- Email: [email protected]
A Patient With Persistent Headache and Numbness
CASE CHALLENGE
A Patient With Persistent Headache and Numbness Susan Alex, MS, APRN, Susan Chaney, EdD, APRN, and Catherine Hill, DNP, APRN INTRODUCTION
H
eadache is a very common disorder and often can be a presenting symptom for many other neurologic disorders. Due to its commonality, several other serious disorders that have similar presentations can be misdiagnosed or left untreated. A very thorough history and physical can often provide information for correct diagnosis and timely management. CASE PRESENTATION
Ms. AB is a 24-year-old, right-handed, Caucasian female with past medical history of pseudotumor cerebri and migraine, who presented with a 1-week history of intermittent, dull frontal headache. Initially, she was able to manage her headaches with over-thecounter ibuprofen, as needed, and rest. Her migraines had been well controlled for > 1 year, since she started taking zonisamide for pseudotumor cerebri. Two days after the initial headache, she had the “worst headache of her life,” when she presented to a local emergency department (ED). She also had transient visual obscurations, associated numbness on her right side, leg itching, and involuntary movements in her right arm and leg, which her mother described as “seizurelike.” The whole episode lasted for about 15-20 minutes. She denied having any change in level of consciousness, nausea, vomiting, or any focal weakness. She was diagnosed with tension headache and was discharged home on ibuprofen. Her headaches during these episodes were clearly different from her usual frontal headaches. She had not been having any aura with her usual frontal migraines. The following day, she had another seizurelike episode and numbness that spread to both of her legs and to the other arm. She was again evaluated in an ED, where computed tomography (CT) of the head was normal and she was started on leviteracetam and butalbital/acetaminophen/caffeine. She was discharged home with instructions to follow-up www.npjournal.org
with her primary care physician (PCP). The next day, she saw her PCP, who referred her for higher level care. Her past medical history included chronic migraine headache, pseudomotor cerebri, asthma, and menorrhagia since age 16. She was on oral steroids and mometasone furoate inhalation for asthma, zonisamide for pseudomotor cerebri, oral contraceptive pills for menorrhagia and ibuprofen for headaches. Her family history was unremarkable, except for a history of 2 miscarriages for her mother in the first trimester. She was a single, full-time law student, social drinker, had never smoked, and denied any illicit drug use. She denied any fever, chills, chest pain, dizziness, cough, shortness of breath, abdominal pain, nausea, vomiting, urgency, frequency, or dysuria. Her pertinent positive review of systems included headache, transient visual disturbance, numbness, and 2 “seizurelike” episodes. She denied any weakness. PHYSICAL EXAM
Her vital signs were stable and as follows: blood pressure 101/59; pulse 44 beats/min; temperature 36.6 C (97.9 F, temporal artery); respiration 16 breaths/min; saturation of peripheral oxygen 97%; weight 198 lb., 6.6 oz. (90 kg); and body mass index 33.02 kg/m2. At admission, it had been 4 days since her last menstrual period. NEUROLOGIC EXAM
She was awake, alert, oriented to person, place, time, and situation, and was a coherent historian with a good fund of knowledge. Her speech was clear and cranial nerves II-XII were intact. Her sensation was intact and she had 5/5 strength bilaterally (according to the Medical Research Council scale), and no drift. Coordination findings showed finger-to-nose and heel-to-shin intact bilaterally. Reflexes were 2þ throughout. Plantar response showed down-going The Journal for Nurse Practitioners - JNP
e17
toes bilaterally and normal gait. Her cardiac exam showed regular S1and S2 sounds; telemetry patterns with normal sinus rhythm; clear chest, with no wheezing or rales; a soft, nondistended abdomen; and bowel sounds positive in all 4 quadrants. Questions to consider: 1. What initial routine diagnostic tests should be considered? 2. What are the possible differential diagnoses? 3. Based on the information, what is the possible diagnosis?
