Headache in children - ED management

Headache is a rare chief complaint in children but more frequently seen in adolescents. ED evaluation should answer the following the questions:

• Primary or Secondary Headache?
• Needs Investigations or Imaging?
• Need for follow up with GP?

Primary headaches (Disabling): Migraine, Tension Headache, Cluster headache (and other trigeminal autonomic cephalalgias); and other primary headaches (such as cough or exertional headache). They are thought to be due to a primary malfunction of neurones. Primary headaches are typically self-limited.

Secondary headaches (a/w Morbidity and Mortality): May show up symptomats of some underlying pathology, e.g. from raised intracranial pressure and space-occupying lesions. Headaches due to a SOL are worse when lying down and morning vomiting is characteristic. There is often a change in mood, personality or educational performance. Causes of secondary headache include brain tumors, vascular malformations, and intracranial abscesses; craniofacial problems, such as sinusitis, dental abscesses, or otitis; systemic disorders, such as lupus cerebritis; and exposure to toxic substances, such as carbon monoxide, lead, or cocaine. Other features suggestive of a space-occupying lesion are i.e Red Flags for Headache:

• Visual field defects – from lesions pressing on the optic pathways, e.g. craniopharyngioma (a pituitary tumour)
• Cranial nerve abnormalities causing diplopia, new-onset squint or facial nerve palsy. Abducens nerve has a long intracranial course and is often affected when there is raised pressure, resulting in a squint with diplopia and inability to abduct the eye beyond the midline. It is a false localising sign. Other nerves are affected depending on the site of lesion, e.g. pontine lesions may affect the VIIth (facial) cranial nerve and cause a facial nerve palsy.
• Abnormal gait (Cerebellar Lesions)
• Torticollis 
• Bradycardia
• Confusion, Seizures
• Growth failure, e.g. craniopharyngioma or hypothalamic lesion
• Papilloedema 
• Cranial bruits – may be heard in arteriovenous malformations 
• Recent change in personality, behaviour or educational performance
• Headache that wakes up a child (different from headache on awakening, not uncommon in migraine)

Headache coinciding with the onset of fever suggests inflammation - sinusitis, pharyngitis, otitis, or meningitis), or may be associated with a more general viral syndrome. The severity of a headache is not helpful to determine the cause. Patients with tension headaches can com- plain of terrible pain, whereas a child with a brain tumor may complain of mild to moderate pain. Nonetheless, complaints of very intense pain should be taken seriously and assessed in context with other historical elements.

The most common causes of headache in chidren are viral and respiratory illnesses and migraneous headaches. A migraine that lasts >72 hours is known as status migrainosus. 

• The mainstay of management is a thorough history and examination. Imaging is unnecessary in the absence of any Red Flag features.
• Among children with intracranial diseases, most are unable to indicate the location of the pain or had an occipital headache. 
• Positional preferences --> space- occupying lesions
• Abdominal pain, nausea, or vomiting--> May be seen in migraine 
• Cluster headaches can be associated with multiple ipsilateral symptoms
• Headache with effortless vomiting but no GI complaints --> suggests elevated ICP
• Family history is commonly seen in migraneous headaches

Examination findings may be normal even if the history suggests a secondary headache. A careful neurologic examination with attention to cranial nerves, gait, strength, and mental status is essential to exclude secondary headache. There is a very low incidence of positive findings on neuroimaging studies in children with headache who have normal findings on physical examination.

Imaging CT or MRI - NCCT is sufficent for most cases that require imaging. CT with contrast is needed when you suspect brain abscess but a normal head CT does not exclude an intracranial mass because the posterior fossa is not well visualized. The posterior fossa is the most common location of brain tumors in children, and MRI of the brain provides better visualization of the posterior fossa. MRA/MRV are useful when vascular malformations or dural sinus thrombosis is suspected. 

Treatment

Do not use narcotics for primary headaches. Long-term use of narcotics can change the pain-modulatory system leading to more intense pain. 

Options: 

• Primary Headaches - Fluid bolus/NSAIDs, Stemetil or Metoclopermide. Metocloperamide and Stemetil can cause extrapyramidal reactions, which are relieved by diphenhydramin, Triptans High Flow Oxygen can also be used to treate Cluster HA.  
• Secondary Headaches need symtom control with Analgesics and further evaluation. 

