Letters to the Editor 2295

functional potential." We discharge people from our stroke unitwhen they and their families are ready for living at home or, if thatproves impossible, in a rest home or geriatric hospital. Rehabilitationcontinues at home, where it is more in context with the patient's lifeinterests. I believe that the in-hospital phase of stroke rehabilitationshould prepare the patient for discharge rather than aim for maximalfunction, which can be achieved later in a more appropriate setting.

Paul Friedman, FRACPStroke Unit

Waikato HospitalHamilton, New Zealand

References1. Kalra L. The influence of stroke unit rehabilitation on functional

recovery fr°m stroke. Stroke. 1994̂ 25:821-825.2. Friedman PJ. Clock drawing in acute stroke. Age Ageing. 1991;2ft

140-145.

ResponseDr Friedman raises three issues in his letter. The first one is that of

probable differences in the initial Barthel activities of daily living(ADL) scores between patients treated on the stroke unit and thosetreated on general wards.1 It is implied that differences in these initialscores may have been masked by use of the median instead of themean for group comparisons and could have been responsible for theobserved differences in outcome. The Barthel ADL score used tomeasure function in my study (and apparently on Dr Friedman'sunit) is the Barthel ADL Index as modified by Wade and colleagues.2

This is an ordinal scale with nonuniform intervals, and the appropri-ate statistical group descriptions would be the median and rangerather than the mean. The mean is a group comparator of interval orratio measures and its use is therefore inappropriate for this index.Multiple regression analysis (stepwise deletion) was undertaken onthe original data to analyze the effects of age, gender, side of stroke,initial Barthel scores, and perceptual problems indicated by Barthelscores at hospital discharge, as suggested by Dr Friedman. Thisanalysis showed that the setting of stroke management was a signif-icant independent variable affecting discharge Barthel ADL scores,as were initial Barthel ADL scores and presence of perceptualproblems. The rate of recovery appeared to be unaffected by initialBarthel scores and was greatest in some of the patients with thelowest initial scores.

Dr Friedman notes that the length of stay on the stroke unit inmy study was longer than the mean length of stay on his unit.Although initial median Barthel ADL scores are comparablebetween the two units, there appears to be a significant differencein the age composition of the two groups. Dr Friedman does notspecify the age of his patients but implies they are all elderly,whereas my study included a significant number of younger strokepatients, in whom rehabilitation needs may be the greatest.3 DrFriedman's patients were selected at least 30 days after the stroke,whereas the subjects in my study were randomized at 14 days. Thiscould well account for the 16-day difference in length of stay.

I agree with Dr Friedman that the inhospital phase of strokerehabilitation should prepare patients for discharge and thatfurther rehabilitation should take place in the home environmentto maximize functional gains after a stroke. A large proportion ofthe overall costs of stroke are related to the length of hospital stayrather than to medical or therapy input. One of the majorobjectives of management in our stroke unit is to achieve safe,supportable, and early discharges with further therapy supportbeing provided at home or in the community.

Lallt Kalra, MD, PhD, FRCPOrpington Clinical Age Research Unit

King's College School of Medicine and DentistryOrpington, KentUnited Kingdom

References1. Kalra L. The influence of stroke unit rehabilitation on functional

recovery from stroke. Stroke. 1994;25:821-825.2. Wade DT. Measurement in Neurological Rehabilitation. Oxford,

England: Oxford University Press; 1992.3. Kalra L. Does age affect benefits of stroke unit rehabilitation?

Stroke. 1994^25:346-351.

Transient Abnormal Behavior AfterPontine InfarctionTo the Editor

In a recent issue of Stroke, Andersen et al1 reported patientswith poststroke pathological crying associated with bilateral pon-tine or hemispheric lesions, and suggested that an involvement ofthe serotonergic system may be related to their symptoms. Theyalso reported a patient with a unilateral pontine lesion who hadtransient pathological crying. We have observed a patient whoexhibited transient abnormal behavior after acute unilateral pon-tine infarction, which may also be attributable to the derangementof serotonergic neurotransmission in the brain.

