(Stroke. 1995;26:1285-1288.)
© 1995 American Heart Association, Inc.
Articles |
Subjective Experiences of 24 Patients Dramatically Recovering From Stroke
From the Department of Neurology, University of Texas Medical School at Houston.
Correspondence to James Grotta, MD, University of Texas Health Science Center, Department of Neurology, 6431 Fannin, Room 7044, Houston, TX 77030.
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Abstract |
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Background There are no reports describing patients' perception of having a stroke and then dramatically recovering.
Summary of Report We interviewed 24 patients randomized at our center to intravenous tissue plasminogen activator or placebo in an ongoing multicenter blinded prospective study. These patients demonstrated at least 50% improvement or an absolute improvement of 5 points on the National Institutes of Health Stroke Scale during the first 24 hours after treatment, with 7 patients returning completely to normal. Twelve of 24 of the strokes involved the right middle cerebral artery, 2 of 24 the right posterior cerebral artery, 8 of 24 the left middle cerebral artery, and 2 of 24 the basilar artery territory. CT scans at 24 hours or 1 week showed infarction in 19 of 24. Most patients (19 of 24) could clearly recall the exact circumstances involving the onset of their stroke, but only 12 of 24 were aware of the magnitude of their neurological deficit (7 of 14 right hemisphere and 4 of 8 left hemisphere patients). Only 6 of 24 were aware of their improvement when it occurred (3 of 14 right hemisphere and 2 of 8 left hemisphere patients). Five of 24 remembered positive phenomena such as warmth or tingling during their recovery, and only 2 patients demonstrated euphoria. Most patients seemed peculiarly unaware or blasé about their deficit and improvement.
Conclusions Most patients with acute stroke are not aware of the severity of their problem, and recovering patients do not remember important events during the next 24 hours. This occurs with either right or left hemisphere lesions and may have a significant impact on early stroke recognition.
Key Words: anosognosia • cerebrovascular disorders • denial • memory • stroke onset
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Introduction |
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Recently we have focused efforts on the early recruitment of patients into a trial of intravenous tissue plasminogen activator (TPA) versus placebo within 3 hours of the onset of ischemic stroke. Patients enrolled in this protocol are followed up very closely during the first 24 hours for clinical improvement or deterioration. In the process of conducting this study during the last 3 years we, like others,1 have observed that many patients dramatically recover during the first 24 hours even though they have severe stable neurological deficits on presentation and ultimately have CT scan evidence of cerebral infarction. The present study was generated by our interest in the subjective experiences of what these patients feel when they have a stroke and then recover. We recognized that this acute interventional study provided a unique opportunity to document dramatic recovery and then record the patient's subjective observations of the experience. We have been unable to find any similar reports in the literature.2
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Subjects and Methods |
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Subjects were patients who were enrolled at our center in the National Institute of Neurological Disorders and Stroke (NINDS) TPA Stroke Study testing intravenous TPA versus placebo. To qualify, these patients had to be randomized within 180 minutes of the onset of stroke symptoms. Other inclusion criteria were a baseline CT scan that did not show hemorrhage and was compatible with the diagnosis of acute ischemic stroke. Exclusions included minor neurological deficit or symptoms that were significantly improving before randomization. After randomization and treatment, patients were followed up at intervals up to 1 year. Follow-up CT scans were obtained at 24 hours and 7 to 10 days. The National Institutes of Health (NIH) Stroke Scale was performed at the time of randomization (baseline), 2 and 24 hours after treatment, and after 7 to 10 days and 3 months. The NIH Stroke Scale is a 46-point scale with normal scored as 0.3 As an example, our patient 17 with global aphasia and right hemiplegia, hemianopia, and hemi-inattention scored 26 points at baseline. He improved to moderate aphasia and hemiparesis at 24 hours (13 points) and to mild aphasia and hand weakness at 1 week (4 points).
To qualify for the present study, patients had to (1) be randomized into the NINDS TPA study; (2) show dramatic improvement during the first 24 hours after randomization as evidenced by a greater than 50% or 5-point improvement on the NIH Stroke Scale from baseline to the 24-hour exam; and (3) have intact memory and ability to communicate verbally at the time of follow-up.
The patients were identified and then interviewed 2 days to 14 months after their stroke by one of the authors (J.G.), who also reviewed all CT scans and case report forms. The exact date of interview was not available for six patients. The interviews were carried out in person or by telephone. No formal questionnaire was used, but the same directed questions were asked to all patients to describe what they could recall about their subjective experiences, in particular their recollection of circumstances at stroke onset; their awareness of the type and severity of their neurological deficit; their recollection of their clinical course in the ambulance, emergency department, and intensive care unit; their improvement; and finally any positive emotional (euphoria) or sensory (tingling, warmth) phenomena that occurred.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Twenty-four patients qualified for this analysis. Seven of the 24 returned completely to normal (NIH Stroke Scale score 0 or 1) by 24 hours. Thirteen of the 24 strokes were cardioembolic. The following arterial territories were involved: right middle cerebral in 12, right posterior cerebral in 2, left middle cerebral in 8, and basilar in 2.