Take Home:

The mainstay of management is a thorough history and examination. Imaging is unnecessary in the absence of any Red Flag features.

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

The Intractable Migraneous Headache

Migraine headaches results from dysfunction of brainstem pathways that normally modulate sensory input, with disordered activity of blood vessels. This leads to neurogenic inflammation in pain-sensitive arteries, the dura, and meningeal tissues, and promotes local vasodilatation. Medications such as sumatriptan and ergot derivatives cause vasoconstriction and relieve the symptoms. These triggers stimulate trigeminovascular axons causing pain and the release of vasoactive neuropeptides from perivascular axons. 

Clinical Presentation

• Headache that lasts from 4 to 72 hours
• Aggravation by routine physical activity
• Classically unilateral and pulsating (May not be unilateral)
• a/w Nausea, vomiting, and photophobia or photophobia 
• May have Scalp Tenderness 
• Aura (most common are visual auras with flashes of lights)

Key Q - Is your headache similar to your usual migraine headaches? If the news is no, then a different cause should be suspected. 

Treatment Options for Migraine

• Acetaminophen - Patients with diagnosed migraine often try paracetamol before arriving to the EDs. There is no harm in adding Paracetamol to routine migraine therapy.
• Fluids - Dehydration is a known trigger of migraine. Persistent nausea and vomiting further exacerbates the migraine. Adequate hydration might improve patient malaise and help those who are dehydrated.
• Anti-emetics - Parenteral metoclopramide, chlorpromazine, and prochlorperazine (Stemetil) all have demonstrated efficacy in randomized trials as monotherapy for acute migraine. Antiemetic medications are efficacious and are recommended for acute migraine in the ED. To reduce the risk of akathisia, diphenhydramine should be included. (Diphenhydramine does not prevent Metoclopramide induced dystonia)
• Oxygen - "High-flow" oxygen has been studied in migraine headaches. When compared with placebo, oxygen used for 15 min was more effective in pain relief with no significant adverse events.
• Steroids - Steroids prevent the lingering of attacks and recurrence as well. Everyone with a migraine attack should receive dexamethasone 10mg IV/IM or a 3 day course of presdqisolone unless there is an obvious contraindication. 
• NSAIDs - NSAIDs are effective in treating acute migraine. Ketorolac is a potent pain killer which often works for migraine.

• Triptans - Evidence suggests that SC delivery is fastest and most effective route. Common side effects include injection site reactions, dizziness, and paresthesias. Triptans are contraindicated in cardiovascular disease, pregnancy, basilar migraines, Prinzmetal angina, and ischemic stroke, and with the use of ergotamines within the previous 24 hours. Studies have also suggested that triptan therapy is less effective in patients with prolonged and severe migraine. Triptans are best reserved for patients who present within 1-2 hours of headache. Given the side effect profile, lack of efficacy in severe migraine, and relative contraindications, triptan use in the ED is of limited value. 
• Butyrophenones - (haloperidol and droperidol). RCTs have demonstrated efficacy of haloperidol and droperidol mono therapy. However, these drugs have been associated with frequent side effects (somnolence, akathisia, anxiety) and also prolong QTc interval. These are generally reserved for rescue therapy in refractory migraine. 
• Ergot Alkaloids - Dihydroergotamine (DHE), a 5-HT_1B/1D serotonin receptor agonist which highly effective in relieving headaches. However, DHE causes vomiting in a significant proportion of patients. Patients therefore should be pretreated with an antiemetic such as metoclopramide or prochlorperazine.
• Opioids - Use opioids only as the last sort for refractory headache. When compared with NSAIDs, DHE, and antiemetic medications, opioids are less effective for migraine. The frequent use of opioids in chronic and recurrent headache conditions may lead to adverse effects and may even exacerbate headaches.
• Propofol - Evidence for using propofol is not robust but it is again something to consider when everything else fails. Follow the procedural sedation protocol and doe as 10-20 mg IVP every 3-4 minutes up to 1 mg/kg. Our aim is mild sedation, not apnea.
• Magnesium - Magnesium is ideally used for refractory migraine, migraine patients with true aura, those with hypoMg. Administer 2 g IV Mg over 20min. Evidence for the use of Migraine is still conflicting though. 

