Archives of Neurology

Fromm, Gerhard H.

doi: 10.1001/archneur.1984.04210080001002pmid: 6721731

Abstract Pain is the most common reason that patients seek medical help. Pain continues to present difficulties, however, as regards both its definition and the methods for accurately measuring it. Our inability to quantify pain adequately has handicapped the comparison of different analgesic drugs, as well as the treatment of pain in general.1 One of the main problems in measuring pain is that the word pain refers to a great variety of sensory experiences rather than a single specific sensation varying only in intensity.2 A number of more sophisticated ways of measuring pain have therefore been proposed, such as the McGill-Melzack pain questionnaire,2 measurements based on signal detection theory,3 and functional measurement scaling.4 Another difficulty in accurately assessing the potency of analgesic drugs is the sizable number of patients who exhibit a substantial placebo response. The importance of the placebo response in the treatment of Pain References 1. Painful communications, editorial . Lancet 1980;1:805. 2. Melzack R: The McGill pain questionnaire: Major properties and scoring methods . Pain 1975;1:277-299.Crossref 3. Clark WC: Pain sensitivity and the report of pain: An introduction to sensory decision theory . Anesthesiology 1974;40:272-287.Crossref 4. Gracely RH, Wolskee PJ: Semantic functional measurement of pain: Integrating perception and language . Pain 1983;15:389-398.Crossref 5. Beecher HK: Measurement of Subjective Responses . New York, Oxford University Press, 1959. 6. Kugelberg E, Lindblom U: The mechanism of the pain in trigeminal neuralgia . J Neurol Neurosurg Psychiatry 1959;22:36-43.Crossref 7. Tomson T, Tybring G, Bertilsson L, et al: Carbamazepine therapy in trigeminal neuralgia: Clinical effects in relation to plasma concentration . Arch Neurol 1980;37:699-703.Crossref 8. Fromm GH, Terrence CF, Chattha AS: Baclofen in the treatment of trigeminal neuralgia: Double-blind study and long-term follow-up. Ann Neurol, in press. 9. Rockliff BW, Davies EH: Controlled sequential trials of carbamazepine in trigeminal neuralgia . Arch Neurol 1966;15:129-136.Crossref 10. Killian JM, Fromm GH: Carbamazepine in the treatment of trigeminal neuralgia: Use of side effects . Arch Neurol 1968;19:129-136.Crossref 11. Tomson T, Bertilsson L: Potent therapeutic effect of carbamazepine-10,11-epoxide in trigeminal neuralgia . Arch Neurol 1984;41:598-601.Crossref

Stein, Bennett

doi: 10.1001/archneur.1984.04210080001001pmid: 6721730

Abstract The article by Khatri et al1 is a contribution to the developing field of lumbar disk diagnosis. Even with the development of water-soluble contrast media in myelography, there is still an aversion on the part of the physician and especially his patient toward myelography. Therefore, the computed tomographic (CT) scan with and without contrast is finding greater use as a primary diagnostic measure for lumbar disk disease and for spinal stenosis and spinal spondylosis. This article sets out to correlate the various diagnostic measures, including electromyogram (EMG), CT scan, myelography, and the findings at surgery. In the group of patients with abnormal findings of disk disease or spinal stenosis, there was excellent correlation between CT and EMG abnormal findings and the pathologic findings at the time of surgery. The conclusion appears justified that in the presence of an abnormal CT scan and EMG a physician can make an accurate References 1. Khatri BO, Baruah J, McQuillen MP: Correlation of electromyography with computed tomography in evaluation of lower back pain . Arch Neurol 1984;41:594-597.Crossref

Khatri, Bhupendra O.;Baruah, Jitendra;McQuillen, Michael P.

doi: 10.1001/archneur.1984.04210080002003pmid: 6232914

Abstract • High-resolution computed tomography (CT) of the lumbar spine in 80 consecutive patients with lower back pain was correlated with electromyography (EMG) and with the clinical outcome at one-year follow-up. Forty-two patients had abnormal EMG findings that could be explained on the basis of anatomical defect(s) seen on CT. Nine had normal CT scans but abnormal EMGs, and five patients had normal EMGs but abnormal CT scans. Thirteen of the 80 patients were further investigated with myelography, 22 patients underwent surgical exploration, and the remainder received conservative therapy. In the majority of cases, surgery confirmed the abnormal CT and EMG findings; in some instances, however, myelography and/or surgery confirmed the abnormality only at the level demonstrated on EMG. The CT and EMG often agree. However, an abnormal EMG seems to correlate better with the demonstrated course of radiculopathy than CT. References 1. Johnson EW, Melvin JL: The value of electromyography in the management of lumbar radiculopathy (abstract) . Arch Phys Med Rehabil 1969;50:720. 2. Johnson EW, Melvin JL: Value of electromyography in lumbar radiculopathy . Arch Phys Med Rehabil 1971;52:239-243. 3. Flax HJ, Berrios R, Rivera D: Electromyography in diagnosis of herniated lumbar disk . Arch Phys Med Rehabil 1964;45:520-524. 4. Gough JG, Koepke GM: Electromyographic determination of motor root levels in erector spinae muscles . Arch Phys Med Rehabil 1966; 47:9-11. 5. Tonzola RF, Ackil AA, Shahahi BT, et al: Usefulness of electrophysiological studies in the diagnosis of lumbosacral root disease . Ann Neurol 1981;9:305-308.Crossref 6. Knuttson B: Comparative value of electromyographic, myelographic, and clinical-neurological examination in diagnosis of lumbar root compression syndrome . Ada Orthop Scand 1961; 49( (suppl) ):1-135. 7. Seppalainen AM, Alaranta H, Soini J: Electromyography in the diagnosis of lumbar spinal stenosis . Electromyogr Clin Neurophysiol 1981; 21:55-66. 8. Sheldon JJ, Sersland T, Leborgne J: Computed tomography of the lumbar vertebral column: Normal anatomy and the stenotic canal . Radiology 1977;124:113-118.Crossref 9. Hammerschlag SB, Wolpert SM, Carter BL: Computed tomography of the spinal canal . Radiology 1976;121:361-367.Crossref 10. Jacobson RE, Gargano FP, Rosomoff HL: Transverse axial tomography of the spine: I: Axial anatomy of the normal lumbar spine . J Neurosurg 1975;42:406-411.Crossref 11. Haughton VM, Syvertsen A, Williams AL: Soft-tissue anatomy within the spinal canal as seen on computed tomography . Radiology 1980; 134:649-655.Crossref 12. Lee BCP, Kazam E, Newman AD: Computed tomography of the spine and spinal cord . Radiology 1978;128:95-102.Crossref 13. Williams AL, Haughton VM, Syvertsen A: Computed tomography in the diagnosis of herniated nucleus pulposus . Radiology 1980;135:95-99.Crossref

