Background:
Non-aneurysmal perimesencephalic subarachnoid hemorrhage (NAPMSAH) is a rare subtype of spontaneous subarachnoid hemorrhage characterized by blood predominantly distributed around the midbrain cisterns and the absence of an identifiable aneurysmal source. It generally has a favorable clinical course and lower complication rates than aneurysmal subarachnoid hemorrhage. Although its precise pathophysiology remains uncertain, transient elevations in intracranial venous pressure associated with Valsalva-like maneuvers have been proposed as a potential mechanism. We report an unusual presentation of NAPMSAH in a hypertensive middle-aged female with recurrent vomiting.
Case Presentation:
A 58-year-old female with a five-year history of systemic hypertension and dyslipidemia presented with an acute-onset severe headache that progressively worsened over one day. The headache was described as the worst headache of her life and was associated with multiple episodes of vomiting, photophobia, and phonophobia. She had no loss of consciousness, seizures, altered sensorium, fever, neck rigidity, or focal neurological deficits. She also had a history of gastroesophageal reflux disease with recurrent episodes of dry cough and vomiting. On presentation, her blood pressure was 160/100 mmHg, while her Glasgow Coma Scale score was 15/15. Non-contrast CT of the brain demonstrated subarachnoid hemorrhage predominantly involving the interpeduncular, ambient, quadrigeminal, and bilateral superior cerebellar cisterns, consistent with a classic perimesencephalic hemorrhage pattern. CT cerebral angiography showed no intracranial aneurysm, arteriovenous malformation, or other vascular abnormality. Conventional digital subtraction angiography was planned but was not performed because the patient declined due to financial constraints. She was managed conservatively with neurological monitoring, nimodipine, seizure prophylaxis, blood pressure control, analgesia, antiemetics, and supportive care.
Outcome:
The patient improved clinically within two days and remained neurologically intact without vasospasm, rebleeding, hydrocephalus, or electrolyte disturbances. She was discharged on the fifth day. At two-week and one-month follow-up, she had complete resolution of headache, no neurological deficits, and had resumed normal daily activities.
Conclusion:
NAPMSAH should be considered in patients presenting with acute severe headache even in the absence of focal neurological or meningeal signs. In this patient, recurrent vomiting as a Valsalva-like event, together with uncontrolled hypertension, may have contributed to transient increases in intracranial venous pressure and precipitated hemorrhage. Although the proposed mechanism remains speculative, careful neurovascular imaging is essential to exclude an aneurysmal source and establish the diagnosis. The favorable clinical recovery in this case further demonstrates the generally benign course of NAPMSAH.