Posterior Reversible Encephalopathy Syndrome (PRES) Diagnosis: A Comprehensive Guide

Posterior Reversible Encephalopathy Syndrome (PRES) is a neurological condition characterized by a variety of symptoms including visual disturbances, seizures, headaches, and altered mental status. Diagnosis is typically achieved by observing specific imaging features on brain MRI, predominantly in the parieto-occipital lobes. Timely recognition and accurate PRES diagnosis are critical for effective treatment and improved patient outcomes in this potentially reversible condition. This article provides a detailed overview of PRES, encompassing its clinical presentation, etiology, epidemiology, pathophysiology, evaluation, differential diagnosis, treatment and management strategies, prognosis, and potential complications. Furthermore, it emphasizes the crucial role of an interprofessional healthcare team in ensuring prompt recognition and treatment of PRES to enhance patient safety, optimize care quality, and improve overall outcomes.

Objectives:

• Enhance the ability to identify PRES symptoms and risk factors for earlier evaluation and treatment.
• Differentiate PRES from emergent conditions with similar presentations and refine diagnostic approaches for better patient outcomes.
• Understand and compare various treatment options for PRES management.
• Emphasize the significance of interprofessional education and communication in improving patient care, safety, and outcomes in PRES, and implement effective strategies for enhanced team coordination.

Access free multiple choice questions on this topic.

Introduction

Posterior Reversible Encephalopathy Syndrome (PRES), also known by several other names including reversible posterior leukoencephalopathy syndrome (RPLS), reversible posterior cerebral edema syndrome, posterior leukoencephalopathy syndrome, hyperperfusion encephalopathy, and brain capillary leak syndrome, is a distinct clinical-radiological entity. The syndrome manifests with a spectrum of neurological signs and symptoms. These can include altered mentation ranging from confusion to stupor, drowsiness, visual impairments (such as visual hallucinations, cortical blindness, hemianopia, quadrantanopia, and diplopia), seizures (both focal and generalized tonic-clonic), and severe headaches.[1] PRES can develop rapidly or gradually, with symptoms evolving over hours to a few days. A significant number of cases are associated with acute, uncontrolled hypertension, often with systolic blood pressure measurements between 160 and 190 mmHg.[2]

The nomenclature of PRES is derived from its key characteristics: (1) radiographic evidence of white matter edema observed as hyperintense T2 or hypointense T1 signals on Magnetic Resonance Imaging (MRI), typically located in the posterior regions of the cerebrum, often symmetrically, though asymmetric presentations are also observed; and (2) the potential reversibility of symptoms, contingent upon timely PRES diagnosis and intervention. However, it is important to note that the term “posterior” can be misleading as edema is not exclusively confined to the posterior cerebral white matter. It can also occur in watershed zones beyond the parieto-occipital regions, the thalamus, and occasionally in the anterior circulation.[2, 3, 4] Furthermore, the condition is not invariably reversible. Without prompt treatment, some patients can experience severe, life-threatening complications, including transforaminal cerebellar herniation and persistent focal neurological deficits.[5, 3]

Image: T2 FLAIR MRI sequence displaying hyperintensities indicative of vasogenic edema in the parieto-occipital regions, a hallmark of PRES diagnosis.

Etiology

Individuals at increased risk of developing PRES typically present with one or more predisposing factors, triggers, or underlying conditions. Hypertension is a major risk factor, alongside preeclampsia, and kidney diseases such as nephrotic syndrome (which can induce hypovolemia and secondary hypertension via renin-angiotensin system activation) and renal failure. Liver disease and exposure to various chemotherapeutic agents, including platinum-based drugs, gemcitabine, CHOP/R-CHOP regimens, cytotoxic medications, and immunosuppressants like tacrolimus, sirolimus, interferon therapies, and certain immunotherapies and monoclonal antibodies such as bevacizumab, pazopanib, sorafenib, and sunitinib, also elevate the risk.[3, 6, 7, 8]

Further risk factors include autoimmune disorders such as hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, eosinophilic granulomatosis with polyangiitis, and systemic lupus erythematosus, as well as sepsis.[2, 9, 10, 11, 12] Among these diverse etiologies, uncontrolled hypertension is the most frequently observed trigger for PRES.[4] However, it is critical to understand that acute hypertension alone does not invariably lead to PRES, and predicting which hypertensive individuals will develop PRES remains a clinical challenge.[2, 13]