e18
The Journal for Nurse Practitioners - JNP
4. What are the possible treatment options available? 5. What important patient and family education is required? 6. What is the recommended follow-up for this individual? Think you know answer to these questions? Test yourself and the go to page e29 to read the answers
Volume 12, Issue 1, January 2016
CASE CHALLENGE
A Patient With Persistent Headache and Numbness (continued from page e18)
s. AB was first evaluated in the ED and was transferred to the stroke neurology service for further management. Brain CT without contrast showed no evidence of acute intracranial abnormality and her basic blood work findings were within normal limits. Brain ischemia is often caused by thromboembolism and occlusive arterial disease.1 In some cases, brain ischemia can also be caused by thrombosis of the dural sinuses and cerebral and cerebellar veins.1 From a neurologic standpoint, key findings in Ms. AB’s exam and history included headache, numbness, shaking movements of arms and legs, use of oral contraceptive pills, oral steroid use for asthma, and a family history of 2 miscarriages for her mother. Findings of visual disturbance and numbness can be consistent with signs of migraine, stroke, or seizures. Her complaint of headache, use of oral contraceptives, and family history of 2 miscarriages for her mother could also suggest a possible hypercoagulable state, including venous sinus thrombosis. 1. What initial routine diagnostic tests are to be considered? a. CT of the brain. b. Magnetic resonance imaging (MRI) of the brain. c. Magnetic resonance venography (MRV). d. Electroencephalography (EEG). e. Blood work. CT scan can be used to detect intracerebral hemorrhage immediately after onset of bleeding.1 MRI or magnetic resonance angiography (MRA) is very useful to confirm the diagnosis of stroke apart from clinical presentation. MRI is more sensitive than CT in detecting early ischemic changes.1 MRA techniques, especially MRV, are also useful in defining dural sinus and cerebral and cerebellar venous occlusions by abnormalities in the normal flow signals, non-opacification of sinuses, and by showing collateral venous channels.1 Blood work, including a complete blood count, basic metabolic panel, erythrocyte sedimentation rate, and measures
M
www.npjournal.org
of the prothrombin time (PT) and activated partial thromboplastin time (PTT), should also be tested for patients with suspected CVT. These studies may reveal abnormalities indicative of an underlying hypercoagulable state, an infectious process, or an inflammatory state, all of which may lead to the development of CVT.2 EEG should also be considered to rule out seizures. 2. What are the possible differential diagnoses? Subarachnoid hemorrhage. Pseudotumor cerebri. Migraine. Stroke. Cerebral venous sinus thrombosis (CVT). Seizures. 3. Based on the information, what is the possible diagnosis? Diagnosis. MR of brain, MRA, and MRV were performed. Brain MR did not show evidence of stroke; however, MRA/MRV showed evidence of obstructed flow along the posterior-superior sagittal sinus extending into the bilateral transverse sinus, consistent with superior sinus thrombosis. Blood work findings, including complete blood count, basic metabolic panel, erythrocyte sedimentation rate, and measures of PT and activated PTT, were within normal limits. Routine EEG showed no epileptiform discharges. Lower extremity Doppler was negative for deep vein thrombosis. Based on the clinical presentation and imaging findings, a diagnosis of CVT was established. CVT is an uncommon form of stroke, usually affecting young individuals.2 Its diagnosis and management are very difficult due to the multiplicity of risk factors and the absence of a standardized treatment approach. Diagnosis is typically based on clinical presentation and imaging confirmation.2 Pathophysiology and the most common causes. Occlusion of the venous system compromises the drainage of blood. As a result, the pressure in the brain tissue drained by the obstructed veins and dural The Journal for Nurse Practitioners - JNP
e29
sinuses increases and cerebral edema develops in the involved territory. Brain hemorrhage can occur if the pressure is high enough to break the capillaries and arterioles.1 There are multiple predisposing causes for CVT. The common causes of dural sinus occlusions include: infections; hormonal factors; pregnancy and puerperium in adults; neoplasms; abnormalities of the blood and coagulation system; systemic illnesses, including nephrotic syndrome; dehydration, which predisposes to high hematocrit and increases in viscosity and hypercoagulability; oral contraceptive use; smoking; use of female hormone prescriptions; and systemic inflammatory diseases, especially ulcerative colitis, and both Crohn’s and Beçhet’s diseases. However, approximately 30% of cases have no underlying cause.3 Oral contraceptive use increases the risk of CVT in women of reproductive age by 7-fold when compared with non-use of this method of contraception.3 Headache is a very common symptom in patients with intracranial venous occlusive disease.1 Based on the assessment and findings, the most likely etiology in this case is the use of oral contraception and perhaps steroid therapy, as well as possible dehydration. 