doi: 10.1001/archneur.1995.00540280009001pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archneur.1995.00540280016002pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archneur.1995.00540280017003pmid: 7710366
Abstract Ahern et al,1 in their otherwise interesting article on multiple personality and temporolimbic epilepsy, described a patient (patient 2) who, following left (dominant)-hemisphere inactivation, in addition to developing right hemiparesis, became "obtunded" and remained so for approximately 7 to 8 minutes. The authors proceeded, then, to say that this "was probably due to cross-fill of amobarbital into the contralateral anterior cerebral arterial territory, which resulted in bilateral frontal deactivation." Granted, transient delta slowing in the electroencephalogram was seen in the right frontal region, in addition to the areas supplied by the left anterior and middle cerebral arteries; but, considering that such electroencephalographic findings are not incompatible with unilateral test results, could not another explanation of the "obtundity" observed be found in the reported role of the dominant hemisphere for speech in matters of consciousness (Terzian2, Serafetinides et al,3 and Hommes and Panhuysen4). Indeed, a careful and References 1. Ahern GL, Herring AM, Tackenberg J, et al. The association of multiple personality and temporolimbic epilepsy . Arch Neurol . 1993;50:1020-1025.Crossref 2. Terzian H. Behavioral and EEG effects of intracarotid sodium amytal injection . Acta Neurochir . 1964;12:230-239.Crossref 3. Serafetinides EA, Hoare RD, Driver MV. Intracarotid sodium amytobarbitone and cerebral dominance for speech and consciousness . Brain . 1965;88:107-130.Crossref 4. Hommes OR, Panhuysen LHHM. Bilateral intracarotid amytal injection: a study of dysphasia, disturbance of consciousness and paresis . Psychiatr Neurol Neurochir . 1970;73:447-459.
doi: 10.1001/archneur.1995.00540280017004pmid: N/A
Abstract In reply I read Serafetinides' letter with interest. My colleagues and I1 did, indeed, attribute the obtundation of patient 2 during the left hemisphere intracarotid sodium amobarbital test as probably being due to cross-fill of amobarbital into the contralateral anterior cerebral artery territory, thereby leading to bilateralfrontal deactivation. Other possibilities were, however, considered, even if they were not discussed in that article. One of these possibilities was that of cerebral dominance for consciousness. The studies mentioned in Serafetinides' letter (eg, Serafetinides et al2) reported that inactivation of the language-dominant (usually left) hemisphere resulted in alterations in consciousness that were only infrequently seen (and were of shorter duration) with inactivation of the other hemisphere. Similar findings have been made in patients with cerebrovascular accidents.3While such findings have profound import for concepts of cerebral lateralization and consciousness, they are not without their share of controversy. In their landmark References 1. Ahern GL, Herring AM, Tackenberg J, et al. The association of multiple personality and temporolimbic epilepsy . Arch Neurol . 1993;50:1020-1025.Crossref 2. Serafetinides EA, Hoare RD, Driver MV. Intracarotid sodium amylobarbitone and cerebral dominance for speech and consciousness . Brain . 1965;88:107-130.Crossref 3. Albert ML, Silverberg R, Reches A, Berman M. Cerebral dominance for consciousness . Arch Neurol . 1976;33:453-454.Crossref 4. Plum F, Posner JB. Diagnosis of Stupor and Coma . 3rd ed. Philadelphia, Pa: FA Davis Co; 1982:22-23. 5. Rosadini G, Rossi GF. On the suggested cerebral dominance for consciousness . Brain . 1967;90:101-112.Crossref 6. Lesser RP, Dinner DS, Lüders H, Morris HH. Memory for objects presented soon after intracarotid amobarbital sodium injections in patients with medically intractable complex partial seizures . Neurology . 1986;36:895-899.Crossref 7. Gotman J, Bouwer MS, Jones-Gotman M. Intracranial EEG study of brain structures affected by internal carotid injection of amobarbital . Neurology . 1992; 42:2136-2143.Crossref 8. Bouwer MS, Jones-Gotman M, Gotman J. Duration of sodium amytal effect: behavioral and EEG measures . Epilepsia . 1993;34:61-68.Crossref 9. Ahern GL, Labiner DM, Hutzler R, et al. Quantitative analysis of the EEG in the intracarotid amobarbital test, I: amplitude analysis . Electroencephalogr Clin Neurophysiol . 1994;91:21-32.Crossref
