Thesis (Ph.D.). / Title from title page of PDF (viewed 2008/01/30). Written for the Dept. of Epidemiology and Biostatistics. Includes bibliographical references.

Diss. (sammanfattning) Linköping : Univ., 2006. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 6 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Umeå : Univ., 2005. / Härtill 4 uppsatser.

Thesis (M.S.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 44 pages. Includes Vita. Includes bibliographical references.

Cerebrovascular accidents are a leading cause of morbidity and mortality in the United States. Many conditions exist which may mimic this disease process including seizures, migraines, metabolic derangements, infections, space-occupying lesions, neurodegenerative disorders, peripheral neuropathy, cervical myelopathy, syncope, other vascular disorders, and functional neurologic disorder. Timely diagnosis and treatment are important in order to preserve functional status in these patients. A 48-year-old male presented to the emergency department with a 28-hour history of worsening left sided numbness, tingling, weakness, and feeling off balance. The patient stated that for the past several months he had noticed these symptoms, but they suddenly became worse the day prior. He also described shooting pains down the left arm with certain movements of his neck. The patient denied any difficulty with speaking, understanding words, performing mental tasks, bowel or bladder incontinence, or right sided symptoms. Physical exam showed intact cranial nerves II-XII, 5/5 strength of upper and lower extremities on the right side, 4/5 strength of upper and lower extremities on the left side. Romberg test was normal, heel to shin and finger to nose were intact bilaterally. Foot drop was noted on the left side and placement of the foot on the ground was noted to be clumsy. Initial head CT in the emergency department showed a frontal lobe hypodensity and was without intracranial hemorrhage. Computed tomography angiography of the head and neck showed no large vessel thrombosis or stenosis. Echocardiography revealed normal chamber sizes, normal left ventricular ejection fraction, no patent foramen ovale, and no left atrial or left ventricular thrombus. Telemetry monitoring throughout the stay remained sinus rhythm. Magnetic resonance imaging of brain and cervical spine was performed showing multifocal acute infarcts of the right and left frontal lobes and severe cervical spondylosis at C4-C6 with spinal cord edema in T2 sequences slightly below that level. The patient subsequently underwent a cervical spine decompression for the spinal cord compression during the hospital stay. Due to the multifocal lesions noted on the brain MRI, a vasculitis workup was performed which returned negative for any abnormal test findings. The patient was also diagnosed with diabetes mellitus type 2 during the stay as he was found to have a glycosylated hemoglobin A1C of >12. He was initially hypertensive during hospitalization, but this resolved on its own after day three of the hospitalization so anti-hypertensives were not required. The patient was discharged home on high intensity statin therapy, dual oral hypoglycemic therapy for his diabetes mellitus, home physical therapy, and he was scheduled to start dual antiplatelet therapy seven days after cervical spine surgery. This dual antiplatelet therapy with clopidogrel and aspirin was to be continued for three weeks after which continuation with low dose aspirin was advised. As seen in this case, patients that present with a cerebrovascular accident should always be evaluated for other etiology behind his or her symptoms and having a low threshold for pursing other additional diagnoses is reasonable.

Thesis (M.S.)--Boston University

Cerebrovascular accidents (CVAs) are a leading cause of morbidity and mortality in the United States. Metabolic derangements such as hypoglycemia, infections, brain masses or lesions, neurodegenerative disorders, neuropathies, myelopathies, seizures, syncope, types of migraines, and many other disorders may mimic CVA. Our case presents a 38-year-old female who was evaluated in the emergency department with a three- hour history of headache, lethargy, left- sided upper extremity weakness, facial droop, and dysarthria. A CVA workup was initiated and she immediately underwent a computed tomography (CT) scan of the head which revealed no intracranial hemorrhage. She was unable to provide a thorough medical history due to lethargy, however she was able to answer yes/no questions to screen for tissue plasminogen activator (tPA) qualification. She qualified based on her screening results and was administered tPA for her presumed ischemic CVA. She was then monitored in the intensive care unit for twenty-four hours. Due to reoccurrence of headache and left-sided weakness, as well as recent administration of tPA increasing risk of hemorrhage, she underwent two subsequent negative non- contrast head CT scans to rule out bleeding during that time. On hospital day two, magnetic resonance imaging (MRI) of the head, neck, and spine were performed which were also negative for infarct or hemorrhage. A more detailed history from our patient revealed previous migraine headaches, but her left sided weakness and dysarthria were new symptoms. With this information, it was suspected that she was suffering from a hemiplegic migraine, a rare mimic of CVA. Prochlorperazine, diphenhydramine, valproic acid, and corticosteroids were administered for migraine treatment, which aborted her symptoms entirely. Topiramate was then started for migraine prophylaxis. Daily low-dose aspirin was also initiated due to inability to fully rule out CVA/transient ischemic attack (TIA). An outpatient neurology follow up was scheduled on discharge. In clinical practice, hemiplegic migraines and CVA/TIA may be difficult to differentiate as symptoms often overlap. A detailed history and physical exam with careful attention to associated symptoms and timing of symptom onset is essential to formulating a correct diagnosis. This must be done quickly, as tPA is a high-risk medication with a narrow time window for administration. In conclusion, not all disease processes have an available “gold standard” diagnostic test to differentiate similar diagnoses. MRI of the brain is usually performed to differentiate ischemic CVA from TIA; however, imaging is not useful to differentiate hemiplegic migraine from TIA. Therefore, performing a thorough history, physical exam, and chart review is paramount to provide patients with the correct treatment as well as prevent adverse outcomes. It is the responsibility of the clinician to make difficult decisions weighing the risks and benefits of providing various treatments or interventions, and to know the complications of those treatments. Disease processes mimicking CVA must be considered in all patients, as treating an incorrect diagnosis can have devastating effects.