• Sphenopalatine Ganglion Block

Bottomline: It is reasonable to start with fluids/O2, Metoclopramide. Do not forget to add steroids. Add Acetaminophen/NSAIDs if symptoms persist. Other  potential options (Ergot Alkaloids/Mg/Propofol, Ganglion Blocks) are all based on your comfort and local protocols. Opioids are your last option. 

References:

• Singhal AB, Maas MB, Goldstein JN, et al. High-flow oxygen therapy for treatment of acute migraine: A randomized crossover trial. Cephalalgia. 2016 May 20.
• Balbin JE, Nerenberg R, Baratloo A, Friedman BW. Intravenous fluids for migraine: a post hoc analysis of clinical trial data. Am J Emerg Med. 2016 Apr;34(4):713-6.
• Bigal ME, Bordini CA, Tepper SJ, Speciali JG. Intravenous magnesium sulphate in the acute treatment of migraine without aura and migraine with aura. A randomized, double-blind, placebo-controlled study. Cephalalgia. 2002 Jun;22(5):345-53.
• Colman I, Friedman BW, Brown MD, Innes GD, Grafstein E, Roberts TE, Rowe BH. Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomised controlled trials for preventing recurrence. BMJ. 2008 Jun 14;336(7657):1359-61.
• Colman I, Rothney A, Wright SC, Zilkalns B, Rowe BH. Use of narcotic analgesics in the emergency department treatment of migraine headache. Neurology. 2004 May 25;62(10):1695-700.
• Friedman BW, Bender B, Davitt M, Solorzano C, Paternoster J, Esses D, Bijur P, Gallagher EJ. A randomized trial of diphenhydramine as prophylaxis against metoclopramide-induced akathisia in nauseated emergency department patients. Ann Emerg Med. 2009 Mar;53(3):379-85.
• Friedman BW, Greenwald P, Bania TC, Esses D, Hochberg M, Solorzano C, Corbo J, Chu J, Chew E, Cheung P, Fearon S, Paternoster J, Baccellieri A, Clark S, Bijur PE, Lipton RB, Gallagher EJ. Randomized trial of IV dexamethasone for acute migraine in the emergency department. Neurology. 2007 Nov
• Regan LA, Hoffman RS, Nelson LS. Slower infusion of metoclopramide decreases the rate of akathisia. Am J Emerg Med. 2009 May;27(4):475-80.
• Soleimanpour H, Taheraghdam A, Ghafouri RR, Taghizadieh A, Marjany K, Soleimanpour M. Improvement of refractory migraine headache by propofol: case series. Int J Emerg Med. 2012 May 15;5(1):19.
• Taggart E, Doran S, Kokotillo A, Campbell S, Villa-Roel C, Rowe BH. Ketorolac in the treatment of acute migraine: a systematic review. Headache. 2013 Feb;53(2):277-87.

Posterior Reversible Encephalopathy Syndrome (PRES)

Introduction

Posterior Reversible Encephalopathy syndrome PRES (also known as reversible posterior leukoencephalopathy syndrome) is a constellation of clinical and radiological findings which presents with rapid onset headache, seizures, altered consciousness, and visual disturbances. 

It strongly associated with with renal disease, vascular and autoimmune diseases, immunosuppressive medications, and organ transplantation. Nearly 3/4 patients with PRES are hypertensive, but others may have normal or only mildly elevated blood pressure.

Pathophysiology

Failure of Cerebral Autoregualtion, endothelial injury, disruption of blood brain barrier leading to Vasogenic edema is a proposed mechanism. However, the exact pathophysiology remains unclear. 

Diagnosis 

Prompt recognition of PRES is important to prevent permanent damage due to ongoing cerebral ischemia. Having a high index of suspicion is important. PRES must be added to our routine list of differentials of Posterior Circulation Stroke, SAH, Cerebral Venous Thrombosis. Focal neurologic deficits are uncommon in PRES and Seizures are the most common presentation. 

It is reasonable to start with CT Head in the Emergency Department to rule out other CNS Catastrophes. However, MRI is a better tool to diagnose PRES. Magnetic Resonance Imaging recordings showing white matter abnormalities without infarction. Classical MRI findings of vasogenic edema involving bilateral parietal-occipital lobes. 