Jeret, Joseph S.;Benjamin, Jeffrey
doi: 10.1001/archneur.1995.00540280018006pmid: N/A
Abstract In reply We thank Wijdicks for finding our study1 "very well done" and containing "important data," but it is not "more important than the authors realized themselves." The legal implications, eg, need for informed consent, are being explored (C. D. Zwiebel, Esq, oral communication). The moral implications of performing a potentially dangerous diagnostic test with no therapeutic implications for the patient2 are also being addressed (Abraham S. Abraham, MD, written communications, January, 21, 1990, and October 21, 1991, and J. David Bleich, PhD, a rabbi, written communication, December 24, 1992). The State University of New York institutional apnea testing protocol has also been modified. The medical implications and dire need to meticulously monitor patients during apnea testing are apparent from our study.We undertook our study because although the fact that "hypotension develops during apnea testing... is well recognized, " formal studies other than anecdotal reports were conspicuously lacking. References 1. Jeret JS, Benjamin J. Risk of hypotension during apnea testing . Arch Neurol . 1994;51:595-599.Crossref 2. Jeret JS. Rabbi Shlomo Zalman Auerbach's p'sak on 'brain death' reconfirmed . Jewish Observ . 1992;25:36-38. 3. Earnest MP, Beresford HR, McIntyre HB. Testing for apnea in suspected brain death: methods used by 129 clinicians . Neurology . 1986;36:542-544.Crossref 4. Allen N, Burkholder JD, Molinari GF, Comiscioni J. Clinical criteria of brain death . In: The NINCDS Collaborative Study of Brain Death . Bethesda, Md: National Institutes of Health; December 1980:77-147. Publication 81-2286. 5. Bruce DL. Blood gas values change slowly in apneic organ donors . Anesthesiology . 1986;65:128.Crossref 6. Caronna JJC. Bedside testing to determine apnea . Neurol Alert . 1992;10:72. 7. Pitts LH, Kaktis J, Caronna J, Jennett S, Hoff JT. Brain death, apneic diffusion oxygenation, and organ transplantation . J Trauma . 1978;18:180-183.Crossref 8. Ropper AH, Kennedy SK, Russell L. Apnea testing in the diagnosis of brain death . J Neurosurg . 1981;55:942-946.Crossref 9. Benzel EC, Gross CD, Hadden TA, Kesterson L, Landreneau MD. The apnea test for the determination of brain death . J Neurosurg . 1989;71:191-194.Crossref
doi: 10.1001/archneur.1995.00540280018005pmid: 7710367
Abstract Maintaining a minimum systolic blood pressure of 90 mm Hg ensures adequate perfusion to all vital organs that may potentially be used for donation. That hypotension develops during apnea testing in certain patients who otherwise fulfill the clinical criteria of brain death is well recognized. Causes of hypotension in brain death may be related to cardiac arrhythmias, cardiac stunning, diabetes insipidus, prior use of diuretics and fluid restriction in the management of primary brain injury, or loss of arterial and venous sympathetic tone as a result of destruction of the pontine and medullary vasomotor structures.1 Neurologists do not like to perform apnea testing, and they do it in an inappropriate manner. In a survey of neurologists in Colorado and California, Earnest et al2 found that only one of eight neurologists vigorously performed apnea testing by providing 100% oxygen during testing and by measuring arterial blood gas levels. One References 1. Darby JM, Stein K, Grenvik A, Stuart SA. Approach to management of the heart beating 'brain dead' organ donor . JAMA . 1989;261:2222-2228.Crossref 2. Earnest MP, Beresford HR, McIntyre HB. Testing for apnea in suspected brain death: methods used by 129 clinicians . Neurology . 1986;36:542-544.Crossref 3. Jeret JS, Benjamin JL. Risk of hypotension during apnea testing . Arch Neurol . 1994;51:595-599.Crossref
Scheinberg, I. Herbert;Sternlieb, Irmin
doi: 10.1001/archneur.1995.00540280019007pmid: 7710368
