Sudden Onset Of Severe Headache Research Articles

Call-Fleming syndrome

Call–Fleming syndrome is a part of reversible cerebral vasoconstriction syndrome (RCVS) group and is thought to be of idiopathic origin. It is classically described to be having multisegmental, focal vasospasms in the cerebral arteries. It is characterized clinically by the sudden onset of severe headache, classically described as thunderclap headache, with or without associated neurological deficits. The importance of it lies in that it is a potentially reversible cause of this clinical presentation, unlike its other counterparts, aneurysmal subarachnoid hemorrhage (SAH) or vasculitis.

Tungsten Coil Disappearance and SAH Recurrence 12 Years After Endovascular Embolisation

A 55-year-old woman presented with a sudden onset of severe headache. Computed tomography (CT) revealed SAH (grade I according to the Hunt and Hess classification), predominantly in the right ambient cistern. digital subtraction angiography (dsA) demonstrated a posterior communicating artery (pCoA) aneurysm (3.2 × 5.1 mm) (Fig. 1c). This patient had suffered sAH because of rupture of a right pCoA 12 years back (Fig. 1a) and had undergone endovascular treatment. Tungsten mechanical detachable coils (MDS; Balt Extrusion, Montmorency, France) were inserted into the aneurysm, and the occlusion was considered to be greater than 90 % (Fig. 1b). she was discharged and returned to normal life without further angiography. After comparing the dsA images of this presentation and the ones 12 years before, the two aneurysms were the same, but the tungsten coils had disappeared. Cranial CT and plain radiographs did not find high radiopacity in other places. On admission, endovascular embolisation was selected. While the patient was under a general anaesthetic, platinum coils (GDC, Boston Scientific, Fremont, CA, USA) were inserted, including two 4 mm × 10 cm coils, a 4 mm × 6 cm coil and a 2 mm × 3 cm coil. The coils were inserted until aneurysmal circulatory exclusion was achieved (Fig. 1d). Whole blood, serum and urine tungsten levels were assayed. The values were 0.00025, 0.00024 and 0.00018 μg/ ml, respectively. The normal serum value is 0.0002 μg/ml. Liver and renal functions were tested, and they were normal. X-ray scan showed no lung fibrosis or dermatitis. Subsequently, she was discharged with no neurological deficit.

Giant necrotic pituitary apoplexy

Apoplexy of the pituitary gland is a rare complication of pituitary adenomas, involving hemorrhage with or without necrosis within the tumor. This condition may be either asymptomatic or may present with severe headache, visual impairment, ophthalmoplegia, and pituitary failure. Transsphenoidal surgery is the treatment of choice, and early intervention is usually required to ensure reversal of visual impairment. Reports of pituitary apoplectic lesions exceeding 60.0mm in diameter are very rare. A 39-year-old man with long-standing history of nasal congestion, decreased libido and infertility presented with a sudden onset of severe headache and diplopia. MRI of the head demonstrated a massive skull base lesion of 70.0×60.0×25.0mm, compatible with a giant pituitary macroadenoma. The lesion failed to enhance after administration of a contrast agent, suggesting complete necrotic apoplexy. Urgent surgical decompression was performed, and the lesion was resected via a transnasal transsphenoidal approach. Pathological analysis revealed evidence of necrotic pituitary apoplexy. At the 2 month follow-up, the patient had near-complete to complete resolution of his visual impairment. To the authors’ knowledge, this report is unique as the patient demonstrated complete necrotic apoplexy and it underlines the diagnostic dilemma in such a case.

Tension pneumocephalus and rhinorrhea related to chronic sinusitis

A 42-year-old woman presented with a sudden-onset severe headache associated with vomiting and a persistent aqueous rhinorrhea. She had an allergic chronic sinusitis. There was no history of head trauma. Neurologic exam disclosed papilledema. The computed tomography (CT) scan showed opacification of the left sphenoid sinus and pneumocephalus extending from frontal region until convexity, compressing the supratentorial ventricular system (Fig 1). The cerebrospinal fluid (CSF) fistula was found in the left pterygoid process (Fig 2). Air probably came through the [...]