PRES appears to be a misnomer as the syndrome is not always reversible, and it may not be localised to either the white matter or the posterior regions of the brain. Atypical features— including hemorrhage, asymmetrical changes, isolated involvement of the frontal lobes, and cortical lesions are common.

Management

• Rapid withdrawal of the trigger (Eclampsia, Drugs)
• Prevent Seizures
• Aggressive blood pressure management 

Take Home:

• PRES should be considered in patients who present with seizures, altered consciousness, visual disturbances, or headache, particularly with acute hypertension.
• PRES has been associated with chronic and acute kidney disease, solid organ transplantation, and use of immunosuppressive drugs.
• Typical MRI findings include reversible, symmetrical, posterior subcortical vasogenic edema.
• If recognized and treated promptly, the rapid-onset symptoms and radiologic features usually fully resolve within days to weeks.

References:

• Hinchey J, Chaves C, Appignani B, et al.  A reversible posterior leukoencephalopathy syndrome. N Engl J Med. 1996;334(8):494-500
• Hobson, E. V., Craven, I., & Blank, S. C. (2012). Posterior Reversible Encephalopathy Syndrome: A Truly Treatable Neurologic Illness. Peritoneal Dialysis International : Journal of the International Society for Peritoneal Dialysis, 32(6), 590–594. http://doi.org/10.3747/pdi.2012.00152
• Fugate, J. E., Claassen, D. O., Cloft, H. J., Kallmes, D. F., Kozak, O. S., & Rabinstein, A. A. (2010). Posterior Reversible Encephalopathy Syndrome: Associated Clinical and Radiologic Findings. Mayo Clinic Proceedings, 85(5), 427–432. http://doi.org/10.4065/mcp.2009.0590
• https://radiopaedia.org/articles/posterior-reversible-encephalopathy-syndrome-1

Author:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

                    

Lets talk about Headache in Adults!

From the Desk of Sagar Galwankar, MBBS, DNB, FACEE, MPH, Diplomat. ABEM, FRCP

• Headache is one of the common symptoms when patients come to the ED.
• Headache can be a Presenting Complaint when the patient arrives. "I got a Headache" and sometimes when patients are being evaluated at bedside for some other symptoms they can add the complaint "..and I also have an Headache"
• History takes paramount importance when a patient complains of Headache as a Primary Symptoms or a Co-Symptom as a part of a Series of Complaints.
• Always evaluate Headache keeping a 360 Degree approach. 
• Always address Headache. via your Thought process, History taking and Clinical Exam.

Vital Signs take a Lot of Importance and ask for them as you immediately prescribe pain medications to treat the PAIN.

Temperature, Pulse, Blood Pressure, Respiration, Pulse Ox, and Bedside Glucose are key stat Bedside Parameters which guide you to a story. Order an EKG Stat and read it.

Remember:  Gender does matter ! Pregnant Females & Females who do not know they are pregnant can come to the ED. Being Pregnant Changes the way you will evaluate these patients. Having abdominal pain, Hyperemesis gravidarum vaginal bleed can come with an headache and evaluating for abdominal emergencies and Ruling out Ectopic Pregnancy at the same time deciding about CT Head and Headache work up is a complex issue. They can also have HELP Syndrome or Eclampsia also can start with Headache.

• Age is crucial before Young Female with Headache and Cold and Cough is different from a 50 Year old with Headache and Blurry Vision.
• History taking should include: When did it start, how severe is it from a scale of 1-10, any other symptoms of Dizziness, Focal weakness, Gen weakness, Vision changes, neck pain, Syncope Seizures, Nausea, Vomiting Diarrhea, Chest Pain, SOB, Neck Pain/Stiffness, Dizziness, Vertigo have to be ruled in or ruled out.
• Past History of DM HTN CAD CVA Cancer HIV Hep B Hep C are important. Is patient on anticoagulants also is key history point.

