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Dissection Is Most Likely Due to Multiple Environmental and Genetic Risk Factors. Also, Recent Infections (Mainly Respiratory) H

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Dissection Is Most Likely Due to Multiple Environmental and Genetic Risk Factors. Also, Recent Infections (Mainly Respiratory) H Synapsea clinical resource SPRING 2017, VOL. 8, ISSUE 1 Vertebral and Carotid Artery Dissections The most important environmental risk factor appears to be Lucian Maidan, MD major or minor trauma caused by events such as chiropractic manipulation, yoga poses, coughing, and sneezing. Trauma Although only 10% of the 750,000 people who annually suff er produces an intimal tear through which blood enters the wall an ischemic stroke in the U.S. are younger than 50, those and forms an intramural hematoma. younger individuals have a higher mortality. Dissection of carotid arteries (CAD) and vertebral arteries (VAD) is second Clinical manifestations of a cervical artery dissection include only to cardioembolic strokes in young people, with an incidence both local signs and symptoms and ischemic and even estimated at up to three per 100,000 people for carotid artery hemorrhagic cerebral events. dissection and 1.5 per 100,000 for the vertebral arteries. Local manifestations of CAD include Horner syndrome The second most common lesion of the cervical arteries after (ipsilateral), neck pain, headache, tinnitus, facial pain, and atherosclerosis, dissection may be either spontaneous or cranial nerve palsies (IX to XII most commonly). secondary to major trauma. The majority of dissections occur Local manifestations of a VAD include severe occipital extracranially—only 10% are intracranial—and in 16% of cases headache, nuchal pain, cervical root involvement (most multiple arteries are involved. commonly C5-C6 level), and lower brainstem compression if the Dissection is most likely due to multiple environmental and dissection extends in the intradural space. genetic risk factors. Also, recent infections (mainly respiratory) Ischemic manifestations of CAD include stroke, most commonly have been associated with dissection. in the middle cerebral artery distribution, amaurosis fugax, A genetic predisposition may be present for an underlying ischemic optic neuropathy, and retinal infarction. structural defect aff ecting the media and adventitia of the An estimated 85% of patients with a VAD will develop ischemic outer wall of superfi cial temporal arteries of patients who have manifestations involving the posterior circulation sometimes had dissections. Also, absence of a demonstrable intimal tear after days or weeks delay. Most often the presentation is a lateral on some histologic examinations suggests that at least some medullary syndrome (Wallenberg syndrome), which consists of dissections are caused by a primary intramural hematoma. ipsilateral facial pain and numbness, Several connective tissue disorders have been associated with contralateral loss of pain and dissection, including vascular Ehlers-Danlos syndrome (type temperature, dysartria, hoarseness, IV), Marfan syndrome, and osteogenesis imperfecta. hiccups, vertigo, nausea, vomiting, ataxia and diplopia. If other areas of the brainstem are involved, Dissection is most likely due to multiple a medial medullary syndrome environmental and genetic risk factors. Also, with characteristic contralateral recent infections (mainly respiratory) have been weakness and numbness, Horner associated with dissection. syndrome or, if the cerebellum is Lucian Maidan, MD continued on page 5 To view Synapse electronically, visit DignityHealth.org/Synapse. For your convenience in neurological referrals, call the Dignity Health Doctor Direct referral line at 855.685.5050. Synapse Idiopathic Intracranial Hypertension standing, and is aggravated by activities that raise ICP, such as coughing, sneezing, bending over, or performing a Valsalva. Peter T. Ska , MD Associated symptoms include transient visual obscuration, Idiopathic intracranial hypertension (IIH), fi rst described photopsia (light fl ashes), pulsatile tinnitus (often described as by Heinrich Quincke in 1893 as “serous meningitis,” is an whooshing), retrobulbar pain or pressure, neck pain or stiff ness, unusual cause of chronic headache. Also referred to as “benign diplopia, and visual loss. Although formal, automated visual intracranial hypertension,” this disorder can result in permanent fi eld testing will demonstrate peripheral vision loss (scotoma) blindness if not recognized and treated promptly and should not in a majority of patients, most will be unaware of the defi cit due be regarded as benign. to preservation of central vision and of visual acuity. Blindness occurs in as many as 5% of cases, and though often gradual, it The common name, pseudotumor cerebri, refers to the presence can be acute. Approximately 10% of patients are asymptomatic, of papilledema without a