Subarachnoid haemorrhage as the presenting feature of lumbar spinal arteriovenous malformation

A 41-year-old man presented with a sudden onset severe occipital headache, vomiting, neck stiffness and photophobia. He had been previously well, aside from chronic mid and lower back pain. There...

Primary sudden onset severe headache: Prognosis and factors influencing it

Sudden onset severe headache, so called thunderclap headache, is a common condition that sometimes indicates a life-threatening conditions such as subarachnoid haemorrhage (SAH). Little is known about the prognosis of primary sudden onset severe headache (PSOH). Objectives To investigate the recurrence rate of sudden onset severe headache with normal brain imaging and lumbar puncture and factors associated with its recurrence.

Idiopathic Lenticulostriate Artery Pseudoaneurysm Protruding into the Lateral Ventricle: A Case Report

We report a rare case of an idiopathic pseudoaneurysm causing intraventricular hemorrhage (IVH). A 28-year-old man presented with sudden onset of severe headache. He underwent external ventricular drainage for an isolated IVH in the right lateral ventricle. Digital subtraction angiography (DSA) revealed that the aneurysm (7.5×4.5 mm) arose from the distal part of the medial lenticulostriate artery. Following removal of the external ventricular drainage catheter, the aneurysm decreased in size (4.0×2.3 mm). However, follow-up DSA revealed a slightly enlarged aneurysm (4.2×3.2 mm) with morphologic change. The aneurysm was clipped via the interhemispheric transcallosal approach, but postoperative DSA revealed a residual aneurysm sac beside the clips. Given the risk of rebleeding, a second operation was planned for complete resection of the aneurysm. After revised craniotomy and careful dissection of the caudate nucleus, the aneurysm sac was completely resected. Histopathological examination revealed that the aneurysm was a pseudoaneurysm. The patient recovered without any neurological sequel and was discharged.To the best of our knowledge, this is the first reported case of an idiopathic lenticulostriate artery pseudoaneurysm protruding into the right lateral ventricle and causing an IVH that was successfully treated with microsurgical resection.

Lateral sinus thrombosis in setting of Acute otitis media: An atypical presentation

Lateral sinus thrombosis (LST) is a rare complication of Acute Otitis Media and associated mastoiditis. Although, in the era of antibiotics, the presentation may be variable and diagnosis is difficult. High index of suspicion is required to diagnose the atypical presentation. We report an atypical presentation of LST wherein a 12-year-old female presented with sudden onset severe occipital headache following ear syringing. Contrast enhanced computed tomography of temporal bone revealed LST without coalescent mastoiditis. Patient was managed conservatively with intravenous antibiotics and low-dose heparin. The management protocols in such cases are discussed and relevant literature reviewed.

Primary sudden onset severe headache: Prognosis and factors influencing it

Primary sudden onset severe headache: Prognosis and factors influencing it

Apoplexy of A Microprolactinoma During Pregnancy: Case Report and Review of Literature

To report a rare case of apoplexy in a microprolactinoma during pregnancy. We present the initial clinical manifestations, laboratory results, radiologic findings, and management in a patient who had pituitary apoplexy during early pregnancy. The pertinent literature and management options are also reviewed. A 37-year-old woman with a history of a microprolactinoma presented during the 16th week of her first pregnancy with a sudden onset of severe headache, nausea, vomiting, and blurred vision. Magnetic resonance imaging showed a sellar heterogeneous mass with suprasellar extension and contact with the optic chiasm, compatible with adenoma apoplexy. The patient's visual fields were normal. Conservative management was followed by rapid clinical improvement and a notable regression of the sellar mass after 5 weeks of cabergoline therapy. Uneventful pregnancy resulted in the delivery of a healthy baby. Repeated magnetic resonance imaging was performed 1 week after delivery and showed resolution of the microadenoma. At 3 months after delivery, the patient had recovered regular menses and had sustained normal prolactin levels without treatment. This case illustrates a rare occurrence of apoplexy in a microprolactinoma during pregnancy, which was managed conservatively and led to a complete regression of the pituitary tumor.