Tomson, Torbjörn;Bertilsson, Leif

doi: 10.1001/archneur.1984.04210080006004pmid: 6721732

Abstract • The clinical effects of carbamazepine-10,11-epoxide were assessed in six patients with trigeminal neuralgia. The patients were first given an optimal therapeutic dose of carbamazepine. Part of or the entire carbamazepine dose was then exchanged for the metabolite carbamazepine-10,11-epoxide for three to six days. The patients were unaware of changes in the therapeutic regimen (single-blind). Carbamazepine dosages ranged from 400 to 1,400 mg/day and carbamazepine10,11-epoxide dosages ranged from 300 to 1,000 mg/day. The clinical effects were assessed by the patients' recordings of pain attacks. When carbamazepine-10,11-epoxide and carbamazepine were given in similar doses, the pain control was comparable. On a plasma concentration basis, carbamazepine10,11-epoxide had a considerably higher pain-relieving potency than carbamazepine. During carbamazepine treatment, the epoxide metabolite contributes to the antineuralgic effect to an extent that might be comparable to that of the parent drug. No side effects were seen during carbamazepine-10,11-epoxide therapy. References 1. Kutt H: Anticonvulsant blood levels in the management of epileptic patients , in Klawans HL (ed): Clinical Neuropharmacology . New York, Raven Press, 1978, pp 1-13. 2. Atkinson AJ Jr, Stec GP, Lertora JJL, et al: Impact of active metabolites on monitoring plasma concentrations of therapeutic drugs . Ther Drug Monit 1980;2:19-27.Crossref 3. Porter RJ: Clinical efficacy and use of antiepileptic drugs , in Woodbury DM, Penry JK, Pippenger CE (eds): Antiepileptic Drugs , ed, 2. New York, Raven Press, 1982, pp 167-175. 4. Blom S: Tic douloureux treated with new anticonvulsant: Experiences with G 32883 . Arch Neural 1963;9:285-290.Crossref 5. Faigle JW, Feldmann KF: Carbamazepine biotransformation , in Woodbury DM, Penry JK, Pippenger CE (eds): Antiepileptic Drugs , ed, 2. New York, Raven Press, 1982, pp 483-495. 6. Faigle JW, Feldmann KF, Baltzer V: Anticonvulsant effect of carbamazepine: An attempt to distinguish between the potency of the parent drug and its epoxide metabolite , in Gardner-Thorpe C, Janz D, Meinardi H, et al (eds): Antiepileptic Drug Monitoring . London, Pitman Press, 1977, pp 104-108. 7. Morselli PL, Gerna M, de Maio D, et al: Pharmacokinetic studies on carbamazepine in volunteers and in epileptic patients , in Schneider H, Janz D, Gardner-Thorpe C, et al (eds): Clinical Pharmacology of Antiepileptic Drugs . Berlin, Springer-Verlag, 1975, pp 166-180. 8. McKauge L, Tyrer JH, Eadie MJ: Factors influencing simultaneous concentrations of carbamazepine and its epoxide in plasma . Ther Drug Monit 1981;3:63-70.Crossref 9. Pynnönen S, Sillanpää M, Frey H, et al: Carbamazepine and its 10,11-epoxide in children and adults with epilepsy . Eur J Clin Pharmacol 1977;11:129-133.Crossref 10. Rane A, Höjer B, Wilson JT: Kinetics of carbamazepine and its 10,11-epoxide metabolite in children . Clin Pharmacol Ther 1976; 19:276-283. 11. Schneider H, Berenguer J: CSF and plasma concentrations of carbamazepine and some metabolites in steady state , in Gardner-Thorpe C, Janz D, Meinardi H, et al (eds): Antiepileptic Drug Monitoring . London, Pitman Press, 1977, pp 264-273. 12. Dam M, Sury J, Christiansen J: Has carbamazepine-10,11-epoxide an independent antiepileptic effect in man? in Penry JK (ed): Epilepsy: The Eighth International Symposium . New York, Raven Press, 1977, pp 143-146. 13. Eichelbaum M, Bertilsson L, Lund L, et al: Plasma levels of carbamazepine and carbamazepine-10,11-epoxide during treatment of epilepsy . Eur J Clin Pharmacol 1976;9:417-421.Crossref 14. Sillanpää M, Pynnönen S, Laippala P, et al: Carbamazepine in the treatment of partial epileptic seizures in infants and young children: A preliminary study . Epilepsia 1979;20:563-569.Crossref 15. Strandjord RE, Johannessen SI: Singledrug therapy with carbamazepine in patients with epilepsy: Serum levels and clinical effect . Epilepsia 1980;21:655-662.Crossref 16. Tomson T, Tybring G, Bertilsson L, et al: Carbamazepine therapy in trigeminal neuralgia: Clinical effects in relation to plasma concentration . Arch Neurol 1980;37:699-703.Crossref 17. Tomson T: Interdose fluctuations in carbamazepine plasma concentration in relation to intermittent side effects. Arch Neurol, in press. 18. Tomson T, Tybring G, Bertilsson L: Single dose kinetics and metabolism of carbamazepine10,11-epoxide . Clin Pharmacol Ther 1983;33:58-65.Crossref 19. Kugelberg E, Lindblom U: The mechanism of the pain in trigeminal neuralgia . J Neurol Neurosurg Psychiatry 1959;22:36-43.Crossref 20. Tomson T, Ekbom K: Trigeminal neuralgia: Time course of pain in relation to carbamazepine dosing . Cephalalgia 1981;1:91-97.Crossref 21. Rockliff BW, Davies EH: Controlled sequential trials of carbamazepine in trigeminal neuralgia . Arch Neurol 1966;15:129-136.Crossref 22. Eichelbaum M, Ekbom K, Bertilsson L, et al: Plasma kinetics of carbamazepine and its epoxide metabolite in man after single and multiple doses . Eur J Clin Pharmacol 1975;8:337-341.Crossref 23. Bertilsson L, Höjer B, Tybring G, et al: Autoinduction of carbamazepine metabolism in children examined by a stable isotope technique . Clin Pharmacol Ther 1980;27:83-88.Crossref