demonstrable, intracranial mass, while and symptomatic IIH can also present without papilledema if IIH is used specifi cally when no other secondary cause of raised, there is chronic optic atrophy with thinning of the retinal neural intracranial pressure (ICP) is discovered. Secondary causes fi ber layer. of pseudotumor cerebri include cerebral venous thrombosis, steroid withdrawal, Addison disease, obstructive sleep apnea, The diagnosis of IIH is made on the basis of clinical history, hypoparathyroidism, and hypervitaminosis A. physical examination, imaging studies, and lumbar puncture. The physical examination should be normal except for The annual incidence of IIH is approximately 1 in 100,000. papilledema and the occasional fi nding of an abducens nerve However, IIH aff ects approximately 1 in 25,000 women of palsy, which can be caused by increased ICP. childbearing age, and the incidence increases to 1 in 5,000 for those with co-morbid obesity. In particular, weight gain over the Modifi ed Dandy Criteria for Diagnosis of IIH: preceding 12 months is the most predictive and well-established 1. Symptoms of raised ICP (e.g., headache, visual loss, risk factor. papilledema) Patients with IIH generally present in one of two ways. Either 2. No localizing signs other than abducens papilledema is incidentally discovered at the time of optometric (6th) nerve palsy or ophthalmological examination, or clinical evaluation 3. The patient is awake and alert of chronic headache is sought. In the fi rst case, further 4. Normal brain imaging without investigation with neuroimaging and referral to a neurologist is evidence of venous thrombosis assured. In the second case, the clinician must maintain a high (e.g., MRI w/ MR Venogram) index of suspicion, make specifi c inquiry into related symptoms and secondary causes, and perform an appropriate physical 5. Lumbar puncture opening exam including vision, eye movement, and fundoscopy. pressure > 250 mm CSF with normal composition The vast majority of patients with IIH present with headache 6. No other explanation for the that is typically holocranial, occurs daily, is worse upon raised ICP awakening or when lying down, is better when sitting or Peter T. Skaff, MD continued on page 3 Dignity Health Neurological Institute | Synapse Editorial Board John Schafer, MD George Luh, MD Alan Shatzel, DO Christopher Wood, FACHE Neurologist and Editor-in-Chief Medical Director Medical Director, Neurology Vice President Dignity Health Neurological Institute Neurointerventional Radiology Dignity Health Neurological Institute Dignity Health Neurological Institute Dignity Health Neurological Institute Richard Beyer, MD Peter T. Skaff, MD Chairman, Specialties Praveen Prasad, MD, FAANS Neurologist, Mercy Medical Group Medicine Division Medical Director, Neurosurgery Director, Neurodiagnostics Woodland Healthcare Dignity Health Neurological Institute Mercy San Juan Medical Center Page 2 SPRING 2017, VOL. 8, ISSUE 1 Guillain Barre Syndrome CSF studies are often normal during the fi rst week of symptoms. Nerve conduction studies are not necessary in all cases, but can Ryan Armour, DO be helpful when the clinical examination and CSF fi ndings are Guillan Barre syndrome (GBS) is the eponym used to insuffi cient to determine the diagnosis. describe a group of rapidly progressive immune mediated polyneuropathies. GBS is caused by autoantibodies binding to Care must be taken to monitor patients for dysautonomia, peripheral nerves causing demyelination and sometimes axonal as this can occur in 70% of patients. Cardiac arrhythmias, loss. Many cases are preceded by a relatively benign viral or gastrointestinal dysmotility and rapid and dangerous blood bacterial illness, vaccination or surgical procedure. Typical pressure fl uctuations may occur suddenly, making patients patients will develop muscle weakness that worsens over the at risk for signifi cant morbidity and sudden death. Severe course of days, beginning in distal lower limb muscles. respiratory weakness requiring ventilatory support may occur rapidly in up to 30% of patients. For these reasons, patients admitted into the hospital must be monitored with cardiac Care must be taken to monitor patients for telemetry. Bedside spirometry with close attention to forced dysautonomia, as this can occur in 70% of patients. vital capacity and negative inspiratory force is critical. Treatment is indicated for patients who have progressively Proximal lower limb muscle, upper limb muscle and facial worsening weakness. Symptoms may relapse after some initial muscle weakness may develop over a few days. Patients will improvement in the eight weeks after initial onset of weakness. complain of back pain throughout the clinical course of the Intravenous immunoglobulin (IVIG) or plasmapheresis have disease. The weakness will progress over the course of two to both been shown to improve recovery time. Physical therapy four
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