sensitivity, specificity & positive & negative predictive values

2
rive serum titer, a CSF lab profile consistent with Lyme disease, and documented vasculitis on angiogram that re- sponds to IV Rocephin ® strongly suggests CNS Lyme dis- ease as the cause (as stated in Halperin's article). There is no doubt that there is a need for more accurate ways to make the diagnosis of active Lyme disease, both CNS or peripheral, and better ways to monitor response treat- ment. Gerard X Brogan, Jr, MD Department of Emergency Medicine State University of New York Stony Brook 1. Reik L, Steers AC, Bartenhagen NH, et ah Neurologic abnormalities of Lyme disease. Medicine 1979;58:281-294. 2. Stiernstedt G: Tick-borne Borrelia infection in Sweden. Scand J Infect Dis 1985;45:1-70. 3. Pachner AR, Steere AC: Neurological findings of Lyme disease. Yale ] Biol Med 1984;57:481-483. 4. Pachner AR: Spirochetal diseases of the CNS. NeuroI Clin 1986;4: 207-222. 5. Uldry PA, Regli F, Bogousslavsky J: Cerebral angiopathy and recurrent strokes following Borrelia burgdorferi infection. J Neurol Neurosurg Psy- chiatry 1987;50:1703-1704. 6. Reik L: Disseminated vasculomyelinepathy: An immune complex dis- ease. Ann Neurol 1980;7:291-296. 7. Halperin JJ, Luft BJ, Anand AK, et ah CNS Lyme disease (letter). Neurol ogy 1990;40:190. Central Cord Syndrome To the Editor: The neurologic deficit described in "Traumatic Central Cord Syndrome in a Patient With Os Odontoideum" by McGoldrick and Marx [December 1989;18:1358-1361], was attributed to a central cord syndrome when, in fact, I be- lieve the symptoms can be more accurately explained by a paralysis' of Bell. A central cord syndrome involves a spinal cord injury from bulging of the ligamenta flava against the anterior vertebral bodies during flexion of the cervical spine. 1 This injury causes injury to the central portion of the spinal cord (hence the name central cord injury) and results in weakness of the arms greater than the legs, loss of bladder function, and a variable degree of sensory loss. The vic- tims are usually elderly, and the level of injury is usually in the lower cervical spine. The paralysis of Bell is an injury to the pyramidal de- cussation, usually as a result of posterior displacement of the odontoid. Anatomically, the pyramidal decussation of the cervical cord is directly posterior to the odontoid, and this accounts for its potential for. injury whenever the odontoid is displaced. I believe the neurologic symptoms that occurred in this patient and the pathophysiology that was proposed to ac- count for this deficit are most likely explained by paral- ysis of Bell and not a central cord syndrome as reported by the author. David J Dula, MD Emergency Medicine Geisinger Medical Center Danville, Pennsylvania 1. Schneider RD, Crosby EC: Traumatic spinal cord syndromes and their management. J Clin Neurosurg 1972;20:424-492. In Reply: Dr Dula brings up the point that the neurologic deficits described in our patient could be explained by a "cruciate paralysis of Bell," which involves injury to the pyramidal tract decussation. The "cruciate paralysis" as described by Bell involves selective bilateral arm paralysis or tetra- plegia. A lesion involving the rostral crossing fibers of the pyramidal decussation may simulate the neurologic pat- tern of "acute central cervical cord injury syndrome." In fact, two of the cases presented in Bell's original paper in- volved a neurologic pattern that was initially classified as acute central cervical cord syndrome. Our patient presented with weakness of the arms greater than the legs without apparent sensory loss and loss of bladder function. We feel this pattern of neurologic deficit is consistent with central cord syndrome. John McGoldrick, MD John Marx, MD Department of Emergency Medicine Denver General Hospital Denver, Colorado Sensitivity, Specificity & Positive & Negative Predictive Values To the Editor." The article, "Fracture of the Carpal Navicular - Effi- cacy of Clinical Findings and Improved Diagnosis With Six-View Radiography" by Mehta and Brautigan [March 1990;19:225-257], contains an error in statistical calcula- tion. Table 1 compares the results of four- and six-view radiography in diagnosing fractures of the navicular. 19:11 November 1990 Annals of Emergency Medicine 1354/175

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Page 1: Sensitivity, specificity & positive & negative predictive values

rive serum titer, a CSF lab profile cons is ten t w i th Lyme disease, and documented vascul i t i s on angiogram that re- sponds to IV Rocephin ® strongly suggests CNS Lyme dis- ease as the cause (as s tated in Halper in ' s article). There is n o doubt that there is a need for more accurate ways to make the diagnosis of active Lyme disease, both CNS or per ipheral , and be t t e r ways to m o n i t o r response t reat- ment .