Zimmer, Reinhilde;Teelken, Albert W.;Trieling, Wilhelm B.;Weber, Werner;Weihmayr, Thomas;Lauter, Hans

doi: 10.1001/archneur.1984.04210080010005pmid: 6721733

Abstract • The investigation of enzyme and neurotransmitter levels and/or their metabolites in the CSF of patients with senile dementia of Alzheimer's type (SDAT) could become a promising approach for a clinical research and diagnostic procedure. To learn more about the metabolic reflections of central metabolism in the CSF of patients with SDAT, we measured CSF levels of γ-aminobutyric acid (GABA) and homovanillic acid (HVA), the dopamine metabolite. In 16 female patients with SDAT and in eight matched control patients, CSF GABA levels were measured by ion exchange with fluorimetric detection, and HVA levels were measured fluorimetrically. The GABA content of the CSF was significantly reduced in patients with SDAT, whereas the HVA level was unchanged. References 1. Pope A, Hess HA, Lewin E: Microchemical pathology of the cerebral cortex in pre-senile dementias . Trans Am Neurol Assoc 1965;89:15-16. 2. Bowen DM, Smith CB, White P, et al: Neurotransmitter-related enzymes and indices of hypoxia in senile dementia and other abiotrophies . Brain 1976;99:459-495.Crossref 3. Davies P, Maloney AYE: Selective loss of central cholinergic neurons in Alzheimer's disease . Lancet 1976;2:1403.Crossref 4. Davies P: Neurotransmitter-related enzymes in senile dementia of Alzheimer type . Brain Res 1979;171:319-327.Crossref 5. Perry EK, Gibson PH, Blessed G, et al: Neurotransmitter enzyme abnormalities in senile dementia . J Neurol Sci 1977;34:247-265.Crossref 6. Rossor MN, Emson PC, Iversen LL, et al: Neuropeptides and neurotransmitters in cerebral cortex of Alzheimer's disease , in Corkin S, Davis KL, Growdon HJ, et al (eds): Aging . New York, Raven Press, 1982, vol 19 7. Alzheimer's Disease: A Report of Progress, pp 15-24. 8. Gottfries CG, Gottfries J, Roos BE: The investigation of homovanillic acid in the human brain and its correlation to senile dementia . Br J Psychiatry 1969;115:563-574.Crossref 9. Winblad B, Adolfsson R, Carlsson A, et al: Biogenic amines in brains of patients with Alzheimer's disease , in Corkin S, Davis KL, Growden HJ, et al (eds): Aging . New York, Raven Press, 1982, vol 19 10. Alzheimer's Disease: A Report of Progress, pp 25-33. 11. Bernheimer H, Birkmayer W, Hornykiewicz O: Homovanillic acid in the cerebrospinal fluid . Experientia 1966;609-610. 12. Gottfries CG, Kjällquist A, Pontén U, et al: Cerebrospinal fluid pH and monoamine and glycolytic metabolites in Alzheimer's disease . Br J Psychiatry 1974;24:280-287.Crossref 13. Soininen H, MacDonald E, Rekonen M, et al: Homovanillic and 5-hydroxy-indole-acetic acid levels in cerebrospinal fluid of patients with senile dementia of Alzheimer type . Acta Neurol Scand 1981;64:101-107.Crossref 14. Growdon JH, Logue M: Choline, HVA and 5-HIAA levels in cerebrospinal fluid of patients with Alzheimer's disease , in Corkin S, Davis KL, Growdon HJ, et al (eds): Aging . New York, Raven Press, 1982, vol 19 15. Alzheimer's Disease: A Report of Progress, pp 35-43. 16. Bowen DM, Sims NR, Benton S, et al: Biochemical changes in cortical brain biopsies from demented patients in relation to morphological findings and pathogenesis , in Corkin S, Davis KL, Growdon HJ, et al (eds): Aging . New York, Raven Press, 1982, vol 19 17. Alzheimer's Disease: A Report of Progress, pp 1-7. 