Juvenile Idiopathic Stabbing Headache

We report on 83 juvenile patients with idiopathic stabbing headache, subjectively perceived as lasting from a fraction of a second to a few minutes. This sample was selected from among 2543 outpatients referred because of recurrent headache to the Paediatric Neurology Services of Ferrara and Padua (Italy). Other painful syndromes were excluded by clinical examination and appropriate tests Idiopathic stabbing headache in the pediatric age group contrary to the adult form, is usually not associated with other primary headache syndromes. We suggest that this clinical picture should be more clearly defined in the future, in order to better understand its relationships with other primary headaches.     

Stabbing Headache as the Presenting Manifestation of Intracranial Meningioma: A Report of Two Patients

Stabbing headache may occur as a primary headache disorder, may accompany other primary headaches, or, in rare instances, may be associated with secondary headache syndromes. We report two patients with intracranial meningioma in whom stabbing headache was the heralding symptom. Headache remitted promptly following surgical resection. These cases stress the importance of excluding underlying pathology in patients presenting with new-onset stabbing headache.     

The Relationship Between Idiopathic Intracranial Hypertension and Obesity

Objective.— Idiopathic intracranial hypertension (IIH) is usually considered to result from deficient intracranial absorption of cerebrospinal fluid, but has also been suggested to be caused by decreased cranial venous flow because of increased intrathoracic pressure resulting from intra‐abdominal obesity. To test this hypothesis, cerebrospinal fluid pressure (Pcsf), extracranial venous pressure (Pvf), intracranial venous pressure, and body mass index (BMI) were studied in patients with IIH with papilledema compared with patients with chronic tension‐type headache (CTTH). Design and Subjects.— The Pcsf and the pressures in frontal veins without (Pvf) and with bilateral compression of the supraorbital branch of the frontal veins and the superficial facial veins (Pvfc), the latter considered to be about equal to Pvfc, were studied in 10 consecutive patients with IIH with papilledema. Ten consecutive CTTH patients were used for controls. Orbital phlebography was performed to confirm that the compression of facial veins other than the frontal veins resulted in adequate communication between the frontal vein used for the studies and the cavernous sinus. Results.— Cerebrospinal fluid pressure was between 200 and 250 mm water in 5 of the CTTH patients and above 350 mm water in all IIH patients. Body mass index was >25 in all CTTH patients and similar in the 2 groups. Cerebrospinal fluid pressure was similar to Pvfc in all 10 CTTH patients but significantly greater in 6 of the 10 IIH patients. Pvf was similar in the 2 groups and related to BMI. Conclusions.— Chronic tension‐type headache patients may be prone to have Pcsf > 200 mm water and BMI > 25. Papilledema because of intracranial hypertension occurred in the present study at Pcsf > 350 mm water. The findings of Pvfc and Pcsf being similar in all CTTH patients support the suggestion that the techniques used for measuring intracranial venous pressure are adequate. The findings of similar BMI in the CTTH and the IIH patients who differed significantly as to Pcsf refute the hypothesis that obesity precedes, and is the cause of, intracranial hypertension in IIH. The difference between Pcsf and Pvfc in 6 of the IIH patients also does not support such a hypothesis but may indicate that IIH is due to deficient intracranial cerebrospinal fluid absorption. Since a relationship between intracranial hypertension and obesity is established and obesity is not found to cause intracranial hypertension in IIH, intracranial hypertension may be suggested to be the primary cause of weight increase in IIH. Obesity, however, may secondarily increase the preexistent IIH.     

Idiopathic Intracranial Hypertension and Seventh Nerve Palsy

Patients with idiopathic intracranial hypertension may occasionally present with coexisting lower motor neuron facial weakness. This study reviews a 6-year experience at Mayo Clinic. The aim of this study was to determine the possible association of idiopathic intracranial hypertension and facial paresis. Two cases were identified. Both fulfilled the modified Dandy's diagnostic criteria for idiopathic intracranial hypertension. Treatment consisted of steroids in one, and emergent optic nerve sheath fenestration in the other. The cranial nerve palsies resolved in both cases.     

Primary and Secondary Stabbing Headache

Eight out of the 33 cases of primary stabbing headache seen in a general neurology clinic (40% have headache as their chief complaint) in the last 3.5 years are presented. The epidemiology, association with other primary headache disorders, secondary associations, testing, and treatment of primary stabbing headache are reviewed.     