4. What are the possible treatment options available? Management. Acute treatment of CVT focuses on anticoagulation and management of other associated problems such as seizures, increased intracranial pressure, venous infarction, and prevention of cerebral herniation.4 Typical management of seizures and increased intracranial pressure in patients with CVT requires a team approach that includes consultations with neurology and neurosurgery.4 The rationale for anticoagulation is to prevent thrombus propagation, recanalize occluded sinuses and cerebral veins, and prevent complications of deep vein thrombosis and pulmonary embolism.4 After acute thrombolysis, oral anticoagulation will be continued for 3-6 months. Ms. AB was started on heparin drip with a PTT goal of 50-70 seconds. Once PTT was therapeutic, coumadin was added. Hydration was maintained with intravenous fluids. Oral levertiracetam 1,000 mg twice a day for possible seizures was continued. Her e30
The Journal for Nurse Practitioners - JNP
headache was managed with ibuprofen every 4 hours as needed, with oral zonisamide 50 mg/day also continued for her history of pseudomotor cerebri. Mometasone furoate and oral steroids for asthma were discontinued as her asthma was well controlled and she was started on albuterol inhalation 2mg/5mL every 4 hours, as needed. She was subsequently weaned off heparin drip and continued on coumadin with an international normalized ratio (INR) goal of 2-3. Ms. AB remained neurologically stable and did not have any complications during her stay. Anticoagulant treatment for CVT appears to be safe and is associated with a potentially important reduction in the risk of death or dependency, although the difference did not reach statistical significance.5 Seizure is a poor prognostic factor. It results in secondary ischemia and brain damage. The control of seizures using antiepileptic agents, both oral and parenteral, remains one of the mainstays of CVT treatment.6 Adequate hydration is also very important in the management of CVT patients. Long-term management is focused on secondary prevention. She was discharged home on coumadin with instructions to follow-up. 5. What important patient and family education is required? Discharge instructions. The patient and family was instructed on the importance of adequate hydration and the importance of staying active so as to avoid long periods of sitting/standing, as it can lead to blood clots. She was also instructed on the importance of continuing all medications. She was advised to stop using any hormonal forms of birth control or steroids. Diet education was given for eating balanced meals. She was also counseled not to drive or operate heavy machinery until being seizure-free for at least 6 months, and were given permission to return to school. Instructions were also given to seek emergency treatment for any signs of internal bleeding, including severe headache, red urine, dark stools, vomiting of blood, or heavy bruising, although some bruising could be expected. She was also instructed to call 911 or go to the nearest emergency room for any symptoms of stroke, such as weakness/numbness in the face, arm, or leg; sudden blurry vision or loss of vision in 1 or both eyes; inability to speak clearly or understand simple statements; loss of coordination or Volume 12, Issue 1, January 2016
balance; or sudden, severe headache—like the “worst headache of her life.” 6. What is the recommended follow-up for this individual? Follow-up. The patient was instructed to followup with neurology within 3 months with repeat MRV and to follow-up with her PCP for INR monitoring to maintain a goal range of 2-3. Continuity of care. Upon follow-up, her repeat MRV showed significant, but not complete, resolution of venous thrombosis. Overall, her headaches improved. She denied any seizurelike symptoms, activities, or events, with INR within the target range. She had no further bleeding complications. She was advised to continue her medications and follow-up again after 3 months with repeat MRV. References 1. Caplan LR. Stroke: A Clinical Approach. 4th ed. Philadelphia, Pa: Saunders Elsevier; 2009.
www.npjournal.org
2. Saposnik G, Barinagarrementeria F, Brown RD, et al. Diagnosis and management of cerebral venous thrombosis. Stroke. 2011;42:1158-1192. 3. Amoozegar F, Ronksley PE, Sauve R, Menon BK. Hormonal contraceptives and cerebral venous sinus thrombosis risk: a systematic review and meta-analysis. Front Neurol. 2015;6:7. 4. Piazza G. Cerebral venous thrombosis. Circulation. 2012;125:1704-1709. 5. Coutinho JM, de Bruijn SF, deVeber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. Stroke. 2012;43:41-42. 6. Mohapatra F, Swain BM, Mohanty J. Prognostic evaluation of cerebral venous sinus thrombosis using clinical and MR sequences. J Neurol Neurophysiol. 2014;5.
Susan Alex, MS, ANP-BC, works as a stroke team NP. She can be reached at [email protected]. Susan Chaney, EdD, RN, FNP-C, FAANP, and Catherine Hill, DNP, APRN, GNP-BC, are faculty members at Texas Woman’s University in Dallas. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a conflict of interest.