18. Yates CM, Allison Y, Simpson J, et al: Dopamine in Alzheimer's disease and senile dementia . Lancet 1979;2:851-852.Crossref 19. Mann DMA, Lincoln J, Yates PO, et al: Changes in the monoamine containing neurones of the human CNS in senile dementia . Br J Psychiatry 1980;136:533-541.Crossref 20. Rinne UK: Parkinson's disease as a model for changes in dopamine receptor dynamics with aging . Gerontology 1982;28( (suppl 1) ):35-52.Crossref 21. Albert E: Senile Demenz und Alzheimer'sche Krankheit als Ausdruck des gleichen Krankheitsgeschehens . Fortschr Neurol Psychiatr 1964;32:625-673. 22. Enna SJ, Stern LZ, Wastek GJ, et al: Cerebrospinal fluid γ-aminobutyric acid variations in neurological disorders . Arch Neurol 1977;34:683-685.Crossref 23. Glaeser BS, Hare TA: Measurement of GABA in human cerebrospinal fluid . Biochem Med 1975;12:274-282.Crossref 24. Huizinga JD, Teelken AW, Muskiet FA, et al: Gamma aminobutyric acid determination in human cerebrospinal fluid by mass fragmentography . J Neurochem 1978;30:911-913.Crossref 25. Enna SJ, Wood JH, Snyder SH: γ-Aminobutyric acid (GABA) in human cerebrospinal fluid: Radioreceptor assays . J Neurochem 1977; 28:1121-1124.Crossref 26. Manyam BNV, Katz L, Hare TA, et al: Levels of γ-aminobutyric acid in cerebrospinal fluid in various neurologic disorders . Arch Neurol 1980;37:352-355.Crossref 27. Rosen WG, Terry RD, Fuld PA, et al: Pathological verification of ischemic score in differentiation of dementias . Ann Neurol 1980; 7:486-488.Crossref 28. Folstein FM, Folstein SE, McHugh PR: 'Mini Mental State': A practical method for grading the cognitive state of patients for clinician . J Psychiatr Res 1975;12:189-198.Crossref 29. Böhlen, P, Schechter PJ, van Damme W, et al: Automated assay of γ-aminobutyric acid in human cerebrospinal fluid . Clin Chem 1978; 24:256-260. 30. Westerink RHC, Korf J: Determination of nanogram amount of homovanillic acid in the central nervous system with a rapid semiautomatic fluorometric method . Biochem Med 1975; 12:106-115.Crossref 31. Zimmer R, Teelken AW, Gündürewa M, et al: Effect of sodium valproate on CSF GABA, cAMP, cGMP and homovanillic acid levels in men . Brain Res Bull 1980;5( (suppl 5) ):585-588.Crossref 32. Zimmer R, Teelken AW, Meider KD, et al: Preliminary studies on CSF gamma-aminobutyric acid levels in psychiatric patients before and during treatment with different psychotropic drugs . Prog Neuropsychopharmacol Biol Psychiatry 1981;4:613-620.Crossref 33. Perry LP, Hansen S, Wall RA, et al: Human CSF GABA concentrations: Revised downward for controls, but not decreased in Huntington's chorea . J Neurochem 1982;38:766-773.Crossref 34. Kolata GB: Clues to the cause of senile dementia: Patients with Alzheimer's disease seem to be deficient in a brain neurotransmitter . Science 1981;211:1032-1033.Crossref 35. Böhlen P, Hout S, Palfreyman MC: The relationship between GABA concentrations in brain and cerebrospinal fluid . Brain Res 1979;167-297-305.Crossref 36. Reisine TD, Yamamura HJ, Bird ED, et al: Pre- and postsynaptic neurochemical alterations in Alzheimer's disease . Brain Res 1978;159:477-481.Crossref 37. Hare TA, Manyam BNV, Glaeser BS: Evaluation of cerebrospinal fluid γ-aminobutyric acid content in neurological and psychiatric disorders , in Wood JH (eds): Neurobiology of Cerebrospinal Fluid . New York, Plenum Publishing Corp, 1980, pp 171-187. 38. Glaeser BS, Vogel WH, Oleweiler DB, etal: GABA levels in cerebrospinal fluid of patients with Huntington's chorea: A preliminary report . Biochem Med 1975;12:380-385.Crossref 39. Lakke JPWF, Teelken AW: Amino acid abnormalities in cerebrospinal fluid in patients with parkinsonism and extrapyramidal disorders . Neurology 1976;26:489-493.Crossref 40. Lakke JPWF, de Jong PJ, Teelken AW: CSF GABA levels in Parkinson's disease, abstract No. 20 . Abstracts of the Seventh International Symposium on Parkinson's Disease , Frankfurt, West Germany, June 1982.

