, triggers, diagnosis, and management of TCH in RCVS. One aim is to underline that the TCH pattern of RCVS is so typical that it enables, according to the 2013 revision of the International Classification of Headache Disorders, the diagnosis of "probable RCVS" in patients with such a headache pattern, normal cerebral angiography, and no other cause. Another objective is to discuss the role of physical and emotional stress in RCVS and in other related conditions involving similar triggers.

Reversible Cerebral Vasoconstriction Syndrome – A Systematic Approach

Aims: Reversible cerebral vasoconstriction syndrome (RCVS) is a rare idiopathic clinical syndrome presenting as reversible multifocal segmental vasoconstriction of cerebral arteries, typically affecting middle aged women. A 52 year old lady with radiological features of RCVS is presented. Presentation of Case: A 52 year old lady presented with recurrent thunderclap headache. Initial laboratory and radiological investigations were normal. Over the course of two weeks she developed stroke like symptoms with haemorrhagic transformation. Serial imaging revealed development and resolution of cerebral arterial stricture. Discussion: RCVS is often an under-diagnosed entity in patients with thunderclap headache. The initial MRI may be normal but the repeat MRI after two to three weeks may show features of stroke with associated vascular abnormalities. The follow up of these cases with radiological investigations may help in precise diagnosis. Conclusion: Differentiating RCVS from other causes of thunderclap headache can significantly alter the management options and further prognosis.

Reversible cerebral vasoconstriction syndrome at the emergency department.

ObjectiveReversible cerebral vasoconstriction syndrome (RCVS) is an underestimated cause of thunderclap headache that shares many characteristics with subarachnoid hemorrhage (SAH). This fact makes the two easily confused by emergency physicians. This study evaluated the clinical manifestations, radiological features, and outcomes of patients with RCVS.MethodsThe electronic medical records of 18 patients meeting the diagnostic criteria of RCVS at our emergency department between January 2013 and December 2014 were retrospectively reviewed.ResultsThe mean patient age was 50.7 years, and 80% were women. Patients with RCVS encountered physicians 4.7 times before receiving an accurate diagnosis. The mean duration of symptoms until diagnosis was 9.3 days. All but one patient experienced severe headache of 8 to 10 on a numerical rating scale. A total of 44% of patients had nausea, and 66% of patients experienced worsening of the headache while gagging, leaning forward, defecating, urinating, or having sexual intercourse. The most frequently affected vessels were the middle cerebral arteries, which demonstrated a characteristic diffuse “string of beads” appearance. Four cases were complicated by SAH.ConclusionPatients with RCVS have a unique set of clinical and imaging features. Emergency physicians should have a high index of suspicion for this clinical entity to improve its rate of detection in patients with thunderclap headache when there is no evidence of aneurysmal SAH.

Reversible Cerebral Vasoconstriction Syndrome

BackgroundReversible cerebral vasoconstriction syndrome (RCVS) is an underappreciated and poorly understood cause of thunderclap headache (TCH). Although self-limited in the majority of patients, incidence is increasing, with presentations overlapping considerably with life-threatening conditions, such as aneurysmal subarachnoid hemorrhage and stroke. In addition, radiographic findings seen in RCVS are also present in primary angiitis of the central nervous system (PACNS). Misdiagnosis of RCVS might subject patients to unnecessary invasive testing and immunosuppressive therapy. Furthermore, the recommended treatment of glucocorticoids used in PACNS can be harmful in RCVS. RCVS is not a benign condition, as patients can have ischemic or hemorrhagic complications leading to persistent neurologic deficits and even death. Current treatments, guided only by expert consensus, have no proven effect on these complications, which argues the need for accurate identification of patients with RCVS and prospective studies to validate treatment and inform prognoses. Case ReportWe describe a previously healthy male who presented to the emergency department after 2 episodes of TCH and angiography consistent with RCVS. Why Should An Emergency Physician Be Aware of This?RCVS is a common but underappreciated cause of TCH. The likelihood of misdiagnosing RCVS following the accepted diagnostic algorithm of acute headache in the emergency department is high due to a lack of clinical awareness and common features shared with other headache syndromes. Emergency department physicians must broaden the differential in patients presenting to the emergency department with TCH to include RCVS and be familiar with the accepted treatments and appropriate follow-up.