Abstract Because of their concern that initial treatment of neurologically manifest Wilson's disease with penicillamine can cause worsening of the neurologic symptoms, Brewer and colleagues1 have used ammonium tetrathiomolybdate as the initial treatment in 11 such patients. Six additional patients, who had been initially treated with penicillamine, were subsequently treated with ammonium tetrathiomolybdate. During 8 weeks of treatment with tetrathiomolybdate, "None of the patients suffered a loss of neurologic function."1 In the follow-up period of 1 to 5 years, during which the patients received only 150mg of zinc acetate daily, there was"... substantial improvement (of neurologic function) in almost all patients."1 In the past 35 years, we ourselves, or as consultants to other physicians, have prescribed initial treatment with penicillamine for hundreds of patients with Wilson's disease, of whom about 40% were affected neurologically. Neurologic worsening occurred in about 10% of the latter group in the weeks following References 1. Brewer GJ, Dick RD, Johnson V, et al. Treatment of Wilson's disease with ammonium tetrathiomolybdate . Arch Neurol . 1994;51:545-554.Crossref 2. Cumings JN. The effects of BAL in hepatolenticular degeneration . Brain . 1951; 74:10-22.Crossref 3. Scheinberg IH, Sternlieb I. Treatment . In: Wilson's Disease . Philadelphia, Pa: WB Saunders Co; 1984:146.
doi: 10.1001/archneur.1995.00540280019008pmid: N/A
Abstract In reply The main point of the letter by Scheinberg and Sternlieb seems to be that penicillamine is an excellent therapy most of the time for patients with Wilson's disease who present with neurologic disease and, when it is not, injections with British anti-Lewisite are often helpful. The apparent implication is that, in their hands, problems with initial therapy are so few that development of an additional agent for this purpose, such as the tetrathiomolybdate therapy that we reported,1 is not worthwhile.The major problem with the assertions of Scheinberg and Sternlieb is that they are based on the notoriously inaccurate "clinical impression" rather than on rigorously established scientific fact. For example, they say that for 35 years "ourselves, or as consultants to other physicians, have prescribed initial treatment with penicillamine for hundreds of patients." Specifically, how many patients is "hundreds"?A scientific study would not say "hundreds," but would References 1. Brewer GJ, Dick RD, Johnson V, et al. Treatment of Wilson's disease with tetrathiomolybdate . Arch Neurol . 1994;51:545-554.Crossref 2. Brewer GJ, Terry CA, Aisen AM, Hill GM. Worsening of neurological syndrome in patients with Wilson's disease with initial penicillamine therapy . Arch Neurol . 1987;44:490-494.Crossref
doi: 10.1001/archneur.1995.00540280024009pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract Neuropsychiatric Disorders is a strikingly beautiful book. The quality, color, and elegance of the figures and illustrations are so far superior to any other publication that I have seen on this topic that I cannot do justice to it in a black-and-white book review. The clinical and research utility of the figures and photographs is also striking. For example, how many times have we wondered in looking at a magnetic resonance or computed tomographic image where the picture cortex was in terms of Brodmann's areas on the cortical surface? The first section of Neuropsychiatric Disorders provides a color-keyed set of serial illustrations of computed tomographic slices showing Brodmann's areas that are illustrated on each coronal cut. One can use this index to match up lesion neuroanatomy in an axial or coronal plane with known neuroanatomy. The next section provides an overview of the neuropsychiatric disorders that produce cognitive loss. Pathologic
doi: 10.1001/archneur.1995.00540280024010pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract Issues of sexuality and disability are arguably among the last to receive attention in the burgeoning field of comprehensive rehabilitation that has taken place over the past 10 to 15 years. As such, there is a relative dearth of professional reading materials and conferences related to this subject. However, the issues of sexuality and disability, especially related to traumatic brain injury (TBI) and stroke, have been receiving increasing attention in terms of the numbers of books, journal articles, and conferences devoted to this issue over the past few years. This book, by Dr Ernest R. Griffith and Sally Lemberg, is a welcome addition to the issues of sexuality and TBI, especially in its emphasis as a resource for family members. The book first provides an overview of human sexual anatomy and function. The second chapter contributes a relatively comprehensive description of brain anatomy and function. Chapters 3 and 4 delineate
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