Levy, Robert J.;Krall, Ronald L.

doi: 10.1001/archneur.1984.04210080013006pmid: 6721734

Abstract • Twenty-one episodes of status epilepticus (SE) were each treated with 1 to 9 mg (mean, 4 mg) of intravenous lorazepam. All patients with generalized tonicclonic (GTC) SE responded within 15 minutes. Nine (82%) of the 11 patients with episodes of partial SE with altered responsiveness responded poorly. Respiratory depression occurred in five instances (two requiring intubation) and was associated with transient loss of brain-stem reflexes, hypotension, and decorticate posturing in three cases. Generalized tonic-clonic SE was transformed into partial SE with altered responsiveness in three patients. In an additional four patients, marked lethargy developed. Lorazepam appears effective in controlling GTC SE but only occasionally effective in partial SE with altered responsiveness. References 1. Delgado-Escueta AV, Bajorek JG: Status epilepticus: Mechanisms of brain damage and rational management . Epilepsia 1982;23( (suppl 1) ):S29-S41.Crossref 2. Treiman DM, Delgado-Escueta AV: Status epilepticus , in Thompson RA, Green JR (eds): Critical Care of Neurological and Neurosurgical Emergencies . New York, Raven Press, 1980, pp 53-99. 3. Chapman AG, Meldrum BS, Siesjö BK: Cerebral metabolic changes during prolonged epileptic seizures in rats . J Neurochem 1977; 28:1025-1035.Crossref 4. Meldrum BS, Horton RW, Brierley JB: Epileptic brain damage in adolescent baboons following seizures induced by allylglycine . Brain 1974;97:407-418.Crossref 5. Meldrum BS, Vigouroux RA, Brierley JB: Systemic factors and epileptic brain damage: Prolonged seizures in paralyzed artificially ventilated baboons . Arch Neurol 1973;29:82-87.Crossref 6. Rowan AJ, Scott DF: Major motor status epilepticus . Acta Neurol Scand 1970;46:573-584.Crossref 7. Whitty CWM, Taylor M: Treatment of status epilepticus . Lancet 1949;2:591-594.Crossref 8. Wasterlain CG, Plum F: Vulnerability of developing rat brain to electroconvulsive seizures . Arch Neurol 1973;29:38-45.Crossref 9. Duffy FH, Lombroso CT: Treatment of status epilepticus , in Klawans HL (ed): Clinical Neuropharmacology . New York, Raven Press, 1978, vol 3, pp 41-56. 10. Delgado-Escueta AV, Wasterlain C, Treiman DM, et al: Management of status epilepticus . N Engl J Med 1982;306:1337-1340.Crossref 11. Celesia GG: Modern concepts of status epilepticus . JAMA 1976;12:1571-1574.Crossref 12. Browne TR: Drug therapy reviews: Drug therapy of status epilepticus . Am J Hosp Pharm 1978;35:915-922. 13. Booker HE, Celesia GG: Serum concentrations of diazepam in subjects with epilepsy . Arch Neurol 1973;29:191-194.Crossref 14. Walker JE, Homan RW, Vasko MR, et al: Lorazepam in status epilepticus . Ann Neurol 1979;6:207-213.Crossref 15. Sorel L, Mechler L, Harmant J: Comparative trial of intravenous lorazepam and clonazepam in status epilepticus . Clin Ther 1981;4:326-336. 16. Amand G, Evard P: Injectable lorazepam in epilepsy . Rev Electroencephalogr Neurophysiol Clin 1976;6:532-533.Crossref 17. Abstracted , Epilepsy Abstracts , 1978, 11/158. 18. Waltregny A, Darjent J: Preliminary study of parenteral lorazepam in status epilepticus . Ada Neurol Belg 1975;75:219-229. 19. Griffith PA, Karp HR: Lorazepam in therapy for status epilepticus . Ann Neurol 1980; 7:493.Crossref 20. Pires de Oliveira RS: Treatment of convulsive seizure with a new benzodiazepine, lorazepam: Pilot study . Rev Bras Clin Ter 1978;7:415-422. 21. Leppik IE, Derivan AT, Homan RW et al: Double-blind study of lorazepam and diazepam in status epilepticus . JAMA 1983;249:1452-1454.Crossref 22. Gluckman MI, Stein L: Pharmacology of lorazepam . J Clin Psychiatry 1978;39:3-10. 23. Greenblatt DJ, Comer WH, Elliott HW, et al: Clinical pharmacokinetics of lorazepam: III. Intravenous injection . J Clin Pharmacol 1977; 17:490-494.Crossref 24. Ameer B, Greenblatt DJ: Lorazepam: A review of its clinical pharmacological properties and therapeutic uses . Drugs 1981;21:161-200.Crossref 25. Cormack RS, Milledge JS, Hanning CD: Respiratory effects and amnesia after premedication with morphine or lorazepam . Br J Anaesth 1977;49:351-361.Crossref 26. Elliott HW, Nomof N, Navarro G, et al: Central nervous system and cardiovascular effects of lorazepam in man . Clin Pharmacol Ther 1971;12:468-481. 27. Denaut M, Yernault JC, DeCoster A: Double-blind comparison of the respiratory effects of parenteral lorazepam and diazepam in patients with chronic obstructive lung disease . Curr Med Res Opin 1975;2:611-615.Crossref 28. Guerrero-Figueroa R, Guerrero-Figueroa E, Sneed GA, et al: Effects of lorazepam on CNS structures: Neurophysiological and behavioral correlations . Curr Ther Res 1974;16:137-146. 29. Browne TR, Penry JK: Benzodiazepines in the treatment of epilepsy . Epilepsia 1973;14:277-310.Crossref 30. Jaffe R, Christoff NJ: Intravenous diazepam in seizure disorders . Electroencephalogr Clin Neurophysiol 1967;23:77-97.Crossref 31. Laguna JF, Korein J: Diagnostic value of diazepam in electroencephalography . Arch Neurol 1972;26:265-272.Crossref 32. Pensky AL, Raff MC, Moore MJ, et al: Intravenous diazepam in the treatment of prolonged seizure activity . N Engl J Med 1967; 276:779-784.Crossref