An infarct responsible for the patients' presenting neurological deficit was seen on follow-up CT scan in 19 of the 24 patients. In 13 of the 20 patients with middle cerebral artery infarcts, there was a characteristic patchy subcortical distribution of hypodensity similar to that described previously in patients with dramatic spontaneous improvement after stroke.1 No patient in this series had either clinical or radiographic evidence of a lacunar infarct.
The subjective experiences, stroke location, presumed etiology, and
baseline and 24-hour NIH Stroke Scale scores for the 24 patients are
summarized in Table 1
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Nineteen of the 24 patients had excellent recollection of their stroke onset. These patients were able to remember very minute details of the circumstances such as whom they were talking to on the telephone, what they were eating, and what chair they were sitting in. In contrast, only 12 of 24 patients in retrospect reported that they were aware of the type or severity of their neurological deficit either immediately after the stroke or in the emergency department. This was true of patients with either right or left hemisphere lesions. Seven of 14 right hemisphere and 4 of 8 left hemisphere patients were subjectively unaware of their deficits.
Even after they improved, many of these patients had to be persuaded
that they had had a significant deficit so that they would finish their
evaluation and follow-up and adhere to stroke prevention therapy. This
unawareness was not due to decreased level of consciousness; only 7 of
the 24 patients were noted to be mildly lethargic, and none were
obtunded or stuporous on the NIH Stroke Scale carried out in the
emergency department. Lethargy was present in 2 of the right
and 2 of the left hemisphere stroke patients who were unaware of their
deficit. The patients unaware of their deficit with either right or
left hemisphere lesions also did not differ from the other patients in
other aspects of the neurological examination or in total NIH Stroke
Scale score (Table 2).
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The CT localization of infarcts in right and left hemisphere patients
with and without awareness of deficit is presented in Table 3. Although the numbers are too small to make conclusive
statements, it appears that patients unaware of their deficit might
have larger infarcts and more frequent involvement of the basal
ganglia. None of the 11 patients unaware of their deficit had normal
scans compared with 3 of 11 patients aware of their deficit, and 7 of
11 patients unaware of their deficit had some brain swelling compared
with 1 of 11 patients aware of their deficit. Subcortical abnormalities
were seen in all (11 of 11) patients unaware of their deficit compared
with 6 of 11 aware of their deficit. The biggest difference was in the
basal ganglia, where 3 of 4 left hemisphere and 5 of 7 right hemisphere
patients unaware of their deficit had lesions compared with 1 of 4 left
hemisphere and 1 of 7 right hemisphere patients who were aware of their
deficit.
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An even smaller percentage of our patients (6 of 24) were aware of the
rather dramatic improvement in their clinical condition. Again, lack of
awareness of improvement occurred after both right and left cortical or
subcortical infarcts. Only 5 of 24 patients noticed paresthesias or
other positive sensory phenomena. Only 2 patients noted euphoria on
recognizing that they had dramatically improved. These results are
summarized in the Figure.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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This study indicates that most patients recovering from major stroke are aware of the circumstances surrounding the onset of their stroke but not of the severity or course of their illness once these strokes occur. This was true regardless of right versus left hemisphere location of the stroke. Since these patients objectively made such a dramatic recovery, we expected that they would provide interesting observations on their experience. However, we were frankly surprised to find that patients were peculiarly unemotional about their problem.
Without more detailed investigation of these patients, it is impossible to fully characterize the cognitive impairment that occurred during the time of the stroke or to understand its etiology. However, patients who later could not recall their deficit did not have a reduced level of consciousness in the emergency department and later were able to remember events occurring at the onset of their stroke. Therefore, we believe that their unawareness of deficit was a form of anosognosia rather than a deficit in memory or global neurological function. Anosognosia is classically defined as denial of hemiplegia, and all 12 of our patients with unawareness of deficit had significant hemiparesis or hemiplegia contralateral to their brain lesion. Anosognosia has usually been linked with right hemisphere dysfunction4 but has also been reported after left carotid Wada testing.5
Anosognosia in 97 patients with right brain damage was associated with left hemiparesis and visual field defect alone or together6 ; in 13 right hemisphere stroke patients it was associated with left hemisensory deficit, neglect, and apathy.7 However, in another study more frontal than posterior deficits in cognition were found.8 At least as could be determined by subcomponents of the NIH Stroke Scale, we could find no apparent differences in any of these neurological deficits in our 7 right hemisphere patients with anosognosia compared with the 7 patients without except that fewer anosognosia patients had visual field deficits.