Some Cluster approaches are:

• Fever, Tachycardia, Headache, Neck Pain: Here Headache can be as simple as a Viral Fever or as severe as early meningitis or even a URI if Cold Cough Sinus Tenderness are present.
• Headache could be a early Bleed (Subarachanoid) or even a CVA when patients have vasculitis, Bleeding disorders, Hypertension , DM.
• Headache can be due to Glaucoma or due to Otitis Media or even early Temporal arteritis.
• Headache can be segmental along a nerve for a early developing Zoster.
• Syncope, Fall, Seizure, Loss of Sensorium, Altered Mental Status with Headache all can be indicating a worse diagnosis  than how the Headache presented.
• Post Ictal Phase can present as Headache.
• Another confounder: MI/ACS can also present as an Headache so can arrhythmia or PE. So EKG Trop are Important.

There have been cases who have presented as an Headache and when you do labs there has been Low Hemoglobin and patient has a GI Bleed and the Immediate anemia has caused an headache.

Be very particular and alert when Patients says "Headache is what brought me to the ED". On the other hand there is tons of Literature of approach to Migraine in ED.

Its very important that you read the literature as there are various combinations of medications used to break the migraine. When a patient says "I have a Migraine attack" you still have to approach it as an HEADACHE.

Sometimes patients present with Neck Pain and Stiffness and we disregard it as "Slept on wrong side or Neck sprain". Evaluating for Cord Compression and keeping Dissection and SAH as a differential is equally important as much as ACS/MI or even a Retro pharyngeal abscess in a URI patient.

What it comes down to is:

• Vitals, Past History, Med List, Clinical Co-Symptoms, History of Complaint, Detail Clinical Exam to include total undressing of patient Neuro Vascular HFN HEENT Exam and Lab Results is crucial.
• Overdose and Drug abuse are important historical points which can indicate Cocaine abuse or even overdose unintentionally on paracetamol ibuprofen trying to self medicate with Over Counter Medications.
• CBC, LFT RFT Trop EKG UA Tox Screen and CT / MRI ESR are a part of the work up in ED.
• In a patients with Hypoglycemia or Hyperglycemia Ketoacidosis versus Toxicity v/s sepsis or infection has to be kept at back of mind.
• In HTN emergency headache can be because of raised BP and Raised BP can cause headache. Treating both is important but also is important ruling out cardiac pathologies a CT Head and look for Posterior Reversible Encephalopathy Syndrome.
• I have also read reports where patients were on anticoagulants and had neck pain and when MRI was done it has Hemomyelia into the spinal cord.
• There have been cases alcoholism where patients wake up with headache in ED but they dont know that Methanol or Toxic alcohols were also drunk and they have an Headache.
• Being very aggressive to rule out meningitis and SAH and using Spinal Taps with Clinical Co relation is important in the ED.
• Patients often return post spinal tap with headache and at this time Blood Patch becomes a choice after you have ruled out any other cause or pathology.
• Patients also have headache after Nitro given for Chest Pain.
• Fever can exacerbate Headache and Hunger can do that too.
• A TIA can be presenting as Headache being one of the Co-Symptoms.

Documentation:

• Always Document in detail the history the clinical exam and the plan for ordering tests and meds and chart your thought process and notes as you reevaluate the patient.
• That helps and maintains the continuum of care at the same time maintaining standards of care.
• Discharge is a crucial part. Here too Educating the patient and giving return instructions is key.

Do not Disregard or Less regard HEADACHE. Its a Part of the PAIN PATHOLOGIES which can cause PAIN if ignored.

Patients have Pain , treat it first but work it up and decipher the cause then treat the cause....  FOR THE PATIENTS !

Author: 

                                                   

Dr. Sagar Galwankar  

MBBS, DNB, FACEE (INDIA), MPH, Dip. ABEM (USA), FRCP (UK)

Chief Academic Officer of the INDO-US Emergency and Trauma Collaborative 

Assistant Professor 

Department of Emergency Medicine 

University of Florida, Jacksonville 

(Follow Dr. Galwankar on Twitter @SagarGalwankar)

Pituitary Apoplexy

Introduction

Pituitary apoplexy (apoplexy: a sudden neurologic impairment) is a neurosurgical and endocrine emergency that constitutes a clinical syndrome caused by the rapid expansion of a pituitary adenoma secondary to ischemia and /or intratumoral hemorrhage which causes compression of the cavernous sinus, chasm,  optic nerves and hormonal imbalance. The diagnosis is often delayed as approximately ~80% of these patients will have no previous history of a pituitary problem. Pituitary apoplexy may also occur in non-adenomatous or even the normal pituitary gland especially during pregnancy. 

