J Stroke Cerebrovasc Dis
1994;4:216-219 © 1994 National Stroke Association
Mental Status Changes and Stroke Selim R. Benbadis, M.D., Cathy A. Sila, M.D., and Richard L. Cristea, M.D.
A retrospective analysis at a tertiary referred center was done to determine the frequency with which an acute confusional state is caused by a stroke and to evaluate the usefulness of performing computed tomography in this setting. We reviewed 127 neurology consultations requested for patients presenting with acute and apparently isolated mental status changes. The mean age was 62. Nine of 127 (7%) were thought to have suffered mental status changes as a result of an acute stroke: one subarachnoid hemorrhage and eight ischemic strokes. There was no intracerebral hemorrhage. The locations of the infarcts were right frontoparietal (four patients), bilateral occipital (two patients), bilateral frontal (two patients), and right pontine (one patient, in whom the causality of the stroke was uncertain). Of those nine strokes presenting with isolated mental symptoms, six (66%) had some focal abnormality on neurological examination. Only three of the 109 patients (2.7%) with no focal findings were ultimately diagnosed as strokes, and one of these had a subarachnoid hemorrhage. Stroke was a relatively rare cause of acute confusional syndrome. The neurological examination had a very high negative predictive value (97%) and was reliable in selecting patients who should undergo an imaging study. Key Words: Stroke-Confusion.
Although cerebral infarcts are classically diagnosed by the acute presentation of a focal neurological deficit, they are often considered in the differential diagnosis of acute alterations in mental status. Confusional, amnestic, or even psychotic states may occasionally be the sole manifestation of a stroke (I), and this is a common basis for a neurological evaluation. A number of studies have analyzed the types of strokes that are likely to produce mental symptoms, but there has been no quantitative study to evaluate how commonly a confusional state is caused by a stroke. From the Department of Neurology, Cleveland Clinic Foundation, Cleveland, OH, U.S.A. Presented at the 19th International Joint Conference on Stroke and Cerebral Circulation (American Heart Association), San Diego, February 17-19, 1994. Address correspondence and reprint requests to Dr. S. R Benbadis at Department of Neurology, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226, U.S.A. 216
J STROKE CEREBROVASC DIS, VOL.4, NO.4, 1994
Patients and Methods We retrospectively reviewed all consecutive requests for neurological consultations from the hospital and emergency room during a 2-year period (January I, 1987, to December 31, 1988). Consultations for acute mental status or behavioral changes, defined as changes of less than 3 days' duration, were selected. Comatose patients were excluded. Patients with psychotic, agitated, or combative behavior were included. All consultations were requested for apparently isolated mental changes (coded as "mental status changes" or "confusion") noted by the primary physician. In all patients, no focal neurological signs were identified by the referring physician. All consultations were performed within 3 days of symptom onset, and 72 (56.7%) during the first 24 h. The consultations were reviewed with particular attention to the neurological examination performed by the consulting neurology team. A minimum exam-
STROKEAND CONFUSION
ination included the following: mental status, cranial nerves excluding I, motor strength and coordination, reflexes (muscle stretch and plantar), sensory (pin prick and light touch), and gait. Mental status examination always included state of alertness, orientation to place, time, and person, immediate memory, attention, and calculation. Significant discrepancies between physicians in training and attending neurologists were rare; when present, the findings of the attending neurologists were used. Magnetic resonance imaging (MRI) and computed tomography (CT) were performed and interpreted in a single radiology department with standard techniques. All patients underwent at least one imaging study. The final diagnosis was made on the basis of the history, neurological examination, clinical course, and neuroimaging, as well as eventual outcome at follow-up visits. If the diagnosis was a stroke, the mechanism and location were analyzed. We determined the correlation between the bedside neurological examination and the presence or absence of a stroke as the etiology of the acute change in mental status. We used Fisher's exact test with a two-tailed p-value significance level of 0.05.
Results Over a 2-year period, a total of 143 neurological consultations were requested for isolated and acute mental status changes. Sixteen patients were excluded: 13 because the changes were not acute and three because they were in a coma. Thus, 127 patients met our criteria and were entered in the study. The population consisted of 78 men and 49 women. The mean age was 62 (range, 28-89). Fifty-seven (45%) of the
Table 1. Case/ age/sex 1I65/F 2162/M
3/71/F 4/86/M 5/66/M 6/S9/M
7/77/F 8/S2/F 9/62/M
Characteristics of thestrokes
Stroke mechanism location
Focal findings
Infarction R frontoparietal Infarction R frontoparietal Infarction R frontoparietal Infarction R frontoparietal Infarction bilateral occipital Infarction bilateral occipital Infarction bilateral frontal Infarction R pontine Subarachnoid hemorrhage
LHHA LHHA L arm drift LVII + HHA HHA & diplopia None None R VII paresis None
Abbreviations: HHA, homonymous hemianopia; L, left; R, right; VII, seventh nerve.