1555-4155/15/$ see front matter © 2016 Elsevier, Inc. All rights reserved. http://dx.doi.org/10.1016/j.nurpra.2015.08.005
The Journal for Nurse Practitioners - JNP
e31
A Patient With Persistent Headache and Numbness Susan Alex, MS, APRN, Susan Chaney, EdD, APRN, and Catherine Hill, DNP, APRN INTRODUCTION
H
eadache is a very common disorder and often can be a presenting symptom for many other neurologic disorders. Due to its commonality, several other serious disorders that have similar presentations can be misdiagnosed or left untreated. A very thorough history and physical can often provide information for correct diagnosis and timely management. CASE PRESENTATION
Ms. AB is a 24-year-old, right-handed, Caucasian female with past medical history of pseudotumor cerebri and migraine, who presented with a 1-week history of intermittent, dull frontal headache. Initially, she was able to manage her headaches with over-thecounter ibuprofen, as needed, and rest. Her migraines had been well controlled for > 1 year, since she started taking zonisamide for pseudotumor cerebri. Two days after the initial headache, she had the “worst headache of her life,” when she presented to a local emergency department (ED). She also had transient visual obscurations, associated numbness on her right side, leg itching, and involuntary movements in her right arm and leg, which her mother described as “seizurelike.” The whole episode lasted for about 15-20 minutes. She denied having any change in level of consciousness, nausea, vomiting, or any focal weakness. She was diagnosed with tension headache and was discharged home on ibuprofen. Her headaches during these episodes were clearly different from her usual frontal headaches. She had not been having any aura with her usual frontal migraines. The following day, she had another seizurelike episode and numbness that spread to both of her legs and to the other arm. She was again evaluated in an ED, where computed tomography (CT) of the head was normal and she was started on leviteracetam and butalbital/acetaminophen/caffeine. She was discharged home with instructions to follow-up www.npjournal.org
with her primary care physician (PCP). The next day, she saw her PCP, who referred her for higher level care. Her past medical history included chronic migraine headache, pseudomotor cerebri, asthma, and menorrhagia since age 16. She was on oral steroids and mometasone furoate inhalation for asthma, zonisamide for pseudomotor cerebri, oral contraceptive pills for menorrhagia and ibuprofen for headaches. Her family history was unremarkable, except for a history of 2 miscarriages for her mother in the first trimester. She was a single, full-time law student, social drinker, had never smoked, and denied any illicit drug use. She denied any fever, chills, chest pain, dizziness, cough, shortness of breath, abdominal pain, nausea, vomiting, urgency, frequency, or dysuria. Her pertinent positive review of systems included headache, transient visual disturbance, numbness, and 2 “seizurelike” episodes. She denied any weakness. PHYSICAL EXAM
Her vital signs were stable and as follows: blood pressure 101/59; pulse 44 beats/min; temperature 36.6 C (97.9 F, temporal artery); respiration 16 breaths/min; saturation of peripheral oxygen 97%; weight 198 lb., 6.6 oz. (90 kg); and body mass index 33.02 kg/m2. At admission, it had been 4 days since her last menstrual period. NEUROLOGIC EXAM
She was awake, alert, oriented to person, place, time, and situation, and was a coherent historian with a good fund of knowledge. Her speech was clear and cranial nerves II-XII were intact. Her sensation was intact and she had 5/5 strength bilaterally (according to the Medical Research Council scale), and no drift. Coordination findings showed finger-to-nose and heel-to-shin intact bilaterally. Reflexes were 2þ throughout. Plantar response showed down-going The Journal for Nurse Practitioners - JNP
e17
toes bilaterally and normal gait. Her cardiac exam showed regular S1and S2 sounds; telemetry patterns with normal sinus rhythm; clear chest, with no wheezing or rales; a soft, nondistended abdomen; and bowel sounds positive in all 4 quadrants. Questions to consider: 1. What initial routine diagnostic tests should be considered? 2. What are the possible differential diagnoses? 3. Based on the information, what is the possible diagnosis?