We found that anosognosia might be more common in patients with more severe lesions and basal ganglia involvement. However, since CT scans were performed at least 24 hours after stroke onset and in some cases after thrombolytic therapy, the CT scan results undoubtedly are a poor reflection of the region of cerebral dysfunction at the time the patients' neurological findings were maximal. In patients with right hemisphere brain damage, anosognosia could not be linked to any anatomic localization in two studies.6 8 In studies of stroke patients, anosognosia has been associated with large lesions7 (similar to our study) and lesions in the internal capsule,7 9 thalamus,7 or parietal cortex7 (not found in our study).
It is possible that diaschisis involving undetermined brain regions could account for temporary unawareness of deficit in our patients. Transient depression of central nervous system activity remote from the focal area of infarction (diaschisis) is characterized by reduced metabolic activity and consequent reduction in cerebral blood flow, presumably due to deafferentation.10 11 Other etiologies are possible, but hypotension, metabolic disturbances, drug effects, and other easily explainable complicating factors were not present in our patients.
One weakness of our methodology is that we did not standardize the timing of the patient interviews. However, recollection of events did not vary based on interval from stroke to interview in those for whom we had this information.
Regardless of the cause, lack of self-awareness of clinical deficit and course in our patients has several implications. First, it may explain why some patients demonstrate a peculiar lack of urgency in seeking attention for their stroke. Failure of patients to seek help after the onset of stroke symptoms has been recognized as an important cause of delay in the treatment of stroke patients12 and may not always be due to the physical inability of a patient to get to a telephone or to call for help. Second, patients who have poor awareness of the severity of their deficit may have difficulty understanding the complexities of signing informed consents and making other decisions pertaining to their care.
In conclusion, most patients dramatically recovering from nonlacunar ischemic stroke do not recollect the severity of their problem and do not remember important events during the first 24 hours. This occurs with either right or left hemisphere lesions.
Received October 10, 1994; revision received March 10, 1995; accepted April 17, 1995.
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References |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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1. Minematsu K, Yamaguchi T, Omae T. Spectacular shrinking deficit: rapid recovery from a major hemispheric syndrome by migration of an embolus. Neurology. 1992;42:157-162.
2.
Ellis S, Small M. Denial of illness in
stroke. Stroke. 1993;24:757-759.
3. Lyden P, Brott T, Tilley B, Welch KMA, Mascha E, Levine S, Haley E, Grotta J, Marler J, and the NINDS TPA Stroke Study Group. Improved reliability of the NIH Stroke Scale using video training. Stroke. 1994;25:2220-2226. [Abstract]
4.
Mesulam M, Waxman S, Geschwind N, Sabin T.
Acute confusional states with right middle cerebral
infarctions. J Neurol Neurosurg
Psychiatry. 1976;39:84-89.
5. Terzian H. Behavioral and EEG effects of intracarotid sodium amytal injections. Acta Neurol (Vienna). 1964;12:230-240.
6. Bisiach E, Vallar G, Perani D, Papagno C, Berti A. Unawareness of disease following lesions of the right hemisphere: anosognosia for hemiplegia and anosognosia for hemianopia. Neuropsychologia. 1986;24:471-482. [Medline] [Order article via Infotrieve]
7.
Levine D, Calvanio R, Rinn W. The pathogenesis
of anosognosia for hemiplegia. Neurology. 1991;41:1770-1781.
8. Starkstein S, Fedoroff P, Price T, Leiguarda R, Robinson R. Neuropsychological deficits in patients with anosognosia. Neuropsychiatry Neuropsychol Behav Neurol. 1993;6:43-48.
9.
Starkstein S, Fedoroff P, Price T, Leiguarda R,
Robinson R. Apathy following cerebrovascular lesions.
Stroke. 1993;24:1625-1630.
10. Von Monakow C. Diaschisis. In: Pribram KH, ed. Brain and Behavior I: Mood States and Mind. Baltimore, Md: Penguin Books; 1969:27-36.
11. Fiorelli M, Blin J, Bakchine S, Laplance D, Baron J. PET studies of cortical diaschisis in patients with motor hemi-neglect. J Neurol Sci. 1991;10:135-142.
12.
Feldmann E, Gordon N, Brooks J, Brass L, Fayad P,
Sawaya K, Nazareno F, Levine S. Factors associated with early
presentation of acute stroke. Stroke. 1993;24:1805-1810.
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