neurology morning report

Neurology Morning ReportCathy Larrain, MD, PGY3Internal MedicineAugust 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”

Differential Diagnoses

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

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 historyAll 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, clammyHorizontal 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 lymphadenopathyFacial symmetry, +ptosis, normocephalic, atraumatic with moist

mucous membranesNeck musculature slightly stiff R>L without meningeal signs or

spinal/paraspinal tendernessLungs clear bilaterally throughout airfieldsHeart sounds unremarkable, normal S1/S2Abdomen obese with old striae, no stigmata of liver disease, no

tenderness or organomegaly, normoactive bowel soundsExtremities without clubbing, cyanosis, edema

Head CT & CTA

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

TTE: Normal but technically limited study. No obvious abnormalities but bubble study not performed and sensitivity for abnormal findings is low due to quality.

Hypercoagulable workup revealed Factor V Leiden mutation

ImpressionsBilateral cerebellar ischemic

infarctsHypertensionHypokalemiaHypocalcemiaHypophosphatemia

Venous Thromboembolism (VTE)

Secondary preventionAspirin

◦ 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

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 VertigoIdentifying likely etiologies

◦Peripheral vestibular dysfunction (40%)

◦Central brainstem vestibular lesion (10%)

◦Psychiatric disorder (15%) ◦Other etiologies (25%), e.g.

presyncope or disequilibrium◦Idiopathic (10%)

Eliciting pertinent history and physical exam findings:

Positional changes in symptomsOrthostatic blood pressure and

pulse changesObservation of gaitDetection 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 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.

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.

http://en.academic.ru/dic.nsf/enwiki/153025

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.

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

artery2. Branches to both PICA regions arising from

one side3. Pressure effect caused by a large PICA infarct4. Hemodynamic mechanism with

hypoperfusion in the most peripheral branches; and

5. 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

In Summary

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

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

Referenceshttp://en.academic.ru/dic.nsf/enwiki/153025Siddiqui M, Khan FS, Salman M. Bilateral

cerebellar stroke with good functional recovery: a case report. Pak J Neurol Sci. 2009; 4(2): 71-73.

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