Epidemiology

Historically, Posterior Reversible Encephalopathy Syndrome has been underdiagnosed, possibly due to limited awareness of the condition. However, with the increasing availability and advancements in neuroimaging technologies, awareness of PRES has grown, leading to a better understanding of its epidemiology. Current data suggests that PRES affects individuals across all age groups, but it is observed more frequently in middle-aged women.[1, 14]

In a retrospective study analyzing demographics, risk factors, and clinical presentations of 113 patients diagnosed with PRES, Fugate and colleagues reported that 51 patients (45%) had an autoimmune disease. The most common presenting symptom in this cohort was seizures (74%), followed by encephalopathy (28%), headache (26%), and visual disturbances (20%).[4] The study identified seizures at presentation as the strongest predictor for PRES diagnosis, with encephalopathy as the second most significant predictor. Recent chemotherapy exposure and underlying renal failure were also identified as crucial predictive factors for PRES development.[15]

Pathophysiology

The precise pathophysiological mechanisms underlying PRES are not fully elucidated, but prevailing theories center on the dysregulation of cerebral autoregulation. Cerebral autoregulation is the brain’s intrinsic ability to maintain consistent cerebral blood flow across a range of blood pressures through vasodilation and vasoconstriction of cerebral blood vessels.[2] Under conditions of significantly elevated blood pressure, typically exceeding a systolic pressure of 160 mmHg, the compensatory vasoconstriction to maintain constant cerebral blood flow reaches its limit, and cerebral blood flow begins to increase with rising blood pressure. This increased hydrostatic pressure can compromise the integrity of the blood-brain barrier, leading to extravasation of intravascular fluid into the surrounding brain tissue and resulting in vasogenic edema.

It is hypothesized that the posterior circulation is more susceptible to these effects in PRES due to potentially fewer adaptive mechanisms regulating extravasation and blood-brain barrier breakdown under high blood pressure, compared to the anterior circulation.[16] This hypothesis is partly supported by findings from a formaldehyde histofluorescence study by Edvinsson et al., which demonstrated a greater density of adrenergic perivascular fibers innervating the anterior cerebral circulation compared to the vertebrobasilar circulation.[17] The degree of sympathetic nerve involvement is thought to be directly related to the effectiveness of autoregulation.[16]

However, the hypertensive-hyperperfusion hypothesis has limitations, as some PRES cases occur in individuals without significantly elevated blood pressure, below the threshold typically considered to overwhelm cerebral autoregulation.[1, 18] Indeed, PRES has been reported in normotensive patients, particularly those receiving cytotoxic therapies like tacrolimus post-liver transplantation. This observation highlights the role of endothelial dysfunction in PRES pathophysiology.[1, 3] Immunosuppressants such as tacrolimus, cyclosporine, and cisplatin can exert direct toxic effects on the endothelium, compromising blood-brain barrier integrity.[3, 16]

Another proposed mechanism involves ischemia resulting from dysregulated cerebral autoregulation, leading to vasoconstriction and subsequent cytotoxic edema. Some radionuclide studies have shown vasoconstriction in PRES patients.[19, 20, 21, 22] However, these findings are not universal, and neuropathological studies have generally failed to demonstrate evidence of ischemia or infarction in PRES lesions.[23]

Beyond hypertension and direct endothelial toxicity, other factors can contribute to blood-brain barrier disruption and PRES development. Immunosuppressants, sepsis, and metabolic disorders like uremia, hypomagnesemia, and autoimmune diseases can induce neuroinflammation. Astrogliosis, microgliosis, and endothelial activation observed in sepsis or endothelial injury in ANCA-associated vasculitides can increase blood-brain barrier permeability, facilitating intravascular fluid extravasation and increasing PRES susceptibility.[12, 24, 25, 26]

History and Physical Examination

A thorough history and physical examination are indispensable for PRES diagnosis, as it is a clinical and radiographic diagnosis. Clinical presentations of PRES are diverse, varying in severity and acuity. Common presenting symptoms include headache (approximately 50% of cases), encephalopathy (28%), visual disturbances like binocular diplopia, vision loss, absent light perception, hemianopia, or quadrantanopia (39%), seizures (up to 80%), and focal neurological deficits (10-15%).[27] Patients may exhibit altered mental status, making history taking challenging, necessitating collateral information from family, friends, or caregivers. While normotension is uncommon, up to 75% of patients present with moderate to severe hypertension at initial evaluation.[18] Some researchers propose that the rapidity of blood pressure elevation, rather than the absolute blood pressure value, might be crucial, analogous to the theory for febrile seizures in children where the rate of temperature increase is significant.