Gerard X Brogan, Jr, M D Depar tmen t of Emergency Medicine State Universi ty of N e w York Stony Brook

1. Reik L, Steers AC, Bartenhagen NH, et ah Neurologic abnormalities of

Lyme disease. Medicine 1979;58:281-294. 2. Stiernstedt G: Tick-borne Borrelia infection in Sweden. Scand J Infect Dis 1985;45:1-70. 3. Pachner AR, Steere AC: Neurological findings of Lyme disease. Yale ] Biol Med 1984;57:481-483. 4. Pachner AR: Spirochetal diseases of the CNS. NeuroI Clin 1986;4: 207-222. 5. Uldry PA, Regli F, Bogousslavsky J: Cerebral angiopathy and recurrent strokes following Borrelia burgdorferi infection. J Neurol Neurosurg Psy- chiatry 1987;50:1703-1704. 6. Reik L: Disseminated vasculomyelinepathy: An immune complex dis- ease. Ann Neurol 1980;7:291-296. 7. Halperin JJ, Luft BJ, Anand AK, et ah CNS Lyme disease (letter). Neurol ogy 1990;40:190.

Central Cord Syndrome

To the Editor: The neurologic deficit described in "Traumat ic Central

Cord Syndrome in a Pat ient Wi th Os Odon to ide um" by McGoldr i ck and Marx [December 1989;18:1358-1361], was a t t r ibuted to a central cord syndrome when, in fact, I be- lieve the symptoms can be more accurate ly explained by a paralysis' of Bell.

A central cord syndrome involves a spinal cord injury from bulging of the l igamenta flava against the anter ior vertebral bodies during f lexion of the cervical spine. 1 This injury causes injury to the central por t ion of the spinal cord (hence the name central cord injury) and results in weakness of the arms greater than the legs, loss of bladder function, and a variable degree of sensory loss. The vic- t ims are usual ly elderly, and the level of injury is usual ly in the lower cervical spine.

The paralysis of Bell is an injury to the pyramida l de- cussation, usual ly as a resul t of poster ior d i sp lacement of the odontoid. Anatomical ly , the pyramida l decussat ion of the cervical cord is direct ly poster ior to the odontoid, and this accounts for i ts po ten t i a l for. in jury w h e n e v e r the odontoid is displaced.

I bel ieve the neurologic symptoms tha t occurred in this pa t ien t and the pa thophys io logy that was proposed to ac- count for this deficit are mos t l ike ly explained by paral- ysis of Bell and not a central cord syndrome as reported by the author.

David J Dula, MD Emergency Medicine Geisinger Medical Center Danville, Pennsylvania

1. Schneider RD, Crosby EC: Traumatic spinal cord syndromes and their management. J Clin Neurosurg 1972;20:424-492.

In Reply: Dr Dula brings up the poin t that the neurologic deficits

described in our pat ient could be explained by a "crucia te paralysis of Bell," which involves injury to the pyramida l tract decussat ion. The "crucia te paralysis" as described by Bell involves se lec t ive b i l a t e ra l arm para lys is or te t ra- plegia. A les ion involving the rostral crossing fibers of the pyramidal decussa t ion m a y s imula te the neurologic pat- tern of "acute central cervical cord injury syndrome." In fact, two of the cases presented in Bell's original paper in- volved a neurologic pa t te rn that was in i t ia l ly classified as acute central cervical cord syndrome.

Our p a t i e n t p r e s e n t e d w i t h w e a k n e s s of the a rms greater than the legs wi thou t apparent sensory loss and loss of bladder function. We feel this pa t te rn of neurologic deficit is cons is ten t w i th central cord syndrome.

John McGoldrick, M D John Marx, M D Depar tment of Emergency Medicine Denver General Hospital Denver, Colorado

Sensitivity, Specificity & Positive & Negative Predictive Values

To the Editor." The article, "Fracture of the Carpal Navicular - Effi-

cacy of Cl in ica l Findings and Improved Diagnos i s W i t h Six-View Radiography" by M e h t a and Braut igan [March

1990;19:225-257], contains an error in s ta t is t ica l calcula- tion. Table 1 compares the results of four- and six-view r a d i o g r a p h y in d i agnos ing f rac tu res of the nav icu la r .

19:11 November 1990 Annals of Emergency Medicine 1354/175

Page 2: Sensitivity, specificity & positive & negative predictive values

CORRESPONOENCE

While the sens i t iv i ty of the four-view study is correct ly reported to be 83%, the specif ici ty and posi t ive predict ive values are given as 70% and 83%, respectively. Their cor- rect values are both 100%. The sensit ivi ty, specificity, and posi t ive predict ive value given for the six-view s tudy are all correct ly reported as 100%.

Perhaps the u t i l i ty of the addit ional two radiographic views that are part of the six-view s tudy is best i l lus t ra ted by the negative predict ive value, which was not given in this article. By the data presented, the negative predict ive

value of the four views is 69%, whi le that of the six views is 100%. This supports the authors ' conclus ion that nei- ther immobi l i za t ion nor fol low-up is needed given a nega- tive six-view study, provided that larger cl inical s tudies verify the resul ts of this invest igat ion.