Kish, Stephen J.;Shannak, Kathleen S.;Rajput, Ali H.;Gilbert, Joseph J.;Hornykiewicz, Oleh

doi: 10.1001/archneur.1984.04210080020007pmid: 6721735

Abstract • Norepinephrine was measured in postmortem cerebellar cortex of 22 non-neurological control subjects and nine patients with Parkinson's disease, using the high-performance liquid chromatography method with amperometric detection. In all control subjects, substantial amounts of norepinephrine were found in cerebellar cortex. There was a moderate negative correlation between age of control subjects and cerebellar norepinephrine concentration. In the patients with Parkinson's disease, the cerebellar cortical norepinephrine levels were significantly below normal. This is in accord with previously reported reduced norepinephrine levels in locus ceruleus and other regions of the parkinsonian brain. Although the main symptoms of Parkinson's disease are primarily caused by disturbed basal ganglia (dopamine) function, cerebellar dysfunction related to norepinephrine may contribute to some abnormalities of motor performance in this disorder. References 1. Hassler R: Zur Pathologie der Paralysis agitans und der post-Encephalitischen Parkinsonismus . J Psychol Neurol 1938;48:387-476. 2. Klaue R: Parkinsonische Krankheit (Paralysis agitans) und post-Encephalitischen Parkinsonismus . Arch Psychiatr Nervenkr 1940; 111:251-321.Crossref 3. Greenfield JG, Bosanquet FD: The brainstem lesions in Parkinsonism . J Neurol Neurosurg Psychiatry 1953;16:213-226.Crossref 4. Moore RY, Bloom FE: Central catecholamine neuron systems: Anatomy and physiology of the norepinephrine and epinephrine systems . Ann Rev Neurosci 1979;2:113-168.Crossref 5. Hgornykiewicz O: Brain dopamine in Parkinson's disease and other neurological disorders , in Horn AS, Korf J, Westerink BHC (eds): The Neurobiology of Dopamine . New York, Academic Press Inc, 1979, pp 633-654. 6. Farley IJ, Hornykiewicz O: Noradrenaline in subcortical brain regions of patients w Parkinson's disease and control subjects , in Birkmayer W, Hornykiewicz O (eds): Advances Parkinsonism . Basel, Switzerland, Editiones Roche, 1976, pp 178-185. 7. Sano I, Gamo T, Kakimoto Y, et al: Distribution of catechol compounds in human brain . Biochim Biophys Ada 1959;32:586-587.Crossref 8. Bertler A: Occurrence and localization of catecholamines in the human brain . Acta Physiol Scand 1961;51:97-107.Crossref 9. Rinne UK, Sonninen V: Brain catecholamines and their metabolites in parkinsonian patients . Arch Neurol 1973;28:107-110.Crossref 10. Mann DMA, Lincoln J, Yates PO, et al: Changes in the monoamine containing neuro es of the human CNS in senile dementia . Br Psychiatry 1980;136:533-541.Crossref 11. Felice U, Felice JD, Kissinger PT: Determination of catecholamines in rat brain parts by reverse-phase ion-pair liquid chromatography . JNeurochem 1978;31:1461-1465.Crossref 12. Farley IJ, Hornykiewicz O: Noradrenaline distribution in subcortical areas of the human brain . Brain Res 1977;126:53-62.Crossref 13. Robinson DS, Niles A, Davis JN, et al: Ageing, monoamines, and monoamine-oxidase levels . Lancet 1972;1:290-291.Crossref 14. Olson L, Fuxe K: On the projections from The the locus caeruleus noradrenaline neurons: cerebellar innervation . Brain Res 1971;28:1 171.Crossref 15. Hoffer BJ, Siggins GR, Oliver AP, et al Activation of the pathway from locus caerule to rat cerebellar Purkinje neurons: Pharmacological evidence of noradrenergic central inhibition . J Pharmacol Exp Ther 1973;184:553-569. 16. Bloom FE, Hoffer BJ, Siggins GR: Studies on norepinephrine-containing afferents to P rkinje cells of rat cerebellum: I. Localization of the fibers and their synapses . Brain Res 1971;25:501-521.Crossref 17. Brody H: An examination of cerebral cortex and brainstem aging , in Terry RD, Gershon S (eds): Neurobiology of Aging . New York, Raven Press, 1976, pp 177-181. 18. Lloyd KG, Davidson L, Hornykiewicz O: The neurochemistry of Parkinson's disease: Effect of l-dopa therapy . J Neurochem 1975;195:453-464. 19. Romero JA, Chalmers JP, Cottman K, et al: Regional effects of l-dihydroxyphenylalaninee LDOPA) on norepinephrine metabolism inn r brain . J Pharmacol Exp Ther 1972;180:277-285. 20. Hoffer BJ, Freedman R, Woodward DJ, e al: A functional role for the adrenergic inpututto the cerebellar cortex: Interaction of norepinep rine with mossy and climbing fiber excitation and GABA-mediated inhibition , in Garatini (ed): Interactions Between Putative Neurotrans-ansmitters in the Brain . New York, Raven Press. 1978, pp 231-243. 21. Moises HC, Woodward PJ, Hoffer BJ, et al: Interactions of norepinephrine with Purkinjec responses to putative amino acid neurotransmit-ters applied by microiontophoresis . Exp Neur 1979;64:493-515.Crossref 22. Moises HC, Woodward DJ: Potentiation of GABA inhibitory action in cerebellum by locus coeruleus stimulation . Brain Res 1980;182:327-344..Crossref 23. Reichart WA, Doolittle J, McDowell FH: Vestibular dysfunction in Parkinson's disease . Neurology 1982;32:1133-1138.Crossref 24. Watson M, McElligot JG: Diminished improvement in acquisition of a specific locomotor task after localized 6-hydroxydopamine induced cerebellar norepinephrine depletion . Neurosci Abstr 1982;8:392.