Utility of Point-of-Care Ultrasound in the Diagnosis of Idiopathic Intracranial Hypertension in the Emergency Department

BackgroundEmergency physicians are frequently required to identify and triage patients with increased intracranial pressure (ICP). Idiopathic intracranial hypertension (IIH) is a possible cause that must be considered. Its prognosis depends on prompt recognition and treatment, and progression of the disease can lead to permanent vision loss and considerable morbidity. Point-of-care ultrasound can rapidly identify elevated ICP. Measurements of the optic nerve sheath diameter (ONSD) and optic disc elevation (ODE) can act as surrogates for ICP.Case SeriesWe describe five cases in which ultrasound was used to identify increased ICP and aid clinical decision-making. In several of the cases, ultrasound was used to confirm a suspicion for IIH and initiate therapy while awaiting the results of a more time-consuming and technically challenging test, such as lumbar puncture or optical coherence tomography. One of the patients was pregnant, and sonographic evidence of elevated ICP helped avoid exposing the patient to unnecessary radiation.Why Should an Emergency Physician Be Aware of This?Ultrasound is a quick and versatile tool for screening patients with neurologic symptoms, and when integrated into the proper clinical context, can reduce the use of more invasive tests. It can be particularly useful in patients with pathology that may not show abnormalities on computed tomography scan or in whom lumbar puncture is technically difficult, making patients at risk for IIH well-suited to examination by ultrasound. We use a cutoff of 5 mm for ONSD and 0.6 mm for ODE, though there are no universally agreed on cutoff values.     

Idiopathic Intracranial Hypertension and Hemophilia A

OBJECTIVE: A patient with hemophilia A and long-standing recurrent symptoms of idiopathic intracranial hypertension is described. During his relapses, he experienced headache, and attention and language disturbance, but no visual symptoms. BACKGROUND: Hemophilia A is a rare inherited coagulation disorder secondary to factor VIII deficiency. Idiopathic intracranial hypertension has been reported in association with prothrombotic conditions and iron deficiency anemia, but not in patients with hemophilia A. Recurrent or chronic headache is not a typical symptom of hemophilia, but headache is a presenting sign of intracranial bleed in persons with hemophilia. METHODS: Medical history review, clinical neurologic examination, brain magnetic resonance imaging, computed head tomography, and electroencephalogram were performed. RESULTS: Neurologic examination revealed bilateral papilledema during relapses of idiopathic intracranial hypertension. Multiple lumbar punctures preceded by the intravenous administration of factor VIII early in the course of the illness confirmed the presence of elevated cerebrospinal fluid pressures and absence of subarachnoid blood. He had no complications from lumbar punctures. Initial electroencephalograms showed background slowing but later normalized. Magnetic resonance imaging of the brain and computerized tomography of the head were normal. Relapses of idiopathic intracranial hypertension were eventually controlled with the administration of acetazolamide. CONCLUSION: Idiopathic intracranial hypertension may develop in patients with hemophilia A in the absence of visual symptoms. Therapeutic and diagnostic lumbar punctures were safe to perform on this patient, following the administration of factor VIII.     

Idiopathic Intracranial Hypertension in a Young Child Without Visual Symptoms or Signs

A 7-year-old boy presented with a 4-week history of daily headache. His parents reported that he was unable to attend school the week prior to presentation. Intermittent nausea without vomiting was reported, but no blurred vision, photophobia, or diplopia were described. There was no history of trauma or recent systemic illness. The physical examination showed mild neck discomfort, no papilledema, and normal cranial nerve, motor and sensory functioning. Both a CT scan of the sinuses and an MRI of the brain were normal. Although the opening pressure was elevated, the cerebrospinal fluid was also normal. In previous accounts idiopathic intracranial hypertension in children, concomitant papilledema, visual symptoms and/or palsy of the sixth cranial nerve are described. This case demonstrates that idiopathic intracranial hypertension in a young child can present as a daily headache without any visual symptoms or signs.     

Cytokines and Chemokines in Idiopathic Intracranial Hypertension

Background.— The pathogenesis of idiopathic intracranial hypertension (IIH) remains unclear and as such it remains a diagnosis of exclusion.
Objectives.— To identify cerebrospinal fluid (CSF) and serum cytokine and chemokine profiles associated with IIH.
Method.— Semiquantitative assessment with cytokine antibody arrays was used to detect the relative expression of 42 different cytokines and chemokines in the CSF and serum of 8 IIH patients and 8 controls. Subsequently, quantitative assay with enzyme linked immunosorbent assay was performed for chemokine CCL2, interleukin-1 alpha (IL-1α), and leptin.
Results.— Cytokine antibody array showed elevated levels of CCL2 in the CSF and CCL7, CCL8, IL-1α, and leptin levels in serum in IIH patients compared with controls. Subsequent quantitative assessment with enzyme linked immunosorbent assay showed significantly elevated CSF CCL2 in IIH patients compared with controls ( P  < .01) but there was no significant difference in leptin and IL-1α levels between the groups.
Conclusion.— This is the first report demonstrating differences in cytokine expression in the serum and CSF in IIH patients compared with controls. Since the pathogenesis of IIH is unclear, the heterogeneity of the cytokine expression reported here may help understand the pathogenesis of this condition.     

