Neurology Morning Report Cathy Larrain, MD, PGY3 Internal Medicine August 3, 2010
41 year-old male with no known past medical history presents with acute onset vertigo and nausea that awoke him from sleep @4am He initially walked without difficulty to the bathroom where he vomited 3-4 times bilious emesis and continued to experience transient dizziness and vertigo for a few hours
He denied tinnitus, ear pain, visual or hearing loss He described recent recovery from cold-like symptoms 4 days prior to symptom onset with cough, sore throat, runny nose which resolved after few days of “cold medicine”
He did not experience further symptoms for the rest of the day apart from headache frontal and occipital locations, dull, 4/10, for which he took aspirin with relief.
The following morning he had trouble swallowing. Family members grew concerned that he appeared short of breath. He denied shortness of breath or chest pain but said talking was cumbersome because of his difficulty swallowing. He reported intermittent diplopia exacerbated by looking at far objects with alternating blurry vision, then developed persistent right hand numbness and could not walk because the sensation of the room tilting to the right.
No known past medical history, generally healthy Had not seen a physician in 15 years Never hospitalized No surgical history All childhood immunizations up to date No known drug allergies Home Medications: occasional Tums & Ibuprofen
He denied smoking and illicit drug use, admitted to rare 2x/yr alcohol use Employed as a salesman for pool/sauna installation “on my feet 8 hours a day” Family History (+)vertigo
In the Emergency Department
He fell backward slightly while ambulating, could not stand because of sensation of room and body tilting to right
T-97.1 BP-188/96 HR-84 RR-20 SpO2-100% RA Glc-140 Morbidly obese gentleman with eyes closed in moderate emotional distress Skin intact, no rash, clammy Horizontal nystagmus gazing to the left not suppressed with visual fixation, diplopia R>L, motor dysmetriaof the RUE, 5/5 strength bilaterally UE/LE, ? Babinski on right No palpable lymphadenopathy Facial symmetry, +ptosis, normocephalic, atraumaticwith moist mucous membranes Neck musculature slightly stiff R>L without meningeal signs or spinal/paraspinal tenderness Lungs clear bilaterally throughout airfields Heart sounds unremarkable, normal S1/S2 Abdomen obese with old striae, no stigmata of liver disease, no tenderness or organomegaly, normoactive bowel sounds Extremities without clubbing, cyanosis, edema
Secondary prevention Aspirin alone or with other antiplatelet drugs, is highly effective in reducing major ARTERIAL thrombotic events in patients who are at risk or who have established atherosclerotic disease. LMWH vs UFH In a meta-analysis of randomized trials comparing the use of UFH versus LMW heparin for the prevention of VTE in medical patients, there was no statistically significant difference in efficacy between the two types of heparin preparations. However, there was a significant 72 percent risk reduction in major bleeding when LMW heparin was compared with UFH (RR 0.28; 95% CI 0.10-0.78).
The JUPITER study was randomized, double-blind, placebo-controlled, multicenter trial of rosuvastatin for the prevention of VTE in men ≥50 years of age and women ≥60 years of age without history of cardiovascular disease, LDL <130 mg/dL and high-sensitivity CRP ≥2.0 mg/L. In this study, 17,802 apparently healthy subjects were randomly assigned in a 1:1 ratio to treatment with oral rosuvastatin (20 mg/day) or a matching placebo. At a median follow-up of 1.9 years (maximum: 5 years), the following results were obtained: Symptomatic VTE occurred in 94 participants: 34 in the rosuvastatin group and 60 in the placebo group, for VTE rates of 0.18 and 0.32 events/100 person-years of follow-up, respectively (hazard ratio with rosuvastatin 0.57; 95% CI 0.37-0.86). Hazard ratios for the use of rosuvastatin for unprovoked VTE, provoked VTE, pulmonary embolism, and DVT were similarly significant at 0.61, 0.52, 0.77, and 0.45, respectively.