Lüders, Hans;Orlowski, James P.;Dinner, Dudley S.;Lesser, Ronald P.;Klem, George H.

doi: 10.1001/archneur.1984.04210080023008pmid: 6721736

Abstract • Auditory evoked potentials (AEPs) were determined in 16 patients with nearmiss sudden infant death syndrome. The AEPs were normal in all patients except one with prolonged I to V interpeak latency (bilaterally) and another with an asymmetry of interear I to V interpeak latency difference. These results indicate that AEPs do not permit detection of infants at high risk for crib death. References 1. Orlowski JP, Nodar RH, Lonsdale D: Abnormal brainstem auditory evoked potentials in infants with threatened sudden infant death syndrome . Cleve Clin Q 1979;46:77-82.Crossref 2. Nodar RH, Lonsdale D, Orlowski JP: Abnormal brainstem potentials in infants with threatened sudden infant death syndrome . Otolaryngol Headead Neck Surg 1980;88;619-621. 3. Naeye RL: Brainstem and adrenal abnormalities in the sudden infant death syndrome . Am J Clin Pathol 1976;66:526-530. 4. Quattrocki JJ, Baba N, Liss L, et al: Sudden infant death syndrome (SIDS): A preliminary study of reticular dendritic spines in infants . Brain Res 1980;181:245-249.Crossref 5. Shannon DC, Kelly DH, O'Connell K: Abnormal regulation of ventilation in infants at risk for sudden-infant-death syndrome . N Engl J Engl J Med 1977;297:747-750.Crossref 6. Gupta PR, Guileminault C, Dorfman LJ: Brainstem auditory evoked potentials in nearmiss sudden infant death syndrome . J Pediatr 1981;98:791-794.Crossref 7. Stockard JJ: Brainstem auditory evoked potentials in adult and infant sleep apnea syndromes, including sudden infant death syndrome (SIDS) and near-miss for sudden infant death . Ann NY Acad Sci 1982;388:433-465. 8. Ziporyn T: Evoked potentials give early warning of sensory and behavioral deficits in high-risk neonates . JAMA 1981;246:1288-1289.Crossref 9. Stockard JE, Stockard JJ: Brainstem auditory evoked potentials in normal and otoneurologically impaired newborns and infants , in Henry CE (ed): Current Clinical Neurophysiology: Update on EEG and Evoked Potentials . New York, Elsevier North Holland Inc, 1981, pp 421-466. 10. Stockard JE, Westmoreland BF: Technical considerations in the recording of the brainstem auditory evoked potentials for neonatal neurologic diagnosis . Am J EEG Technol 1981;21:31-54.