Table 2.
Stroke Other diagnosis Total
Frequency and distribution of focal findings Focal signs
No focal signs
Total
6 12 18
3 106 109
9 118 127
consults followed a cardiac procedure, 16 (12.6%) were requested in the emergency room, and 54 (42.4%) were referred by various medical or surgical services. No patient was under the primary care of neurology, neurosurgery, or psychiatry. Of our 127 patients, 67 (52%) underwent one head CT scan, 51 (40%) had 2 head CTscans, and 22 (17%) underwent MRI. In 41 patients (32.3%), initial head CTwas obtained by the referring service in the first 24 h. Of 118 CT scans, 108 included intravenous contrast material. At the completion of the neurological evaluation, nine patients (7%) were thought to have suffered mental status changes on the basis of an acute stroke. The stroke syndromes are shown in Table 1. There were eight cerebral infarcts and one subarachnoid hemorrhage. There was no intracerebral hemorrhage. The locations of the cerebral infarcts were: right frontoparietal (four patients), bilateral occipital (two patients), bilateral frontal (one patient), and right pontine (one patient). The relationship between neurological examination and diagnosis is summarized in Table 2. The etiologies of the mental status changes in the remaining 118 patients were not recorded in detail. They were often unclear or multifactorial, and the diagnosis was often presumptive; the vast majority consisted of several metabolic or toxic disturbances (medications) .
Comments Stroke appeared to be a relatively uncommon cause of acute confusional syndrome. The most significant result was that the neurological examination had a negative predictive value of 0.97. Of the 109 patients who had a "nonfocal" examination, only 3 (2.7%) were ultimately diagnosed as having a stroke, including one with a subarachnoid hemorrhage, where focal findings would not be expected, and 2 (1.8%) with a cerebral infarct. The patient with the subarachnoid hemorrhage had complained of severe headache prior to the onset of mental symptoms. ] STROKE CEREBROVASCDIS, VOL. 4, NO.4, 1994
217
S. R BENBADISIT AL
Of the 8 patients with cerebral infarction, 6 (75%) had subtle focal neurological signs on careful examination. Those were elicited in all 4 patients with right frontoparietal infarcts, who displayed various combinations of hemianopsia, subtle hemiparesis (decreased rate of rapid alternating movements), and Babinski sign. Cerebral infarction in the right (nondominant) middle cerebral artery distribution is a well-described cerebrovascular cause of acute confusion, particularly when it involves the inferior division ("mirror of Wernicke''). It is often marked by agitation when the temporal 10be is involved. Of the 5 cases reported by Price et al. (2),4 had a subtle hemiparesis, and 1 displayed left visual extinction. All of the 10 patients reported by Caplan et al. (3) had a left homonymous hemianopsia, and 4 had a left hemiparesis. In Schmidley et al.'s (4) series of 46 patients with right middle cerebral artery infarcts, only 2 presented with acute confusion, and a repeat examination after 2 h revealed hemianopsia, hemiparesis, or extensor plantar response. Although left homonymous hemianopsia, visual neglect, and hemiparesis are almost always present, they can be difficult to detect, and this is the most likely stroke syndrome to present without obvious focal findings (2,4-7). It has been noted that the confusional state associated with a right middle cerebral artery infarct is usually transitory (8). One of the two patients with bilateral occipital infarcts displayed a visual field deficit. Left and bilateral occipital lobe infarcts have also been reported as a cause of acute confusion. They are usually associated with visual loss or other visual signs. Of the four patients reported by Devinsky et al. (9), one had a homonymous hemianopsia and a Babinski sign, two had a facial droop, and one had an arm drift. The "top of the basilar" syndrome is usually accompanied by a myriad of visual, oculomotor, and motor signs (10,11). One of our patients had a pontine infarct, which would not be expected to cause mental symptoms; the infarct, confirmed by MRI, was most likely unrelated to the acute confusional syndrome. Nevertheless, a stroke was diagnosed in this case, and despite the probable lack of cause-and-effect relationship, this subject was counted as a stroke. Several other stroke syndromes have been reported to cause altered mentation. Confusional states in thalamic infarcts have been described and are particularly common when the anteromedial portion of the thalamus is involved (12). This syndrome typically consists of retrograde amnesia with aphasia. It should be noted that sensation is usually preserved if the infarct is purely anteromedial (tuberothalamic artery). Four of the five patients in the above series displayed 218