Thunderclap Headache

Thunderclap headache (TCH) is a sudden severe headache that peaks to maximum intensity within 1 minute. Subarachnoid hemorrhage is the most commonly identified etiology for this headache, however, other secondary etiologies should be considered. Sentinel headache, reversible cerebral vasoconstriction syndrome, arterial dissection, cerebral venous sinus thrombosis, pituitary apoplexy, intracranial hemorrhage, ischemic stroke, reversible posterior leukoencephalopathy, spontaneous intracranial hypotension, colloid cyst, and intracranial infections are other possible causes of TCH. Investigations for the etiology of TCH begin with noncontrast CT head and lumbar puncture. MR brain, CT angiogram, MR angiogram, or CT/MR venogram may need to be performed if the initial investigations are negative. Treatment and prognosis depend on the etiology of the TCH.

Call-Fleming Syndrome: Headache in a 16-Year-Old Girl

Call-Fleming syndrome, also known as reversible cerebral vasoconstriction syndrome, is an important cause of severe headache characterized by segmental constriction of cerebral arteries in multiple vascular distributions. It is commonly described in adults, with a female predominance. We report a case of a 16-year-old girl with history of anxiety, attention deficit hyperactivity disorder, and migraines on several medications presenting with 2 weeks of worsening headaches. Cranial computed tomography was normal, but magnetic resonance imaging revealed cortical subarachnoid hemorrhage. Follow-up imaging demonstrated extensive vasoconstriction of small- to medium-sized cerebral arteries. Sertraline and methylphenidate were discontinued, and nifedipine was started. Symptoms rapidly improved, and repeat angiography at 2 months showed no vasoconstriction. Call-Fleming syndrome is an important cause of thunderclap headache and should be considered in the pediatric population, especially in the setting of certain medication usage and other known risk factors.

Thunderclap headache as the only presentation of herpes simplex meningitis: a review of uncommon causes of thunderclap headache

Thunderclap headache as the only presentation of herpes simplex meningitis: a review of uncommon causes of thunderclap headache

Thunderclap headache as the primary clinical feature of a supratentorial embolic cerebral infarct

A formula for the diagnostic assessment of thunderclap headache (TCH) should be established. The management of this type of headache is controversial. The established diagnostic assessment of TCH includes a computer tomography (CT) of the head and cerebrospinal fluid (CSF) examination to exclude a subarachnoid haemorrhage. In patients whose CT scans and CSF analyses are normal, further testing is rarely considered to be indicated by most clinicians [1]. However, others suggest that in circumstances where CT and CSF are normal, further diagnostic assessment with magnetic resonance imaging (MRI), magnetic resonance angiography (MRA) of the brain and neck, and magnetic resonance venography is necessary [2]. Articles differ in their conclusions and recommendations. A MRI-verified supratentorial embolic cerebral infarct with TCH as the primary clinical feature is to my knowledge not hitherto reported. Here is described a patient who experienced a TCH as the primary clinical feature of an embolic insula/temporal lobe infarct. A 41-year-old woman appeared in the emergency department following an acute and sudden onset of severe headache. The pain was located in the left temporal region, it reached its maximum intensity in \1 min and lasted for about 7 h. At the time of admission to hospital, the patient reported that the headache had waned. There was no previous history of headaches. Vital signs and physical examination were normal. Neurological examination was normal. Laboratory testing was within the normal range. Blood pressure monitoring was normal. An electrocardiogram (ECG) showed sinus rhythm. Cerebrospinal fluid (CSF) examination revealed a normal opening pressure (140 mmH2O), a normal closing pressure, a normal cell count, glucose and protein. Spectrophotometry disclosed no bilirubin. A CT scan of the head was normal. A magnetic resonance imaging (MRI) of the brain was carried out to exclude other causes of TCHs. It revealed an acute ischaemic lesion in the left insula/ temporal lobe (Fig. 1). A magnetic resonance angiography (MRA) was ordered to exclude intracranial aneurysms, cerebral venous thrombosis, dissection and reversible cerebral vasoconstriction syndrome. These investigations revealed an acute embolic occlusion of a main M2 segment branch of the left middle cerebral artery (Fig. 2). No dissection, reversible cerebral vasoconstriction syndrome or other abnormalities could be detected. Further investigations with ECG telemetry and echocardiography were normal. An additional MRI and MRA of the cervical arteries/intracerebral circulation 2 days later confirmed the cerebral infarct and the occlusion. An extensive laboratory testing revealed normal results. No source of the cerebral embolus could be found. The patient could be discharged and remains well. At follow-up after 6 months, she reported no headache. TCH is a very rare manifestation of a cerebral infarct. In 2006, a case report was published where a TCH was the presenting clinical feature of embolic cerebellar infarcts, in the absence of neurological findings [3]. Gossrau et al. [4] presented a similar case (cerebellar infarct) in 2008. Headache is not uncommon in ischaemic stroke, but is usually overshadowed by other manifestations such as aphasia and neglect [5]. It is usually focal and mild [5]. The character of the headache is throbbing [5]. The severity of the headache is not related to the size of the infarct or the location of the lesion [5]. B. Edvardsson (&) Department of Neurology, Faculty of Medicine, Lund University Hospital, 221 85 Lund, Sweden e-mail: Bengt.Edvardsson@med.lu.se

