Neurology Morning Report


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  • Classic Meniere’s triad of symptoms: episodic vertigo (a true spinning sensation that has an onset and an offset), sensorineural hearing loss and tinnitus

    Perilymphatic fistula: infrequent complication of head injury, barotrauma, or heavy lifting in which a fistula develops at the otic capsule, permitting a transfer of pressure changes to the macular and cupular receptors. This explains the clinical syndrome of episodic vertigo and/or hearing loss provoked by sneezing, lifting, straining, coughing, and loud sounds. The latter, so-called Tullio phenomenon, occurs because sound-induced pressure waves are abnormally distributed through the inner ear.
    -The diagnosis is difficult as clinical tests are insensitive. Computed tomography (CT) scanning may show fluid in the region of the round window recess. Treatment with bed rest, head elevation, and avoidance of straining is the first step; failure to resolve after several weeks of conservative therapy is an indication to consider a surgical patch. Recurrences occur in 10 percent.

    Semicircular canal dehiscence syndrome — In semicircular canal dehiscence syndrome, the bone overlying the superior aspect of the superior semicircular canal becomes thin or even absent, thereby allowing pressure to be transmitted to the inner ear. Vertigo is provoked by coughing, sneezing, and Valsalva maneuver. Patients may experience nausea and instability during brief episodes of vertigo. Diagnosis by MRI or high resolution CT of the temporal bone. Some patients benefit by surgical repair of their anatomical deficit.

    Cogan’s syndrome: autoimmune condition that can cause interstitial keratitis and vestibuloauditory dysfunction.
    -Patients have Meniere's-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, which is the perception of objects jiggling back and forth after abruptly turning the head to one side or the other. Caloric testing often reveals absent vestibular function.
    -Systemic steroids and other immunosuppressants may be required

    Wallenberg’s or lateral medullary syndrome

    Chiari malformation: congenital anomaly in which the cerebellar tonsils extend below the foramen magnum. This is usually asymptomatic but may be associated with a constellation of neurologic deficits (headache or neck pain, weakness with long tract signs, dysphagia, and other lower cranial nerve impairments) [53]. Vertigo and gait imbalance are common complaints in symptomatic individuals and may represent cerebellar or brainstem pathology
    -when present, vertigo is often positionally induced, particularly by neck extension, perhaps manifesting pressure on brainstem and cerebellar structures or their blood supply [53]. Vertiginous symptoms are generally mild and often resolve when the patient alters his or her head position. Downbeating nystagmus is often associated with this syndrome, but other patterns of central nystagmus may be seen as well. The diagnosis is confirmed with sagittal MRI.
    -Surgical decompression may be required to relieve symptoms and is usually successful

    Episodic ataxia type 2 (EA-2): autosomal dominant condition caused by mutations in a brain-specific P/Q type calcium channel gene on chromosome 19. Attacks of severe vertigo, nausea, and vomiting, and ataxia begin in childhood or early adult life. These can last a few hours or a few days. Gaze-evoked, rebound, or downbeat nystagmus may be evident not only during but also between attacks. The attacks respond to acetazolamide in a dose of 250 to 750 mg/day
  • CT head without contrast: Bilateral ischemic infarcts of the cerebellar hemispheres R>L without significant compression of the 4th ventricle

    CTA of head and neck: 1. Nonvisualization of both posterior inferior cerebellar arteries in this patient with acute/subacute bilateral cerebellar infarcts. Nonvisualization of the vessels maybe due to thrombus/occlusion of the vessels versus less likely nonvisualization due to small size. 2. No dissection. 3. Mild atherosclerotic narrowing of the right V4 segment. 4. No hemodynamically significant stenosis of the proximal cervical internal carotid arteries. 5. Limited study. 6. Right vertebral artery is slightly smaller than the left throughout the neck. Intracranially, the right vertebral artery Becomes diminutive. These findings likely congenital. Origin of the left vertebral artery which is dominant and not optimally visualized due to artifact from high density venous contrast
  • Causes of bilateral cerebellar ischemia to be discussed, but he has FV Leiden mutation, obesity, mild atherosclerosis, hypertension, congenital ?dominant L vertebral artery. Plans aspirin, anticoagulation, LMWH,
    Causes of his hypertension needs to be further investigated. Cushings vs primary aldosteronism vs salt intake vs ?r/o licorice intake. Check plasma renin & aldosterone to r/o primary aldosteronism (both have diurnal variation. Highest in early morning)
  • Patient is on full strength aspirin, low dose statin, previously only on prophylactic anticoagulation

    There is little evidence that aspirin has a significant effect on the prevention of VENOUS thromboembolic events in medical patients.

    LMWH vs UFH study from 2009 Cochrane database: 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 [88]. 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).
  • Hong JM, Bang OY, Chung CS, Joo IS, Huh K. Frequency and clinical significance of acute bilateral cerebellar infarcts. Cerebrovasc Dis. 2008;26(5):541-8. Epub 2008 Oct 6. Department of Neurology, Ajou University School of Medicine, Suwon, South Korea.

