What Is Perimesencephalic Subarachnoid Hemorrhage?

Perimesencephalic subarachnoid hemorrhage (PMSAH) is a specific type of non-aneurysmal subarachnoid hemorrhage that occurs around the midbrain. Unlike aneurysmal hemorrhages, which often have severe outcomes, PMSAH generally follows a more benign course with lower risks of complications. While its exact cause remains unclear, it is thought to result from venous bleeding rather than arterial rupture.

Recognizing PMSAH is crucial because its clinical course and management differ significantly from other types of subarachnoid hemorrhages. Identifying it correctly ensures appropriate treatment while avoiding unnecessary interventions.

Clinical Presentation

The hallmark symptom of PMSAH is a sudden, severe “thunderclap” headache that reaches peak intensity within seconds, often localized to the occipital or posterior head. Unlike aneurysmal subarachnoid hemorrhages, which may cause widespread neurological deficits, PMSAH is less likely to impair neurological function beyond the headache itself. Some patients report nausea, vomiting, photophobia, and neck stiffness, which can mimic other forms of subarachnoid hemorrhage.

Neurological examination is often unremarkable, with most patients maintaining full consciousness and a Glasgow Coma Scale (GCS) score of 15. Unlike aneurysmal hemorrhages, which frequently cause altered mental status and focal deficits, PMSAH rarely leads to significant cognitive impairment. While some individuals may experience transient confusion or mild drowsiness, profound neurological dysfunction is uncommon. Meningismus, characterized by neck stiffness and discomfort with passive neck flexion, may be present but is generally mild.

In rare cases, mild oculomotor disturbances such as transient diplopia or subtle pupillary asymmetry occur due to the hemorrhage’s proximity to the midbrain. Seizures are exceedingly uncommon, distinguishing PMSAH from aneurysmal subarachnoid hemorrhages, where seizures occur in up to 26% of cases. Systemic symptoms such as transient hypertension and tachycardia may also appear as physiological responses to the acute headache and stress.

Diagnostic Processes

Accurately diagnosing PMSAH is essential to distinguish it from aneurysmal subarachnoid hemorrhage, which requires different management strategies. Diagnosis typically involves neuroimaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI), with cerebrospinal fluid analysis via lumbar puncture when necessary. Cerebral angiography may be performed to rule out vascular abnormalities.

CT

Non-contrast CT is the first-line imaging modality, highly sensitive in detecting acute subarachnoid hemorrhage within the first 24 hours. PMSAH appears as localized hyperdensity of blood in the perimesencephalic cisterns, particularly around the midbrain and pons, without significant extension into the lateral Sylvian fissures or interhemispheric fissure. This distribution helps differentiate PMSAH from aneurysmal hemorrhages, which typically present with more diffuse blood spread.

A study published in Stroke (2012) found that CT scans performed within six hours of symptom onset had nearly 100% sensitivity for detecting subarachnoid hemorrhage. However, as time progresses, the sensitivity of CT decreases due to blood resorption, necessitating further evaluation if initial imaging is inconclusive.

MRI

MRI, particularly fluid-attenuated inversion recovery (FLAIR) and susceptibility-weighted imaging (SWI) sequences, can detect subarachnoid blood when CT findings are equivocal. FLAIR enhances cerebrospinal fluid abnormalities by suppressing normal fluid signals, while SWI is effective in identifying hemosiderin deposits indicative of prior hemorrhagic events.

MRI is not typically the first-line modality due to longer acquisition times and limited availability in emergency settings but is valuable when CT scans are negative despite high clinical suspicion. A 2018 study in Neuroradiology reported that MRI detected residual blood in 85% of patients with subarachnoid hemorrhage who had negative CT scans beyond 24 hours.

Lumbar Puncture

Lumbar puncture (LP) is used when imaging does not confirm hemorrhage but clinical suspicion remains high. Cerebrospinal fluid (CSF) analysis can reveal xanthochromia, a yellow discoloration caused by hemoglobin breakdown, which appears within six to twelve hours and persists for up to two weeks. The presence of red blood cells in serially collected CSF samples can also indicate subarachnoid hemorrhage, though traumatic taps must be considered.