Neues bei Kopfschmerzen 2008

Chronic migraine without medication overuse is now widely accepted as a unique headache entity. Although the lifetime prevalence of migrainous vertigo is 1 %, it is most likely that most patients are not correctly diagnosed or treated. Further prospective studies have revealed triggers and premonitory symptoms signalling migraine attacks. Animal models of cortical spreading depression are being increasingly established to help understand migraine aura and headache. The combination of sumatriptan and naproxen is more effective in comparision to each of the substances alone. Recent trials have shown the efficiacy of topiramate in the treatment of medication overuse headache, chronic migraine and tension-type headache. There is further evidence for a cessation of migraine preventive therapy with topiramate after six months regarding a long-term benefit. However, there is no evidence from randomised trials for short-term prophylaxis of menstrual migraine with estrogen, NSAIDs or triptans. Venlaflaxine is effective for preventive therapy of chronic tension-type headache. Bilateral stimulation of the occipital nerve might be an option for patients suffering from refractory chronic cluster headache instead of deep brain stimulation. Reversible cerebral vasoconstriction may represent a frequent cause of thunderclap headache.

Cerebral venous sinus thrombosis as a rare cause of thunderclap headache and nonaneurysmal subarachnoid haemorrhage

Sirs: In a clinical setting, isolated thunderclap headache is commonly assumed to be benign in origin once subarachnoid haemorrhage (SAH) has been excluded [1]. However, cerebral venous sinus thrombosis (CVST) is an infrequent, alternative cause of sudden-onset headache and is not conclusively excluded by normal conventional CT and LP. CVST is also a recognised rare cause of SAH. Here, we report a case of CVST presenting with thunderclap headache and complicated by delayed SAH. A previously well 53-year-old woman presented with spontaneous, sudden-onset occipital headache as her sole symptom. Neurological examination including fundoscopy was normal, with no evidence of meningism. Acute head CT and subsequent LP performed 16 hours after onset were unremarkable (opening pressure 19 cm, CSF acellular with no bilirubin detectable on spectrophotometry). The headache resolved completely within 24 hours and the patient was discharged with a diagnosis of primary thunderclap headache. The following day, she represented with sudden-onset headache at rest accompanied by mild neck stiffness. Her symptoms resolved before a further suddenonset headache occurred two days later. Examination remained normal throughout. Repeat, unenhanced head CT demonstrated a small, high left frontal SAH along the cranial convexity without involvement of the basal cisterns (Fig. 1a). CT angiography detected no arterial aneurysm, but its venous phase showed changes suggestive of superior sagittal sinus thrombosis, which was confirmed on MR venography (Fig. 1b). Screening for secondary causes of thrombosis was negative. She was initially treated with intravenous unfractionated heparin to allow rapid reversal in case of rebleeding, before being warfarinised under cover from low molecular weight heparin. She remained well at follow-up six months later. Repeat MR angiography showed resolution of the superior sagittal sinus thrombosis, with no other vascular or brain parenchymal abnormalities. Thunderclap headache is an unusual presentation of CVST, perhaps seen in fewer than 20 % of cases [2]. Rarely, there may be no concomitant findings to suggest the presence of a CVST, such as focal neurological signs, seizures or features of raised intracranial pressure. Most patients with CVST have a raised opening pressure and abnormal CSF constituents, but absence of these features does not conclusively rule out the diagnosis. In a previous series of 38 cases, nine patients had both opening pressure and CSF constituents measured, and in one of them all parameters were normal [3]. SAH is a very rare complication of cerebral venous thrombosis, with only 30 cases reported to date. It has been suggested that venous intraparenchymal haemorrhages may rupture into the subarachnoid space, thus causing sudden-onset headache in CVST [2, 4]. However, we hypothesise that our patient’s first headache was caused by the CVST, as there was no evidence of SAH on initial brain CT and bilirubin was not detectable in the CSF. The second or third episode of headache may have been caused by SAH. LETTER TO THE EDITORS