e18
The Journal for Nurse Practitioners - JNP
4. What are the possible treatment options available? 5. What important patient and family education is required? 6. What is the recommended follow-up for this individual? Think you know answer to these questions? Test yourself and the go to page e29 to read the answers
Volume 12, Issue 1, January 2016
CASE CHALLENGE
A Patient With Persistent Headache and Numbness (continued from page e18)
s. AB was first evaluated in the ED and was transferred to the stroke neurology service for further management. Brain CT without contrast showed no evidence of acute intracranial abnormality and her basic blood work findings were within normal limits. Brain ischemia is often caused by thromboembolism and occlusive arterial disease.1 In some cases, brain ischemia can also be caused by thrombosis of the dural sinuses and cerebral and cerebellar veins.1 From a neurologic standpoint, key findings in Ms. AB’s exam and history included headache, numbness, shaking movements of arms and legs, use of oral contraceptive pills, oral steroid use for asthma, and a family history of 2 miscarriages for her mother. Findings of visual disturbance and numbness can be consistent with signs of migraine, stroke, or seizures. Her complaint of headache, use of oral contraceptives, and family history of 2 miscarriages for her mother could also suggest a possible hypercoagulable state, including venous sinus thrombosis. 1. What initial routine diagnostic tests are to be considered? a. CT of the brain. b. Magnetic resonance imaging (MRI) of the brain. c. Magnetic resonance venography (MRV). d. Electroencephalography (EEG). e. Blood work. CT scan can be used to detect intracerebral hemorrhage immediately after onset of bleeding.1 MRI or magnetic resonance angiography (MRA) is very useful to confirm the diagnosis of stroke apart from clinical presentation. MRI is more sensitive than CT in detecting early ischemic changes.1 MRA techniques, especially MRV, are also useful in defining dural sinus and cerebral and cerebellar venous occlusions by abnormalities in the normal flow signals, non-opacification of sinuses, and by showing collateral venous channels.1 Blood work, including a complete blood count, basic metabolic panel, erythrocyte sedimentation rate, and measures
M
www.npjournal.org
of the prothrombin time (PT) and activated partial thromboplastin time (PTT), should also be tested for patients with suspected CVT. These studies may reveal abnormalities indicative of an underlying hypercoagulable state, an infectious process, or an inflammatory state, all of which may lead to the development of CVT.2 EEG should also be considered to rule out seizures. 2. What are the possible differential diagnoses? Subarachnoid hemorrhage. Pseudotumor cerebri. Migraine. Stroke. Cerebral venous sinus thrombosis (CVT). Seizures. 3. Based on the information, what is the possible diagnosis? Diagnosis. MR of brain, MRA, and MRV were performed. Brain MR did not show evidence of stroke; however, MRA/MRV showed evidence of obstructed flow along the posterior-superior sagittal sinus extending into the bilateral transverse sinus, consistent with superior sinus thrombosis. Blood work findings, including complete blood count, basic metabolic panel, erythrocyte sedimentation rate, and measures of PT and activated PTT, were within normal limits. Routine EEG showed no epileptiform discharges. Lower extremity Doppler was negative for deep vein thrombosis. Based on the clinical presentation and imaging findings, a diagnosis of CVT was established. CVT is an uncommon form of stroke, usually affecting young individuals.2 Its diagnosis and management are very difficult due to the multiplicity of risk factors and the absence of a standardized treatment approach. Diagnosis is typically based on clinical presentation and imaging confirmation.2 Pathophysiology and the most common causes. Occlusion of the venous system compromises the drainage of blood. As a result, the pressure in the brain tissue drained by the obstructed veins and dural The Journal for Nurse Practitioners - JNP
e29
sinuses increases and cerebral edema develops in the involved territory. Brain hemorrhage can occur if the pressure is high enough to break the capillaries and arterioles.1 There are multiple predisposing causes for CVT. The common causes of dural sinus occlusions include: infections; hormonal factors; pregnancy and puerperium in adults; neoplasms; abnormalities of the blood and coagulation system; systemic illnesses, including nephrotic syndrome; dehydration, which predisposes to high hematocrit and increases in viscosity and hypercoagulability; oral contraceptive use; smoking; use of female hormone prescriptions; and systemic inflammatory diseases, especially ulcerative colitis, and both Crohn’s and Beçhet’s diseases. However, approximately 30% of cases have no underlying cause.3 Oral contraceptive use increases the risk of CVT in women of reproductive age by 7-fold when compared with non-use of this method of contraception.3 Headache is a very common symptom in patients with intracranial venous occlusive disease.1 Based on the assessment and findings, the most likely etiology in this case is the use of oral contraception and perhaps steroid therapy, as well as possible dehydration. 