The use of rosuvastatin significantly reduced the composite end point of first cardiovascular event, VTE, or death (hazard ratio 0.66; 95% CI 0.57-0.76). The number of patients needed to treat for 4 or 5 years to prevent one of these events was 23 and 18, respectively. Consistent effects were observed in all of the subgroups examined. No differences in the rates of bleeding were noted between the two treatment arms. In a second population-based case control study, an analysis restricted to persons without a history of cardiovascular events indicated that the current use of statins significantly reduced the incidence of VTE (adjusted relative risk 0.75; 95% CI 0.61-0.91)
Vertigo is the predominant symptom that arises from an acute asymmetry of the vestibular system, which includes vestibular apparatus in the inner ear vestibular nerve and nucleus within the medulla connections to and from the vestibular portions of the cerebellum
Evaluation of Vertigo Identifying likely etiologies Peripheral vestibular dysfunction (40%) Central brainstem vestibular lesion (10%) Psychiatric disorder (15%) Other etiologies (25%), e.g. presyncopeor disequilibrium Idiopathic (10%)
Eliciting pertinent history and physical exam findings: Positional changes in symptoms Orthostatic blood pressure and pulse changes Observation of gait Detection of nystagmus
Bilateral Cerebellar Infarcts
Ischemic strokes in the posterior circulation are caused by atherosclerosis or embolism. Cerebellar infarction accounts for 2% of acute strokes and in order of frequency posterior inferior cerebellar artery (PICA) 40% superior cerebellar artery (SCA) 35% border zone infarcts 20% anterior inferior cerebellar artery (AICA) 5% posterior inferior cerebellarartery (PICA) rare PICA arises from the intracranial vertebral artery (VA) and supplies Lateral medullarytegmentum, inferior cerebellar peduncle, the ipsilateralportion of the inferior vermis and the inferior surface of the cerebellar hemispheres. The medial branch of PICA supplies the medial cerebellum and the dorsal medulla oblongata, and the lateral branch supplies the inferoposterolateralaspect of the cerebellum.
The clinical presentation of acute cerebellarinfarcts depend upon involved territory involved and the presence or absence of forth ventricular / brainstem compression. Presentation of sudden onset of occipital headache, severe vertigo, nausea, vomiting, ataxia of gait and trunk, ipsilateralaxial lateropulsion, dysarthria and impairment of consciousness. Brainstem compression results in increasing headache, decreased level of alertness, head tilt and tonsillarherniationthrough the foramen magnum. These infarcts usually involve PICA, AICA or both.
Cerebellar infarction in the territory of posterior inferior cerebellarartery (PICA) is usually unilateral, as the origin of PICA arises from a single vertebral artery (VA). Very few patients with acute bilateral cerebellar infarcts in the territory of PICA have been described in literature to date.
Different hypotheses have been put forth to explain the pathogenesis of bilateral cerebellar infarcts in the PICA territory: Both PICAs arising from an occluded basilar artery Branches to both PICA regions arising from one side Pressure effect caused by a large PICA infarct Hemodynamic mechanism with hypoperfusion in the most peripheral branches; and Double, simultaneous embolic stroke
PICA is the most variable cerebellar artery. It is absent in 20% of VA angiogram; in the majority of these instances, the AICA supplies the PICA territory. In cases when both PICAs are asymmetrical, branches of one PICA partially feed the territory of the other.Furthermore, an "extensive“ PICA may supply the cerebellum bilaterally
Secondary prevention of VTE: aspirin, UFH vs LMWH, statin Warfarinis not appropriate for immediate and short-term prevention of VTE in medical patients When evaluating for a patient with vertigo and/or dizziness, localize the symptoms/type/timing to help identify etiology Peripheral: ear pain, tinnitus, abnormal hearing Central: numbness, weakness, gait impairment, diplopia, dysarthria Life threatening causes of vertigo include brainstem ischemia and cerebellar infarction or hemorrhage Cerebellar strokes comprise 2% of acute strokes Symptoms of acute cerebellar stroke include sudden onset of occipital headache, severe vertigo, nausea, vomiting, ataxia of gait and trunk, ipsilateral axial lateropulsion, dysarthria and impairment of consciousness. Keep in mind the concern for brainstem compression and worsening mental status
Ischemic strokes in the posterior circulation are caused by atherosclerosis or embolism (of a dominant PICA). Cerebellarinfarction in the territory of PICA is usually unilateral with very few bilateral infarcts described in literature thus far Bilateral cerebellar infarction is hypothesized to occur when Both PICAs arising from an occluded basilar artery or other anatomical variation Branches to both PICA regions arising from one side Pressure effect caused by a large PICA infarct Hemodynamic mechanism with hypoperfusion in the most peripheral branches; and Double, simultaneous embolic stroke
References http://en.academic.ru/dic.nsf/enwiki/153025 Siddiqui M, Khan FS, Salman M. Bilateral cerebellar stroke with good functional recovery: a case report. Pak J Neurol Sci. 2009; 4(2): 71-73. UpToDate