Reversible Cerebral Vasoconstriction Syndrome 3 Months after Blood Transfusion

Reversible cerebral vasoconstriction syndrome is characterized by the prolonged but reversible constriction of cerebral arteries accompanied by a sudden onset of severe headache, and is sometimes complicated by subarachnoid hemorrhage or cerebral infarction. It is associated with various clinical conditions and treatments, although the precise pathophysiology is not understood. In particular, several cases of this syndrome have been described to occur in middle-aged women within 1 week of a blood transfusion. We encountered a patient with a reversible cerebral vasoconstriction syndrome who became symptomatic 3 months after a blood transfusion. No other cause for the syndrome was found. This case suggests that the risk for the reversible cerebral vasoconstriction may persist for months after blood transfusion.

Simultaneous Presentation of Two Cerebral Aneurysms

A 48-year-old woman experienced sudden onset of severe headache. Computed tomography showed subarachnoid hemorrhage (SAH) and intracerebral hematoma in the right frontal lobe. Digital subtraction angiography revealed three aneurysms in the anterior communicating artery (AcomA), the right posterior communicating artery (PcomA), and the right middle cerebral artery. The AcomA aneurysm was treated with endovascular coiling. However, her oculomotor nerve palsy was aggravated after the procedure. Embolization of the right PcomA aneurysm was conducted immediately and her oculomotor nerve palsy recovered completely 3 months later. Simultaneous presentation of multiple aneurysms with separate symptoms is rare. We speculate that the progressive oculomotor nerve palsy was caused by tiny enlargement or morphological change of the aneurysm caused by elevated blood pressure and pulsatile effect after SAH.

Massive subarachnoid hemorrhage after radiofrequency trigeminal rhizotomy

A 40-year-old man developed massive subarachnoid hemorrhage following attempted radiofrequency ablation for trigeminal neuralgia. The patient had a 10-year history of trigeminal neuralgia at the ophthalmic and maxillary branches of the left trigeminal nerve. After the procedure, the patient’s pain resolved completely, but one hour later sudden onset of severe headache in the frontal region was appeared. Computed tomography (CT) scan of the cranium showed massive subarachnoid hemorrhage, and an air bubble was observed in the left cavernous sinus. Herein, we present the CT feature of this rare complication. Keywords: Radiofrequency ablation; subarachnoid hemorrhage; traumatic; trigeminal neuralgia

Ganglioneuroma Originating From the Trigeminal Nerve in the Middle Cranial Fossa

A 55-year-old man present with a case of ganglioneuroma manifesting as sudden onset of severe headache. T(1)-weighted magnetic resonance imaging demonstrated a heterogeneously enhanced mass (3 × 3 × 2.5 cm) in the left middle cranial fossa compressing the left cavernous sinus. The tumor was totally removed through a frontozygomatic approach. The histological diagnosis was ganglioneuroma originating from the second division of the trigeminal nerve in the middle cranial fossa. Ganglioneuroma can occur wherever ganglion cells exist, but ganglioneuroma originating from the trigeminal nerve is rare, with only two cases reported.