A systematic review in The Lancet Neurology (2016) found that LP had a sensitivity of nearly 100% for detecting subarachnoid hemorrhage when performed after 12 hours. However, LP is generally reserved for cases where imaging is inconclusive, as it is an invasive procedure with potential complications such as post-lumbar puncture headache.

Angiography

Cerebral angiography, particularly digital subtraction angiography (DSA), is used to exclude vascular abnormalities such as aneurysms or arteriovenous malformations. In PMSAH, angiography typically reveals no underlying vascular pathology. Some clinicians advocate for a single angiographic study if the CT pattern is characteristic of PMSAH, while others recommend follow-up imaging to ensure no missed vascular lesions.

A retrospective study in the Journal of Neurosurgery (2019) found that repeat angiography in PMSAH cases rarely identified new aneurysms, suggesting that a single negative angiogram is sufficient in most cases. However, in patients with atypical hemorrhage distribution or persistent clinical concerns, follow-up angiography may be warranted.

Radiological Findings

Imaging plays a decisive role in differentiating PMSAH from aneurysmal and other non-aneurysmal hemorrhages. The hallmark radiological feature on non-contrast CT is hyperdense blood localized to the perimesencephalic cisterns, particularly around the midbrain and upper pons. Unlike aneurysmal hemorrhages, which often present with diffuse blood extending into the Sylvian fissures and interhemispheric fissure, PMSAH remains confined to the prepontine and interpeduncular cisterns.

Timing of imaging affects radiological appearance. In the acute phase, typically within the first 24 hours, blood appears as a high-attenuation signal on CT. As time progresses, blood products undergo resorption, making detection more difficult. By the end of the first week, CT sensitivity declines, necessitating alternative imaging if suspicion remains high. MRI, particularly FLAIR sequences, can detect residual blood by highlighting abnormal cerebrospinal fluid signal intensity. SWI is also valuable for identifying hemosiderin deposition, which may indicate prior hemorrhagic episodes.

Cerebral angiography, often performed to exclude vascular abnormalities, typically shows no evidence of aneurysm or arteriovenous malformation in PMSAH cases. Digital subtraction angiography (DSA) remains the gold standard for vascular imaging. In patients with classic PMSAH distribution on CT, a single negative angiogram is often considered sufficient, though repeat angiography may be warranted in atypical cases.

Management Approaches

Treatment focuses on symptom control, monitoring for complications, and ensuring no underlying vascular abnormality is missed. Unlike aneurysmal subarachnoid hemorrhage, PMSAH does not require surgical intervention. Hospital admission for 24 to 48 hours is generally recommended for observation.

Blood pressure management is considered, with some clinicians opting for cautious control to prevent rebleeding, though PMSAH is not associated with recurrent hemorrhage. Labetalol or nicardipine may be used to maintain systolic blood pressure below 160 mmHg, though overly aggressive lowering is avoided to prevent cerebral hypoperfusion.

Headache management is a priority, with non-opioid analgesics such as acetaminophen or NSAIDs as first-line treatments. Short-term opioids may be considered in refractory cases. Patients with associated nausea or vomiting may benefit from antiemetics such as ondansetron or metoclopramide. Given the potential for mild transient hydrocephalus, serial neurological assessments are performed to monitor for signs of increased intracranial pressure.

Prognostic Factors

Long-term outcomes in PMSAH are generally favorable, with most patients experiencing full neurological recovery. The absence of arterial rupture reduces the risk of vasospasm, delayed cerebral ischemia, or rebleeding—complications that contribute to poorer outcomes in aneurysmal cases.

Studies tracking PMSAH patients over several years have found that most return to baseline functional status with little to no residual neurological deficits. Some individuals report persistent headaches or subtle cognitive complaints, such as difficulty with concentration or mild fatigue, which may persist for months.

Functional recovery is excellent, with Glasgow Outcome Scale scores indicating favorable results in over 95% of cases. While some patients experience prolonged psychological effects, including anxiety related to the sudden onset of symptoms, reassurance about the low recurrence rate and lack of long-term neurological decline can be beneficial. Long-term monitoring beyond the initial recovery period is rarely necessary, though some may benefit from periodic neurological assessments if persistent symptoms occur.