Most cases of pituitary apoplexy present in the fifth or sixth decade with a slight male preponderance and the most common presenting symptoms is sudden severe headache, which is frequently retro-orbital in location.

Pathophysiology

Because of the rich and the complex vascular system pituitary adenomas have a greater propensity to bleed in contrast to other brain tumours. The pituitary gland is located in a bony cavity called the sella turcica covered by the diaphragma sellae superiorly. It lies in close proximity with hypothalamus, optic chiasma and the cavernous sinus. 

Possible reasons for a hemmorhage could be:

• Rapid tumor growth that outstrips the arterial supply
• Constriction of the thin vascular network and finally ischemia, necrosis and haemorrhage
• Aggressive and invasive tumoral behaviour and hemorrhage 

Clinical Presentation

• Headache (present in 95% of the cases)
• Nausea and Vomiting
• Diplopia
• Changes in visual fields
• Ptosis

                            

Risk Factors

• Hypertension
• Head Trauma
• Major Surgery (CABG)
• Coagulopathy
• Dynamic testing of pituitary gland

How is pituitary apoplexy different from Sheehan Syndrome?

Sheehan syndrome refers to pituitary apoplexy of a nontumorous gland, presumably due to postpartum arterial spasm of arterioles supplying the anterior pituitary and its stalk. Normally, the pituitary gland hypertrophies in pregnancy and this hypertrophy, combined with locally released factors, mediates vascular spasm and renders the pituitary more susceptible to infarction from compromised blood flow. It typically presents years later or as inability to lactate after delivery due to prolactin deficiency and amenorrhea due to gonadotrophin deficiency. Also, after delivery, pubic hair fail to grow, and waxy skin depigmentation develops. Signs of hypothyroidism and hypoadrenalism may develop.

Differential Diagnosis 

• Subarachnoid haemorrhage
• Meningitis
• Hypertensive encephalopathy
• Brain abscess 
• Cavernous sinus thrombosis
• Intracerebral hematomas
• Ophthalmoplegic migraine

Diagnosis and Management

MRI is the investigation of choice in a patient with suspected pituitary apoplexy. However, if a MRI scan is not possible, a dedicated pituitary CT is another alternative. 

Medical treatment consists of the following:

• IV Fluids and administer high-dose corticosteroids. Corticotropic deficiency is present in most patients with pituitary apoplexy and it may be life-threatening. Hydrocortisone can be administered as 100–200 mg intravenous bolus followed either by continuous intravenous infusion of 2-4 mg/hour. 
• Immediately evaluate electrolytes, glucose, and pituitary hormones (random serum cortisol, TSH, free T4, prolactin, IGF-1, LH, FSH)
• Administer appropriate endocrinologic replacement therapy alone or combined with transsphenoidal surgical decompression.
  
  
  
  
  Clinically, the most important endocrine dysfunction is adrenocorticotroph hormone (ACTH) deficiency. Resolution of hypersecretory states have been reported following apoplexy, also described as ‘auto-hypophysectomy’. 
  

  
  

Management is controversial in terms of surgical intervention as some experts advocate early surgical decompression in all patients, whereas others adopt a more conservative approach for selected patients (without visual acuity or field defects and with normal consciousness). Outcome is similar with either conservative management or surgery in more recent studies. Long term with follow-up with hormonal evaluation is required to replace the deficient hormones.

Take Home:

• Pituitary Apoplexy is a life threatening cause of acute onset headache
• Maintain a high index of suspicion in any patient with acute headache and a negative conventional CT scan
• Steroid replacement and maintaining the hemodynamic stability for the cornerstone of management

References:

1. Ranabir, Salam, and Manash P. Baruah. “Pituitary Apoplexy.” Indian Journal of Endocrinology and Metabolism 15.Suppl3 (2011): S188–S196. PMC. Web. 17 Apr. 2016.
2. Rajasekaran, S., Vanderpump, M., Baldeweg, S. et al. (2011) UK guidelines for the management of pituitary apoplexy. Clinical Endocrinology, 74, 9-20. 
3. Solomon, Adriana Elena, et al. "Pituitary apoplexy: clinical features, management and outcome. Clinical study and review of the literature." Romanian Neurosurgery 22.1 (2015): 69-77.