A 54-year-old hypertensive man suddenly developed dysarthriafollowed by a series of unusual behaviors. He called his wiferepeatedly to his room, but would not let her in when she came.When he was later asked why, he said "I suddenly becamesuspicious and angry about her infidelity, but I don't know why.I've had a relatively good marital life so far." He also becameirritable, impulsive, and dysphoric. He called his friends and askedthem to join him in drinking alcohol. Normally, he did not enjoydrinking and had not had alcohol for 1 year prior to this episode.When his friends declined, he went out alone to a bar and becameintoxicated. That night, he brought home a pork cutlet anddevoured it, saying repeatedly, "I have to eat this," even though hehad had his dinner just a few hours before. The next day, he haddifficulty writing because of his weak and clumsy right hand. Hefelt excessively fatigued, lost his appetite, and continued to besuspicious about his wife. At one time, he found a dirty, used gasrange discarded by his neighbor outside the house and brought ithome, saying, "Let's use it." When later asked about this, he said"I really don't know why I did that." When the patient wasexamined at our hospital the next day, he was irritable andimpulsive though alert and oriented. There was moderate dysar-thria, mild right lower facial palsy, and slight weakness and ataxiaof the right arm. The results of routine laboratory tests were allwithin normal limits. Brain magnetic resonance imaging showed aninfarction in the left pons (see Figure). After admission to thehospital, the patient did not exhibit definitely abnormal behavior.However, at 6-month follow-up, he remained slightly more impul-sive and less tolerant than before.

This patient had dysarthria-clumsy hand syndrome due to aparamedian pontine infarction. The coincidental appearance ofthe bizarre behavior and its improvement over a few days suggestthat this transient abnormal behavior was also related to thestroke. Drake et al2 reported 2 patients with pontine base infarc-tion who had manic symptoms including grandiosity, sleeplessness,irritable mood, and hyperactrvity. Our patient's symptoms, whichincluded suspicion of his wife's infidelity, bizarre behavior, irrita-bility, and impulsiveness, do not conform to mania, but areconsistent with acute transient psychosis. These were probably notdue to a stress reaction to his stroke, because they started beforehe realized that he had suffered one.

There is accumulating evidence that altered serotonin metabo-lism is related to the pathogenesis of psychic disturbances.3 Lowlevels of 5-hydroxyindoleacetic acid, a serotonin metabolite, in thecerebrospinal fluid are related to agitation,4 delusion,5 sadness,5 orsuicidal ideas.6 In the human brain stem, raphe nuclei, whichcontain neurons synthesizing serotonin, are located from themedulla to the midbrain.7 The principal ascending fibers arisefrom serotonin cell bodies in the dorsal nucleus and the superior

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22% Stroke Vol 25, No 11 November 1994

Trweigrited magnetic resonance Image showing an Infarct In theleft paramedian pons.

central nucleus, a rostral extension of the pontine raphe nuclei.7 Inour patient, magnetic resonance imaging revealed a paramedianupper pontine lesion, which might have involved the superiorcentral nucleus or the ascending serotonergic fibers. The conse-quent derangement of serotonin neurotransmission may be asso-ciated with the psychotic symptoms seen in this patient.

Jong S. Kim, MDJay H. Lee, MD

Myoung C. Lee, MDDepartment of Neurology

Sung D. Lee, MDDepartment of Psychiatry

University of UlsanAsan Medical Center

Seoul, South Korea

References1. Andersen G, Ingeman-Nielsen M, Vestergaard K, Riis JO. Patho-

anatomic correlation between poststroke pathological crying anddamage to brain areas involved in serotonergic neurotransmission.Stroke. 1994;25:1050-1052.

2. Drake ME Jr, Pakalnis A, Phillips B. Secondary mania after ventralpontine infarction. J Neuropsych Clin NeuroscL 1990;2:322-325.

3. Stan] SM, Wets K. Indolamines and schizophrenia. In: Henn FA,DeUsi LE, eds. Handbook of Schizophrenia, Vol 2: Neurochemistryand Neuropharmacology of Schizophrenia. New York, NY: ElsevierScientific Publisher BV; 1987:257-296.

4. Rimon R, Roos BE, Rakkolainen V, Alanen Y. The content of5-bydroxyindoleacetic acid and homovanillic acid in the cerebro-spinal fluid of patients with acute schizophrenia. / Psychosom Res.1971;15J75-378.