Ruptured Aneurysm With Delayed Distal Coil Migration Requiring Surgical Treatment

A 64-year-old woman with subarachnoid hemorrhage manifesting as sudden onset of severe headache visited our hospital on post-onset day 8. Diagnostic cerebral digital subtraction angiography revealed an aneurysm located at the left internal carotid-anterior choroidal artery with diffuse cerebral arterial spasm. Coil embolization was selected because of diffuse spasm in spite of parent artery elongation at the extra-cranial portion. A small portion of the coil migrated to the parent artery, but coil embolization was successfully completed. The patient developed delayed spasm, which required arterial fasudil hydrochloride injection. After the acute phase of subarachnoid hemorrhage, the patient's symptoms disappeared. However, on day 24 after subarachnoid hemorrhage, the patient showed right hemiparesis and total aphasia, and skull radiography revealed that the migrated coil had moved into the M1 portion of the left middle cerebral artery. Craniotomy was performed to retrieve the coil and clip the aneurysm neck. However, the migrated coil could not be retrieved because of adhesion to the arterial wall. Delayed coil migration is very rare in the chronic phase.

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

Sudden and Unexpected Death from Pituitary Tumor Apoplexy

Pituitary tumor apoplexy refers to a clinical syndrome precipitated by the expansion of a pituitary adenoma by hemorrhage or infarction. Individuals may present with myriad signs, including sudden onset of severe headache, visual changes, altered mental status, cranial nerve palsies, and hormonal dysfunction. This disorder constitutes a medical emergency and warrants an expedited evaluation, diagnosis, and treatment to prevent the potential sequelae of permanent visual loss, endocrine abnormalities, or death. We report a case of sudden death from undiagnosed pituitary tumor apoplexy. The decedent was evaluated by medical personnel on three occasions in the week prior to her death for severe headache, nausea, vomiting, and photophobia. Postmortem examination demonstrated a hemorrhagic infarction of a pituitary adenoma with necrosis and expansion out of the sella turcica. The recognition of and treatment for a patient with pituitary tumor apoplexy requires a rapid multidisciplinary effort. Failure of prompt diagnosis may be fatal and require a medico-legal death investigation for sudden and unexpected death.

Cervical Spine Dural Arteriovenous Fistula With Coexisting Spinal Radiculopial Artery Aneurysm Presenting as Subarachnoid Hemorrhage

We present a patient with a cervical spine dural arteriovenous fistula associated with a radiculopial artery aneurysm at the same vertebral level presenting with subarachnoid hemorrhage. A 45-year-old Native American man presented with sudden-onset severe headache, lethargy, and right hemiparesis. Computed tomography (CT) of the head showed subarachnoid hemorrhage and hydrocephalus. A subsequent CT of the neck showed an anterior spinal subdural hematoma from C2 to C4 causing mild cord compression. Carotid and vertebral angiography failed to demonstrate an intracranial aneurysm, but showed a spinal dural arteriovenous fistula originating from the right vertebral artery at the C5 neuroforamen. The severity of the patient's symptoms, atypical for rupture of a dural arteriovenous fistula, prompted more thorough angiographic evaluation. Thus, injection of the right thyrocervical trunk was performed, demonstrating a 4-mm spinal radiculopial artery aneurysm. Following ventriculostomy, a hemilaminectomy from C4 to C7 was performed with disconnection of the fistula from its drainage system. Subsequent resection of the aneurysm, which was determined to be the cause of the hemorrhage, was accomplished. The patient improved neurologically and was discharged to rehabilitation. Spinal cord aneurysms from a separate vascular distribution may coexist with spinal dural arteriovenous fistulas. In the setting of spinal hemorrhage, especially in situations with an atypical clinical presentation, comprehensive imaging is indicated to rule out such lesions.

Extensive central nervous system involvement in Merkel cell carcinoma: a case report and review of the literature