4. What are the possible treatment options available? Management. Acute treatment of CVT focuses on anticoagulation and management of other associated problems such as seizures, increased intracranial pressure, venous infarction, and prevention of cerebral herniation.4 Typical management of seizures and increased intracranial pressure in patients with CVT requires a team approach that includes consultations with neurology and neurosurgery.4 The rationale for anticoagulation is to prevent thrombus propagation, recanalize occluded sinuses and cerebral veins, and prevent complications of deep vein thrombosis and pulmonary embolism.4 After acute thrombolysis, oral anticoagulation will be continued for 3-6 months. Ms. AB was started on heparin drip with a PTT goal of 50-70 seconds. Once PTT was therapeutic, coumadin was added. Hydration was maintained with intravenous fluids. Oral levertiracetam 1,000 mg twice a day for possible seizures was continued. Her e30
The Journal for Nurse Practitioners - JNP
headache was managed with ibuprofen every 4 hours as needed, with oral zonisamide 50 mg/day also continued for her history of pseudomotor cerebri. Mometasone furoate and oral steroids for asthma were discontinued as her asthma was well controlled and she was started on albuterol inhalation 2mg/5mL every 4 hours, as needed. She was subsequently weaned off heparin drip and continued on coumadin with an international normalized ratio (INR) goal of 2-3. Ms. AB remained neurologically stable and did not have any complications during her stay. Anticoagulant treatment for CVT appears to be safe and is associated with a potentially important reduction in the risk of death or dependency, although the difference did not reach statistical significance.5 Seizure is a poor prognostic factor. It results in secondary ischemia and brain damage. The control of seizures using antiepileptic agents, both oral and parenteral, remains one of the mainstays of CVT treatment.6 Adequate hydration is also very important in the management of CVT patients. Long-term management is focused on secondary prevention. She was discharged home on coumadin with instructions to follow-up. 5. What important patient and family education is required? Discharge instructions. The patient and family was instructed on the importance of adequate hydration and the importance of staying active so as to avoid long periods of sitting/standing, as it can lead to blood clots. She was also instructed on the importance of continuing all medications. She was advised to stop using any hormonal forms of birth control or steroids. Diet education was given for eating balanced meals. She was also counseled not to drive or operate heavy machinery until being seizure-free for at least 6 months, and were given permission to return to school. Instructions were also given to seek emergency treatment for any signs of internal bleeding, including severe headache, red urine, dark stools, vomiting of blood, or heavy bruising, although some bruising could be expected. She was also instructed to call 911 or go to the nearest emergency room for any symptoms of stroke, such as weakness/numbness in the face, arm, or leg; sudden blurry vision or loss of vision in 1 or both eyes; inability to speak clearly or understand simple statements; loss of coordination or Volume 12, Issue 1, January 2016
balance; or sudden, severe headache—like the “worst headache of her life.” 6. What is the recommended follow-up for this individual? Follow-up. The patient was instructed to followup with neurology within 3 months with repeat MRV and to follow-up with her PCP for INR monitoring to maintain a goal range of 2-3. Continuity of care. Upon follow-up, her repeat MRV showed significant, but not complete, resolution of venous thrombosis. Overall, her headaches improved. She denied any seizurelike symptoms, activities, or events, with INR within the target range. She had no further bleeding complications. She was advised to continue her medications and follow-up again after 3 months with repeat MRV. References 1. Caplan LR. Stroke: A Clinical Approach. 4th ed. Philadelphia, Pa: Saunders Elsevier; 2009.
www.npjournal.org
2. Saposnik G, Barinagarrementeria F, Brown RD, et al. Diagnosis and management of cerebral venous thrombosis. Stroke. 2011;42:1158-1192. 3. Amoozegar F, Ronksley PE, Sauve R, Menon BK. Hormonal contraceptives and cerebral venous sinus thrombosis risk: a systematic review and meta-analysis. Front Neurol. 2015;6:7. 4. Piazza G. Cerebral venous thrombosis. Circulation. 2012;125:1704-1709. 5. Coutinho JM, de Bruijn SF, deVeber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. Stroke. 2012;43:41-42. 6. Mohapatra F, Swain BM, Mohanty J. Prognostic evaluation of cerebral venous sinus thrombosis using clinical and MR sequences. J Neurol Neurophysiol. 2014;5.
Susan Alex, MS, ANP-BC, works as a stroke team NP. She can be reached at [email protected]. Susan Chaney, EdD, RN, FNP-C, FAANP, and Catherine Hill, DNP, APRN, GNP-BC, are faculty members at Texas Woman’s University in Dallas. In compliance with national ethical guidelines, the authors report no relationships with business or industry that would pose a conflict of interest.
1555-4155/15/$ see front matter © 2016 Elsevier, Inc. All rights reserved. http://dx.doi.org/10.1016/j.nurpra.2015.08.005
The Journal for Nurse Practitioners - JNP
e31