During physical examination, key findings to note include hemianopia, quadrantanopia, visual neglect, cortical blindness, horizontal gaze palsy with preserved vestibulo-ocular reflex, papilledema, oral trauma (tongue biting indicative of seizures), hyperreflexia, active seizures, and urinary or fecal incontinence.[28, 29]

Evaluation for PRES Diagnosis

Neuroimaging is paramount and considered the gold standard for PRES diagnosis, as clinical symptoms alone are insufficient for definitive diagnosis.[30] Initially, a head CT scan is crucial to rule out neurological emergencies that can mimic PRES, such as intracranial hemorrhage. However, MRI of the brain without intravenous (IV) contrast is the preferred imaging modality for PRES diagnosis. MRI is highly sensitive in detecting vasogenic edema, which appears as a hyperintense signal on T2-weighted and Fluid-Attenuated Inversion Recovery (FLAIR) sequences. While the parieto-occipital lobes are most commonly affected, other regions including the temporal lobe, frontal lobe (superior frontal gyrus), cerebellum, brainstem, and deep white matter can also be involved.[4] It is theorized that the cortex, being more densely packed, may be more resistant to edema accumulation compared to white matter, leading to a greater relative involvement of the cortex in some PRES cases. MRI also aids in differentiating PRES from other potential diagnoses, such as hypoxic-ischemic encephalopathy, posterior circulation stroke, and primary central nervous system vasculitis.[2] In cases involving the classic posterior cerebral hemispheres, PRES can be distinguished from posterior cerebral artery infarction by the typical sparing of the calcarine and paramedian occipital lobe regions in PRES. Diffusion-weighted imaging (DWI) is also valuable in differentiating PRES from stroke, typically showing hypo- or isointense signals in PRES, unlike the hyperintensity often seen in acute ischemic stroke.

Vascular imaging, such as CTA or Magnetic Resonance Angiography (MRA) of the brain, is usually normal in PRES but can be helpful in excluding CNS vasculitis, which may present with focal vasoconstriction or vasodilation patterns. Magnetic Resonance Venography (MRV), also typically normal in PRES, can rule out sagittal sinus thrombosis as a differential diagnosis.[31]

The diagnostic workup for PRES diagnosis should also include investigations to identify potential underlying etiologies, as this is critical for management. Blood tests can assess for electrolyte imbalances (e.g., uremia, hypomagnesemia), hypoalbuminemia, protein deficiencies, and autoimmune markers. Cerebrospinal fluid (CSF) analysis may be indicated to exclude infections (e.g., herpes simplex encephalitis) or autoimmune conditions. Blood glucose measurement helps rule out severe hypoglycemia. Lumbar puncture is often performed in immunocompromised patients or when infection is suspected to evaluate for encephalitis.

Electroencephalography (EEG) can be a useful adjunct in PRES diagnosis and management. In patients with persistent altered mental status without overt seizures, EEG can detect subclinical seizure activity. However, EEG findings in PRES are generally non-specific.[32]

Image: FLAIR MRI of a patient with PRES demonstrating characteristic hyperintensities in the posterior regions, crucial for PRES diagnosis.

Treatment and Management

Effective management of PRES hinges on identifying and treating the underlying cause and carefully managing hypertension. Currently, there is no established, specific antihypertensive protocol for PRES-associated acute hypertension.[33] Antihypertensive treatment is generally recommended when blood pressure exceeds 160 mmHg systolic or 110 mmHg diastolic, with a target range of 130-150 mmHg systolic and 80-100 mmHg diastolic.[29] Rapid or excessive blood pressure reduction can induce cerebral hypoperfusion and increase the risk of ischemia. Therefore, blood pressure should be lowered gradually, not exceeding a 25% reduction from the initial presenting pressure within the first six hours.[29] This careful blood pressure management often necessitates admission to the intensive care unit (ICU) for continuous monitoring and titration of intravenous antihypertensives such as nicardipine, clevidipine, or labetalol until blood pressure stabilization is achieved. Subsequently, maintaining target blood pressure is crucial in both inpatient and outpatient settings. The optimal duration of antihypertensive therapy post-acutely is patient-specific and not definitively established.