Howard Blumstein, MD Medical College of Pennsylvania Philadelphia

Echocardiography to Rule Out Metastat ic

To the Editor. We w o u l d l ike to c o m m e n t on the case confe rence

"Ethical Considera t ions in Emergency Depa r tmen t Man- agement of Termina l ly Ill Pat ients" by Strange et al [Octo- ber 1989;18:1085-1088[. This case discussion involved the ethics of aggressive t rea tment and resusci ta t ion in a 78- year-old m a n wi th k n o w n ca rc inoma of the lung (diag- nosed two months pr ior to the presentat ion) who appar- en t ly developed an acute myocardia l infarction. This new diagnosis was based on "ECG changes compa t ib l e wi th acute an te ro la te ra l myoca rd i a l in fa rc t ion , " a l though the specifics of these ECG changes are not given.

We consider the discussion fol lowing the case presenta- t ion to be an excel lent one and our only concern was wi th the ini t ia l diagnost ic possibi l i t ies in this patient.

In any k n o w n cancer pa t ien t who presents wi th p r imary cardiac s igns /symptoms, the poss ibi l i ty of cardiac meta- s tases m u s t be en ter ta ined . The improved surv iva l af- forded by today's aggressive, m u l t i m o d a l i t y t r ea tmen t of m a n y m a l i g n a n c i e s has inc reased the f r e q u e n c y w i t h w h i c h m e t a s t a t i c d i sease is seen in c l i n i ca l p rac t i ce . 1 Metas ta t ic disease to the heart is one specific area where an increased incidence has been noted.~, 3 The mos t com- mon pr imary tumor responsible for cardiac metas tases is carc inoma of the bronchus, wi th breast, leukemias , lym- phomas, and mal ignant me lanomas l is ted in order of de- creasing frequency. The inc idence of me tas t a ses to the heart , inc lud ing the pe r ica rd ium, ranges f rom 1.5% to 20.6% of autopsies on pat ients wi th known mal ignan t dis- ease.4, 5

This patient , then, wi th no previous known cardiac his- tory and who presented wi th a chief compla in t of weak- ness, was found to have an abnormal ECG two mon ths after having lung cancer diagnosed. Electrocardiographic changes in m e t a s t a t i c d isease are qui te nonspecif ic , al- though Ha r tman et al have proposed that prolonged and p ronounced loca l ized S-T segment e leva t ion in the ab- sence of Q waves is a p a t h o g n o m i c sign of myoc a rd i a l t umor invasion. 6

Our only suggestion, wi th regard to this patient , is that a bedside 2D echocardiogram could have been def ini t ive in de te rmin ing the presence or absence of me tas ta t i c car- diac disease~, 2 and that w i th this knowledge, the decisions regarding aggressive ICU support versus pal l ia t ive treat- men t or specific oncologic therapy may be less controver- sial.

Disease

fi)hn M Tallon, MD Foothills Hospital

David R Montoya, MD, FRCP(C) Calgary General Hospital Calgary, Alberta, Canada 1. Stark RM, Derloff JK, Glick }H, et ah Clinical recognition and manage- ment of cardiac metastatic disease: Observations in a unique case of alveo- lar soft-part sarcoma. Am J Med 1977;63:653-659. 2. Hanfling SM: Metastatic cancer to the heart: Review of the literature and report of 127 cases. Circulation 1960~22:474-483. 3. Lockwood WB, Broghamer WL Jr: The changing prevalence of secondary cardiac neoplasms as related to cancer therapy. Cancer 1980;45:2659-2662.

4. Lammers RJ, Bloor CM: Tumors of the heart and pericardium. Modern Concepts of Cardio~'~scular Disease 1986i551-554. 5. Rosenthal DS, Braunwald E: Hematological-ontological disorders and heart disease, in Braunwald E {ed): Heart Disease, ed 3. Philadelphia, Wig Saunders, 1988, p 1284-1305. 6. Hartman RB, Sehulman P: Pronounced and prolonged ST segment eleva- tion: A pathognomic sign of tumour invasion to the heart. Arch Intern Med 1982;142:1917q919.

1~ Reply: I thank Drs Tal lon and M o n t o y a for the i r c o m m e n t s

and the addi t ion of another diagnost ic poss ib i l i ty to the discussion of the case. It is indeed possible that this pa- t ien t had metas ta t i c disease involving the heart. At the t ime of his arrest and unsuccessful resusci ta t ion, no addi- t iona l tests , e i ther cardiac e nz yme s or eehocard iogram, had been obtained. Your suggestion that bedside echoear- diography would have been defini t ive in rul ing out meta- s tases is also appreciated. Th is is an e n t i t y tha t is no doubt underdiagnosed.

As for the ethical considerat ions, they seem to me to remain pre t ty much the same regardless of the et iology of the ECG abnormal i ty . In e i the r case, pha rmaco log ic or electr ical therapy may have some shor t - te rm effect, but the under lying process remains progressive and terminal .

Gary Strange, MD, FACEP University of Illinois Affiliated Hospitals

Emergency Medicine Residency Chicago

176/1355 Annals of Emergency Medicine 19:11 November 1990