IntroductionMerkel cell carcinoma is a rare malignant cutaneous neoplasm that is locally invasive and frequently metastasizes to lymph nodes, liver, lungs, bone and brain. The incidence of Merkel cell carcinoma has increased in the past three decades.Case presentationA 65-year-old Caucasian man presented with a sudden onset of severe headache and a three-month history of balance disturbance. Magnetic resonance imaging revealed a large meningeal metastasis. The radiologic workup showed retroperitoneal and inguinal lymph node metastases. Biopsy of the inguinal lymph nodes showed metastases of Merkel cell carcinoma. Biopsy from three different suspected skin lesions revealed no Merkel cell carcinoma, and the primary site of Merkel cell carcinoma remained unknown. Leptomeningeal metastases, new axillary lymph node metastases, and intraspinal (epidural and intradural) metastases were detected within six, seven and eight months, respectively, from the start of symptoms despite treating the intracranial metastasis with gamma knife and the abdominal metastases with surgical dissection and external radiotherapy. This indicates the aggressive nature of the disease.ConclusionTo the best of our knowledge, this is the first report in the literature of an intracranial meningeal metastasis of Merkel cell carcinoma treated with gamma knife and of intraspinal intradural metastases of Merkel cell carcinoma. Despite good initial response to radiotherapy, recurrence and occurrence of new metastases are common in Merkel cell carcinoma.

Use of the pipeline embolization device for the treatment of recurrent intracranial aneurysm after previous stent-assisted embolization

Aneurysmal subarachnoid haemorrhage remains an important cause of stroke mortality and morbidity. With the advance of endovascular treatment, increasingly more ruptured intracranial aneurysms are being treated with endovascular embolization. Endovascular treatment has a unique form of recurrence and complication, and the recurrence of intracranial aneurysm treated by stent-assisted embolization is a significant challenge. The pipeline embolization device (PED), a dedicated flow-modifying device, has been available in Hong Kong since September 2008. The PED (eV3, Irvine, CA, USA) is a woven wire mesh tube made of 25% platinum and 75% cobalt-nickel alloy; it is designed to provide 30–35% metal coverage of the inner surface of the target vessel with a pore size of 0.02–0.05 mm (approximately three times more than other commonly used intracranial stents). Here, we illustrate the PED treatment of a recurrent intracranial aneurysm after stent-assisted embolization. A 46-year-old man presented with the sudden onset of severe headache; computed tomography of his brain showed diffuse basal cistern subarachnoid haemorrhage. Computed tomographic angiography showed a left internal carotid artery aneurysm (5.4 mm height and 2.9 mm neck). He was treated with endovascular embolization, which was complicated with coil protrusion. Emergency stent (Neuroform3; Boston Scientific, Natick, MA, USA) deployment to avoid further coil dislodgement was undertaken and embolization continued to occlude the aneurysm. On 1-year follow-up angiography, the aneurysm had recurred with a wide neck (3.5 mm height, 3.8 mm neck). After discussing different treatment and management options, the patient decided to undergo treatment with the PED. He was given 75 mg clopidogrel and 160 mg aspirin daily for 5 days before the procedure. Under general anaesthesia and right femoral arterial puncture, a guiding catheter was inserted into the cavernous segment of his left internal carotid artery. A 3-F microcatheter was placed across the neck of the aneurysm under microguidewire guidance. The PED, mounted on a delivery wire and constrained within a sheath, was inserted into the rotating haemostatic valve and introduced into the hub of the microcatheter. Under heparinization, by pushing the delivery wire, the PED was advanced through the whole length of the microcatheter. The PED delivery wire was then held in place while the microcatheter retracted, supplemented by delivery wire rotation, to initiate deployment. Mainly through forward pressure on the delivery wire, the device was further deployed to create a tight mesh. Finally, the microcatheter was advanced to compress the proximal end of the PED, and the delivery wire was retracted. Check angiography showed aneurysm contrast stasis and layering within the dependent portion, forming an eclipse sign on the subtracted venous phase image. The patient did not experience new focal neurological deficit after the procedure. He was prescribed 75 mg clopidogrel and 160 mg aspirin daily for 3 months and 160 mg aspirin for another 3 months. On 3-month follow up angiography, the patent aneurysm sac had decreased in size. The aneurysm is expected to gradually thrombose after 6 to 12 months. In conclusion, the availability of the PED enhanced the set of tools available for the endovascular treatment of recurrent wide-necked intracranial aneurysm.