Severe complications like status epilepticus or coma can occur in PRES, requiring intensive care management.[34] There is no consensus on specific antiseizure medications for PRES-related seizures, and dedicated studies are lacking. However, commonly used agents such as levetiracetam and phenytoin are frequently employed.[33] Antiepileptic treatment is often initiated during the acute phase of PRES and may be discontinued upon resolution of the syndrome.[35] In some cases, epilepsy may develop as a long-term sequela, necessitating chronic antiepileptic therapy.[1]

Corticosteroids have been proposed to alleviate PRES symptoms by reducing vasogenic edema. However, clinical evidence supporting their efficacy is lacking, and corticosteroids have even been implicated as a trigger for PRES in some patients, such as those treated for asthma.[36] If PRES is attributed to immunosuppressants like bevacizumab, pazopanib, sorafenib, or sunitinib, dose reduction or agent substitution is recommended.[37]

Differential Diagnosis

The differential diagnosis for PRES is broad and includes several critical conditions that must be considered:[2]

• Intracranial hemorrhage (including intracerebral, subdural, and subarachnoid hemorrhage)
• Cerebral sinus venous thrombosis
• Posterior circulation ischemic or hemorrhagic stroke
• Basilar artery thrombosis
• Encephalitis (both autoimmune and infectious, such as HSV encephalitis)
• Uremic encephalopathy
• Hypoglycemia

Prognosis

The prognosis for PRES is generally favorable if PRES diagnosis is prompt and treatment is initiated early. Symptom improvement or complete resolution typically occurs within days to weeks.[2, 14] Visual symptoms often resolve completely, particularly with early intervention, although some cases report residual visual deficits persisting (albeit improved) at 3 to 4 months post-onset.[27] The factors predicting prolonged visual deficits or persistent seizures remain unclear. Delayed treatment can lead to irreversible neurological damage. Extensive cerebral vasogenic edema worsens the prognosis, as increased pressure on cerebral blood vessels can impair blood flow and lead to ischemia.[16] Brainstem involvement also carries a poorer prognosis.[16] Recurrence of PRES is possible, particularly in patients undergoing dialysis.[2]

Complications

Failure to promptly treat PRES can result in significant complications, including focal neurological deficits due to ischemic injury, epilepsy, and life-threatening conditions such as transforaminal cerebellar herniation. Cerebellar herniation is a particularly concerning complication, especially in children following hematopoietic stem cell transplantation.[5, 38, 5]

Deterrence and Patient Education

Early recognition and treatment are crucial for reducing PRES complications and improving patient outcomes. Increased awareness and comprehensive education are vital for effective PRES management, including understanding its risk factors and etiologies. Patient education on blood pressure management can reduce the risk of cerebral autoregulation dysfunction, preventing PRES and other hypertensive complications. Healthcare provider awareness of the potential effects of cytotoxic immunosuppressants on the blood-brain barrier, even in normotensive patients, is essential for timely PRES diagnosis in patients receiving these medications.

Enhancing Healthcare Team Outcomes

Optimizing healthcare team outcomes for PRES necessitates education and effective communication among all members of the care team, including physicians, nurses, technicians, therapists, and especially patients and their families. Given the diverse clinical presentations of PRES and the need for specialized imaging for accurate PRES diagnosis, teamwork is paramount. While CT scans are essential to rule out hemorrhage, MRI is the cornerstone for diagnosing PRES. Radiologist involvement is critical for interpreting imaging findings. Effective communication and awareness of PRES facilitate prompt diagnosis and treatment, preventing potentially lethal complications. Collaboration between neurology and critical care services is essential, particularly for managing blood pressure with titratable intravenous medications, requiring close coordination between nursing and pharmacy practitioners. Shared decision-making, clear communication, and collaborative care pathways are key elements for achieving positive neurological outcomes in PRES management. Interprofessional care should follow an integrated, evidence-based approach to planning and evaluating all joint activities.

Review Questions

(Note: Review questions from the original article are accessible via the provided link.)

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Disclosure: Jaime Zelaya declares no relevant financial relationships with ineligible companies.

Disclosure: Lama Al-Khoury declares no relevant financial relationships with ineligible companies.