Chang, Rowland W.;Bell, Carolyn L.;Hallett, Mark

doi: 10.1001/archneur.1984.04210080026009pmid: 6326716

Abstract • The initial appearance and course of 19 patients with mononeuropathy multiplex due to systemic vasculitis were evaluated. Neuropathy first occurred within one year of the onset of systemic vasculitis in all patients and within one year of the onset of rheumatoid arthritis in four of nine patients. Concurrent cutaneous arteritic lesions and elevated ESRs occurred more frequently in patients with rheumatoid arthritis than in those without it. The overall six-month and five-year survival rates were approximately 80% and 60%, respectively. Significant nerve improvement was noted in 86% of surviving patients after one year. There were no factors at initial appearance predictive of outcome. References 1. Conn DL, Dyck PJ: Angiopathic neuropathy in connective tissue diseases , in Thomas PK, Lambert EH (eds): Peripheral Neuropathy . Philadelphia, WB Saunders Co, 1975, pp 1149-1165. 2. Moore PM, Fauci AS: Neurologic manifestations of systemic vasculitis . Am J Med 1981;71:517-524.Crossref 3. Epstein WV, Engleman EP: The relation of the rheumatoid factor content of serum to clinical neurovascular manifestations of rheumatoid arthritis . Arthritis Rheum 1959;2:250-258.Crossref 4. Hart FD, Golding JR: Rheumatoid neuropathy . Br Med J 1960;1:1594-1600.Crossref 5. Ferguson RH, Slocumb CH: Peripheral neuropathy in rheumatoid arthritis . Bull Rheum Dis 1961;11:251-254. 6. Pallis CA, Scott JT: Peripheral neuropathy in rheumatoid arthritis . Br Med J 1965;1:1141-1147.Crossref 7. Chamberlain MA, Bruckner FE: Rheumatoid neuropathy: Clinical and electrophysiological features . Ann Rheum Dis 1970;29:609-616.Crossref 8. Dyck PJ, Conn DL, Okazaki H: Necrotizing angiopathic neuropathy . Mayo Clin Proc 1972; 47:461-475. 9. Conn DL, McDuffie FL, Dyck PJ: Immunopathologic study of sural nerves in rheumatoid arthritis . Arthritis Rheum 1972;14:135-143.Crossref 10. Vantis JM, Jenulkens FG: Immunofluorescence studies in a case of rheumatoid neuropathy . J Neurol Sci 1977;33:313-321.Crossref 11. Schmid FR, Cooper NS, Ziff M, et al: Arteritis in rheumatoid arthritis . Am J Med 1961;30:56-83.Crossref 12. Bywaters EGL: Peripheral vascular obstruction in rheumatoid arthritis and its relationship to other vascular lesions . Ann Rheum Dis 1957;16:84-103.Crossref 13. Mongan ES, Cass RM, Jacox RF, et al: A study of the relation of seronegative and seropositive rheumatoid arthritis to each other and to necrotizing vasculitis . Am J Med 1969;47:23-35.Crossref 14. Abel T, Andrews BS, Cunningham PH, et al: Rheumatoid vasculitis: Effect of cyclophosphamide on the clinical course and levels of circulating immune complexes . Ann Intern Med 1980;93:407-413.Crossref 15. Scott DGI, Bacon PA, Tribe CR: Systemic rheumatoid vasculitis: A clinical and laboratory study of 50 cases . Medicine 1981;60:288-297.Crossref 16. Weisman MH, Zvaifler NJ: Vasculitis in connective tissue diseases . Clin Rheum Dis 1980;6:351-371. 17. Cupps TR, Fauci AS: The Vasculitides . Philadelphia, WB Saunders Co, 1981, pp 26-49, 72-98. 18. Vertzman L: Polyarteritis nodosa . Clin Rheum Dis 1980;6:297-317. 19. Hoekstra JA, Fauci AS: The granulomatosus vasculitides . Clin Rheum Dis 1980;6:373-388. 20. Fauci AS, Haynes BF, Katz P: The spectrum of vasculitis . Ann Intern Med 1978;89:660-676.Crossref 21. Fan PT, Davis JA, Somer T, et al: A clinical approach to systemic vasculitis . Semin Arthritis Rheum 1980;9:248-304.Crossref 22. Wolff SM, Fauci AS, Horn RG, et al: Wegener's granulomatosis . Ann Intern Med 1974;81:513-525.Crossref 23. Travers RL, Allison DJ, Brettle RP, et al: Polyarteritis nodosa: A clinical and angiographic analysis of 17 cases . Sem Arthritis Rheum 1979;8:184-199.Crossref 24. Armitage P: Statistical Methods in Medical Research . New York, John Wiley & Sons Inc, 1971. 25. Kaplan EL, Meier P: Nonparametric estimation from incomplete observations . J Am Stat Assoc 1958;53:457-481.Crossref 26. Frohnert PP, Sheps SG: Long-term followup study of periarteritis nodosa . Am J Med 1967; 43:8-14.Crossref 27. Sack M, Cassidy JT, Bole GG: Prognostic factors in polyarteritis . J Rheumatol 1975;2:411-420. 28. Cohen RD, Conn DL, Ilstrup DM: Clinical fetaures, prognosis, and response to treatment in polyarteritis . Mayo Clin Proc 1980;55:146-155.

Rao, Stephen M.;Hammeke, Thomas A.;McQuillen, Michael P.;Khatri, B. O.;Lloyd, David

doi: 10.1001/archneur.1984.04210080033010pmid: 6721737

Abstract • Forty-four patients with chronic progressive multiple sclerosis (MS) were compared with age- and education-matched control groups on a battery of clinical and experimental memory measures. Patients with MS performed substantially below the control groups on both immediate learning and delayed recall tasks, particularly in the retrieval of spatial information. The MS sample was subdivided into three groups using a cluster analytic procedure. One group (N = 9) performed well below expectations on memory tasks, exhibited signs of global cognitive disturbance, and had an atypical personality adjustment, characterized by irritability, social withdrawal, and apathy. A second group (N = 19) showed mild memory disturbance, associated with a greater use of psychotropic medications and a higher incidence of reactive depression. A third group (N = 16) performed normally on memory measures. The three groups of patients with MS did not differ in length or overall severity of illness. 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