5. Lindstrom L. Low HVA and normaJ 5-HIAA CSF levels in drugfree schizophrenic patients compared to healthy volunteers: corre-lations to symptomatology and family history. Psychiatry Res. 1985;14:265-273.

6. Ninan PT, Van Kammen DP, Scheinin M, Unnoila M, Bunney W,Goodwin F. CSF 5-hydroxyindoleacetic acid in suicidal schizo-phrenic patients. Am J Psychiatry. 1984;141:566-569.

7. Carpenter MB, Sutin J. Human Neuroanatomy. 8th ed. Baltimore,Md: Williams & Wilkins; 1983:358-409.

ResponseIt is well known that bizarre behavior may accompany occlusive

vascular disease of the rostral basilar artery and infarction of themidbrain, thalamus, and portions of the temporal and occipitallobes, usually without prominent motor dysfunction.1

Kim et al report a case of transient abnormal behavior after aparamedian left pontine infarction, with symptoms of dysphoricmood, irritability and impulsiveness, and suspiciousness. The caseillustrates a complex behavior that, although it is not uncommon,cannot be distinguished from the large group of heterogeneous

conditions reported with rostral brain stem infarctions. It istherefore highly speculative to attribute such a complex behavior,although transient, to derangement of a single neurotransmissionsystem. However, part of the behavior described, namely the lossof control of temper (ie, aggression and irritability), might beattributable to derangement of serotonin metabolism because drugtrials with the selective serotonin reuptake inhibitor citalopramhas been effective in the treatment of such emotional disturbancesin demented patients.2

We find it very important and illuminating to attempt to localizesingle symptoms such as uncontrolled crying or laughing, uncon-trolled temper, sleeplessness, central pain, and amnesia after stroke,and to explore which neurotransmitter systems might be involved.This approach makes possible specific treatment, which is very muchneeded in rehabilitation to improve quality of life after stroke.

Grethe Andersen, MDDepartment of NeurologyArhus University Hospital

Arhus

Karsten Vestergaard, MDDepartment of Neurology

Aalborg HospitalAalborg, Denmark

References1. Caplan LR. "Top of the basilar" syndrome. Neurology. 1980;30:

72-79.2. Nyth AL, Gottfries CG. The clinical efficacy of citalopram in

treatment of emotional disturbances in dementia disorders: aNordic multi-center study. Br J Psychiatry. 1990;157:894-901.

Apo E Phenotype in Atheromatous PlaquesTo the Editor

The association of apolipoprotein (apo) E4 alleles and cere-brovascular disease has been discussed in some recent articles inStroke.1'2 According to the latest epidemiological research, there isan increased frequency of apo E4 phenotype in patients affectedby multi-infarct dementia, which should not be surprising sincehigh apo E4 level increases cardiovascular risk. These patientsconstitute an interesting reference group because of their in-creased risk. It must be remembered that the three apo Evariants—apo E2, apo E3, and apo E4 —have different bondingcapacities with low-density lipoprotein (LDL) (apo E has thegreatest and apo E2 the least), so homozygotes for apo E2 are atrisk of cardiovascular disease because of their increased incidenceof type HI hyperlipidemia, and homozygotes for apo E4 are atgreater risk because the more efficient bond of apo E4 to the LDLreceptor causes reduced activity of the receptor in hepatocytes andan increase in levels of cholesterol and trigfycerides.

It is possible to identify which of the three apo E alleles ispresent in carotid atheromatous fibrous plaques by using a methodthat amplifies a portion of genomic DNA from the plaques. Weanalyzed 35 carotid plaques and 5 femoral ones. One carotidplaque showed an apo E4/E2 allele and the other 39 plaques(98%) showed an apo E3/E3 homozygote isoform. Our conclusionis that apo E alleles in plaques are nearly all E3/E3, in a frequencythat is not different from that in a control population (whoseDNA, for the study of apo E, is taken from peripheral blood ratherthan from plaques). It is important in assessing these findings toconsider the technique of genetic phenotyping used; also, incom-plete separation of bands or uncertain interpretation and identi-fication of the same could lead to erroneous classification of thealleles.

Domenico VenamcdDepartment of Clinical Chemistry

INRCAFermo, Italy

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J S Kim, J H Lee, M C Lee and S D LeeTransient abnormal behavior after pontine infarction.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1994 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.25.11.2295

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