Key Factors Distinguish Transient Post-Stroke Symptoms

Nancy A. Melville

August 15, 2017

Investigators have identified key risk factors, triggers, and clinical features of transient post-stroke recrudescence (PSR) in findings that may help clinicians distinguish this phenomenon from new stroke symptoms.

"This is the first comprehensive characterization of poststroke recrudescence, so all our results are novel," senior author, Aneesh B. Singhal, MD, from the Department of Neurology at Massachusetts General Hospital (MGH) and Harvard Medical School in Boston, told Medscape Medical News.

"We believe it is important to counsel patients about recrudescence, the triggers that should be avoided if possible, and the importance of treating vascular risk factors," he said.

The study was published online August 7 in JAMA Neurology.

Key Triggers

Although transient stroke-like deficits are common following a stroke, there is a lack of evidence to help clinicians distinguish between PSR (a condition in which previous stroke-related deficits reemerge) and new brain ischemia.

To better identify the characteristics of PSR, the investigators evaluated data on 1700 random patients in the MGH Research Patient Data Repository.

They identified 164 episodes among 153 patients who had a primary or secondary diagnosis of cerebrovascular disease, available brain magnetic resonance images, and the term "recrudescence" included in their clinical notes.

All of the patients had previous major strokes: 145 ischemic and 8 hemorrhagic. Patients had a mean age of 67 years, and 92 (60%) were women.

Symptoms emerged at a mean of 3.9 years after the initial stroke and lasted a mean of 18.4 hours. Among 91 (69%) of 131 episodes with documented resolution time, the symptoms resolved on day 1. Twenty-three cases (17.5%) resolved on day 2, and the remainder resolved on subsequent days.

Deficits typically appeared abruptly and were mild to moderate, not exceeding the severity of the previous stroke deficits. They primarily involved motor-sensory or language function, with no cases involving isolated gaze paresis, isolated hemianopia, or isolated neglect.

"The predominant face, arm, and leg involvement combined with the infrequent altered consciousness, gaze paresis, hemianopia, and extinction or inattention suggests that the long white matter tracts are more susceptible," the authors write.

The key triggers appearing to be higher in patients with PSR than in a control group of 65 admissions without PSR included infection (P < .001), hypotension (P = .04), hyponatremia (P = .01), and use of benzodiazepines (P = .02). Insomnia and stress were somewhat higher, but not statistically significantly so (P = .06).

Symptom resolution was more gradual than onset and corresponded with the removal or treatment of the symptom trigger.

Better Diagnosis, Management

Compared with 1861 patients in the MGH Stroke Registry who also did not have recrudescence, 145 patients who did were more likely to be African American, female, or self-identifying race as "other" (P < .001 for all).

Those with recrudescence also had higher rates of diabetes (P < .001), dyslipidemia (P = .001), smoking (P = .03), and more severe neurologic deficits at the time of stroke, as indicated by National Institutes of Health Stroke Scale (NIHSS) score (P < .001).

In terms of stroke severity, the mean NIHSS score immediately before the recrudescence was 2.8. In 62 episodes, the NIHSS deficits were limited to a single item. The score during the episode worsened by a range of 1 to 12 points, with a mean change of 2.5 points; the mean maximum score during the recrudescence was 5.2.

There were significantly more small-vessel infarcts and more strokes from other definite causes, such as dissection, in the recrudescence group.

The authors speculated that mechanisms behind PSR may include subtle involvement of undamaged brain regions.
"Given the diverse and systemic nature of these triggers and the fact that PSR involves a subset of prior stroke symptoms without new neurologic symptoms, the triggers likely act via subtle effects on the undamaged ipsilateral and contralateral brain regions that subserve poststroke plasticity," they note.

They add that various biological and social factors may explain the higher rates of women and African-Americans experiencing PSR.

"Women, African American individuals, and those of other race/ethnicity are more frequently affected, possibly because of variances in neuronal susceptibility, disparities in health care resulting in more triggers such as infections, or other unmeasured confounders," the authors write.

Importantly, PSR is likely more prevalent than is realized, said Dr Singhal.

"It is highly likely that the syndrome is actually quite prevalent," he said. "We suspect that patients are currently frequently coded as having a transient ischemic attack or TIA since there is no ICD-10 [International Classification of Diseases, 10th Revision] diagnostic code for 'post-stroke recrudescence.' We hope our data will raise awareness and enable better diagnosis and management of this syndrome."

Ask Questions

In an accompanying editorial, Louis R. Caplan, MD, Beth Israel Medical Center, Boston, Massachusetts, underscored that the patients in the study had been admitted to the hospital for their symptoms, meaning they represent important examples of cases that physicians had initially failed to recognize as PSR.

More information is needed about patients with symptoms who were not hospitalized, Dr Caplan notes.

"Characterizing the phenomenological, epidemiological, and ecological components of recrudescence may help ward off unnecessary imaging, trips to EDs [emergency departments], and hospitalizations," he writes.

Dr Caplan adds that discussion of the possible re-emergence of symptoms with stroke patients can help them better respond when such symptoms arise.

"When I see patients after a stroke, I almost always ask about residual abnormalities. Their observations and my pointing out leftover dysfunctions make them more aware of even rather subtle deficits and they become less concerned [about these symptoms]," he says.

"Certain external forces bring out the subtle residual deficits — not that these deficits are an indication of new damage. With time, patients stop mentioning the residual symptoms," Dr Caplan adds.

The new findings, he said, underscore the importance of asking key questions to help identify PSR vs a new stroke.

"The distinction between new ischemia and recrudescence is history — that is, the patient's story."

 Dr Caplan notes that even if the findings are validated, many clinicians may still err on the side of caution when stroke patients present with neurologic symptoms.

"I am skeptical because many [of those patients] go to emergency rooms [ERs]," he said. "ERs are often manned by young people who use guideline recipes and overuse imaging," he said.

The authors and Dr Caplan have disclosed no relevant financial relationships.

JAMA Neurol. Published online August 7, 2017. Abstract, Editorial

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