J STROKECEREBROVASCDIS, VOL.4, NO.4, 1994
at least one of the following: hemiparesis, facialweakness, homonymous hemianopsia, and aphasia. Only one had a "nonfocal" examination, and the CT in this patient showed bilateral thalamic infarcts. Fusiform and calcarine cortex infarcts can also cause behavioral symptoms. This syndrome is usually marked by agitation with dense hemianopsia (13, 14). It is interesting to note that a total of 140 imaging studies were performed (118 CT and 22 MRI scans; this represents 1.1 study per patient), and a yield of 6.4%. In the current climate of cost containment, this suggests that neuroimaging could be used more selectively. No patient in this series was diagnosed as being aphasic, a situation that can potentially be misdiagnosed as mental status changes. We recognize several limitations of our study. Its retrospective nature did not allow for strict control and standardization of the neurological examination, and the definition of isolated change in mental status depends on the skill of the examiner. For practical purposes, and because it reflects the reality of referrals, we included all patients in whom the referring physician did not elicit any focal finding. Despite new imaging techniques, there is no absolute gold standard to establish the diagnosis of stroke with certainty, and occasionally it has to be presumptive. Finally, the cause-and-effect relationship between a cerebral infarct and an acute confusional syndrome may be difficult to ascertain, and the stroke may be an incidental finding, as illustrated by our case with a pontine infarct. Our study took place in a tertiary referral center, and our population may not be representative of a general population in which other etiologies, such as subdural hematomas, are probably more common. The over-representation of patients with heart disease or status following a cardiac procedure in this study obviously introduces a bias. However, this does not weaken our conclusion, since stroke would be expected to be, if anything, more frequent in this group than in a "general" populaton.
Conclusions In our population, stroke was an uncommon cause of acute changes in mental status. The neurological examination had a very high negative predictive value. Without focal signs, other causes such as metabolic abnormalities were by far more common. Obtaining CT scans on all patients to exclude an infarct did not seem warranted. There was no case of intracerebral hemorrhage.
STROKEAND CONFUSION
References 1. Victor M, Adams R Principles ofneurology; 4th ed. New York: McGraw-HiIl, 1989:687. 2. Price BH, Mesulam M. Psychiatric manifestations of right hemisphere infarctions. [Nero Ment Dis 1985;173: 610-4. 3. Caplan LR, Kelly M, Kase CS, et al. Infarcts of the inferior division of the right MCA. Neurology 1986;36: 1015-20. 4. Schmidley JW,Messing RO. Agitated confusional states in patients with right hemisphere infarctions. Stroke 1984;5:883-5. 5. Mesulam MM, Waxman SG, Geschwind N, Sabin TD. Acute confusional states with right middle cerebral artery infarctions. J Neurol Neurosurg Psychiatry 1976; 39:84-9. 6. Berthier M, Starkstein S. Acute atypical psychosis following a right hemispheric stroke. Acta Neurol Belg 1987;87:125-31. 7. Mori E,Yamadori A. Acute confusional state and acute agitated delirium. Occurrence after infarction in the right middle cerebral artery territory. ArchNeuro11987; 44:1139-43.
8. Hijdra A. Vascular dementia. In: Bradley WG, Daroff RB,Fenichel GM, Marsden CD, eds. Neurology in clinicalpractice, vol II. Stoneham, MA: Butterworth-Heinlmann, 1991:1426. 9. Devinsky 0 , Bear D, Volpe BT. Confusional states following posterior cerebral artery infarction. Arch Neutol 1988;45:160-3. 10. Mehler MF. The rostral basilar artery syndrome. Neurology 1989;39:9-16. 11. Caplan LR. ''Top of the basilar" syndrome. Neurology 1980;30:72-9. 12. Graff-Radford NR, Eslinger PJ,Damasio AR,YamadaT. Nonhemorrhagic infarction ofthe thalamus. Behavioral, anatomic, and physiologic correlates. Neurology 1984;34:14-23. 13. Horenstein 5, Chamberlain W, ConomyJ. Infarction of the fusiform and calcarine regions: agitated delirium and hemianopsia. Trans Am Neurol Assoc 1967;92:859. 14. Medina JL,Rubino FA,Ross E. Agitated delirium caused by infarctions of the hippocampal formation and fusiform and lingual gyri: a case report. Neurology 1974; 24:1181-3.
J STROKECEREBROVASCDIS, VOL.4, NO.4, 1994
219