    Baseline demographics were not significantly different between unilateral cerebellar infarction (UCI) and bilateral cerebellar infarction (BCI), except for initial stroke severity (modified NIH Stroke Scale and infarct volume) and diabetes. Large-artery atherosclerosis was significantly higher in BCI, whereas undetermined causes were higher in UCI (p = 0.028). By multiple regression analysis, BCI was the only independent radiological factor for poor prognosis (odds ratio, 6.96; 95% CI, 1.80-26.92), and represented a significantly more unstable hospital course, longer hospital stay, worse mRS at discharge, and higher mortality.
  • Neurology Morning Report

    1. 1. Neurology Morning Report Cathy Larrain, MD, PGY3 Internal Medicine August 3, 2010
    2. 2.  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
    3. 3.  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”
    4. 4. Differential Diagnoses
    5. 5. Peripheral Causes  Benign paroxysmal positional vertigo  Vestibular neuritis  Otitis media  Herpes zoster oticus (Ramsay Hunt syndrome)  Meniere’s disease  Acoustic neuroma  Semicircular canal dehiscence syndrome  Cogan’s syndrome  Perilymphatic fistula  Amioglycoside toxicity Central Causes  Migrainous vertigo  Brainstem ischemia  Cerebellar infarction or hemorrhage  Chiari I malformation  Multiple sclerosis  Episodic ataxia (type 2)  Coronary-subclavian steal syndrome
    6. 6.  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.
    7. 7.  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.
    8. 8.  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
    9. 9.  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
    10. 10. In the Emergency Department
    11. 11.  He fell backward slightly while ambulating, could not stand because of sensation of room and body tilting to right
    12. 12. 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 dysmetria of the RUE, 5/5 strength bilaterally UE/LE, ? Babinski on right No palpable lymphadenopathy Facial symmetry, +ptosis, normocephalic, atraumatic with 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
    13. 13. Head CT & CTA
    14. 14.  Na-144 / K-3.0 / Cl-108 / CO2-23 / BUN-12 / Cr-1.0 / Glc-98 / Ca-8.0 / Phos-2.1 / Mg-2.0  WBC-10.3 / Hb-15.6 / Htc-43.9 / Plt-245  PT-12.4 / PTT-24.2 / INR-1.1  TC-160 / TG-198 / HDL-36 / LDL-84 / VLDL- 40  UDS negative
    15. 15.  TTE: Normal but technically limited study. No obvious abnormalities but bubble study not performed and sensitivity for abnormal findings is low due to quality.
    16. 16.  Hypercoagulable workup revealed Factor V Leiden mutation
    17. 17. Impressions  Bilateral cerebellar ischemic infarcts  Hypertension  Hypokalemia  Hypocalcemia  Hypophosphatemia
    18. 18. Venous Thromboembolism (VTE)
    19. 19. 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).
    20. 20.  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.
    21. 21. ◦ 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)
    22. 22. Vertigo
    23. 23.  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
    24. 24. Evaluation of Vertigo  Identifying likely etiologies ◦ Peripheral vestibular dysfunction (40%) ◦ Central brainstem vestibular lesion (10%) ◦ Psychiatric disorder (15%) ◦ Other etiologies (25%), e.g. presyncope or disequilibrium ◦ Idiopathic (10%)
    25. 25. Eliciting pertinent history and physical exam findings:  Positional changes in symptoms  Orthostatic blood pressure and pulse changes  Observation of gait  Detection of nystagmus
    26. 26. Bilateral Cerebellar Infarcts
    27. 27.  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 cerebellar artery (PICA) rare  PICA arises from the intracranial vertebral artery (VA) and supplies ◦ Lateral medullary tegmentum, inferior cerebellar peduncle, the ipsilateral portion 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 inferoposterolateral aspect of the cerebellum.
    28. 28.  The clinical presentation of acute cerebellar infarcts 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, ipsilateral axial lateropulsion, dysarthria and impairment of consciousness.  Brainstem compression results in increasing headache, decreased level of alertness, head tilt and tonsillar herniation through the foramen magnum.  These infarcts usually involve PICA, AICA or both.
    29. 29.
    30. 30.  Cerebellar infarction in the territory of posterior inferior cerebellar artery (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.
    31. 31.  Different hypotheses have been put forth to explain the pathogenesis of bilateral cerebellar infarcts in the PICA territory: 1. Both PICAs arising from an occluded basilar artery 2. Branches to both PICA regions arising from one side 3. Pressure effect caused by a large PICA infarct 4. Hemodynamic mechanism with hypoperfusion in the most peripheral branches; and 5. Double, simultaneous embolic stroke
    32. 32.  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
    33. 33. In Summary
    34. 34.  Secondary prevention of VTE: aspirin, UFH vs LMWH, statin ◦ Warfarin is 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
    35. 35.  Ischemic strokes in the posterior circulation are caused by atherosclerosis or embolism (of a dominant PICA).  Cerebellar infarction 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
    36. 36. References   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