A Comparison of Idiopathic Intracranial Hypertension With and Without Papilledema

Objective.— To compare clinical features, visual characteristics, and treatment of idiopathic intracranial hypertension patients with and without papilledema. Background.— Idiopathic intracranial hypertension does not often occur without papilledema. This study estimates the prevalence and compares the clinical characteristics of idiopathic intracranial hypertension patients with and without papilledema. Methods.— We performed a cross‐sectional analysis of all idiopathic intracranial hypertension patients diagnosed at the University of Utah Neuro‐Ophthalmology Unit between 1990 and 2003. Patient records were reviewed for presence of papilledema and other signs, symptoms, and treatment characteristics. Each patient without papilledema was matched to the patient with papilledema who was closest to his/her age and sex. McNemar's and Wilcoxon‐signed rank sum tests were used to compare characteristics between matched pairs. Results.— Among all patients (n = 353), the prevalence of those without papilledema was 5.7% (n = 20). Patients without papilledema reported photopsias (20%), and were found to have spontaneous venous pulsations (75%) and non‐physiologic visual field constriction (20%) more often than did those with papilledema. Mean opening pressure, although above normal, was lower in patients without papilledema (mean = 309 mm cerebrospinal fluid) compared with those with papilledema (mean = 373 mm cerebrospinal fluid, P = .031). Idiopathic intracranial hypertension patients without papilledema had more frequent diagnostic lumbar punctures than did patients with papilledema. Visual acuities and treatment were similar between groups. Conclusions.— The clinical presentation of idiopathic intracranial hypertension without papilledema is only somewhat different from that of idiopathic intracranial hypertension with papilledema. The lower opening pressure in patients without papilledema may explain variations in symptoms and signs between the 2 groups. When there are visual field changes in idiopathic intracranial hypertension without papilledema, non‐physiologic visual loss should be considered.     

Idiopathic intracranial hypertension and postlumbar puncture headache

Idiopathic intracranial hypertension and low cerebrospinal pressure are 2 conditions that are thought to be on opposite ends of the cerebrospinal pressure spectrum. Headache is the prominent component of both conditions. We describe a patient whose evaluation for idiopathic intracranial hypertension resulted in a postlumbar puncture headache. Although not entirely intuitive, we suggest that the 2 conditions can be present in the same patient.     

Cerebellar Tonsillar Herniation After Weight Loss in a Patient With Idiopathic Intracranial Hypertension

( Headache 2010;50:146-148)
Acquired cerebellar tonsillar herniation is a known complication of lumboperitoneal shunt (LPS) for any indication, including idiopathic intracranial hypertension (IIH), also known as pseudotumor cerebri. ¹ While the underlying pathophysiology of IIH remains unknown, increasing body mass index is a clear risk factor for the development of IIH. We describe an obese patient with IIH unresponsive to LPS who developed symptoms of intracranial hypotension and cerebellar tonsillar herniation after bariatric surgery and a 50-kg weight loss.     

Intracranial hypertension and levofloxacin: a case report

This is a case report of a 15-year-old boy who developed benign intracranial hypertension after 3 weeks of levofloxacin intake. The headache, diplopia, and papilledema resolved within a week after levofloxacin was withdrawn. Physicians must be aware that quinolone antibiotics can potentially cause intracranial hypertension.     

Utility of CSF pressure monitoring to identify idiopathic intracranial hypertension without papilledema in patients with chronic daily headache

The aim of the present study was to report on the utility of continuous Pcsf monitoring in establishing the diagnosis of idiopathic intracranial hypertension without papilledema (IIHWOP) in chronic daily headache (CDH) patients. We report a series of patients (n = 10) with refractory headaches and suspected IIHWOP referred to us for continuous Pcsf monitoring between 1991 and 2000. Pcsf was measured via a lumbar catheter and analysed for mean, peak, highest pulse amplitude and abnormal waveforms. A 1-2 day trial of continuous controlled CSF drainage (10 cc/ h) followed Pcsf monitoring. Response to CSF drainage was defined as improvement in headache symptoms. Patients with abnormal waveforms underwent a ventriculoperitoneal (VPS) or lumboperitoneal (LPS) shunt insertion. All patients had normal resting Pcsf (8 +/- 1 mmHg) defined as ICP < 15 mmHg. During sleep, all patients had B-waves and 90% had plateau waves or near plateau waves. All patients underwent either a VPS or LPS procedure. All reported improvement of their headache after surgery. Demonstration of pathological Pcsf patterns by continuous Pcsf monitoring was essential in confirming the diagnosis of IIHWOP, and provided objective evidence to support the decision for shunt surgery. Increased Pcsf was seen mostly during sleep and was intermittent, suggesting that Pcsf elevation may be missed by a single spot-check LP measurement. The similarity between IIHWOP and CDH suggests that continuous Pcsf monitoring in CDH patients may have an important diagnostic role that should be further investigated.