Non-Traumatic Causes of Acute Right Basal Ganglia Hemorrhage
Hypertension is the most common cause of non-traumatic basal ganglia hemorrhage, accounting for the majority of deep intracerebral hemorrhages in this location, followed by cerebral amyloid angiopathy (though CAA typically causes lobar hemorrhages), vascular malformations, coagulopathy, and less commonly moyamoya disease, tumors, and venous thrombosis. 1, 2, 3, 4
Primary Etiologies to Consider
Most Common Causes
Hypertensive hemorrhage is the leading etiology for basal ganglia hemorrhage. Deep hemorrhages in the basal ganglia, thalamus, pons, or cerebellum in patients with a history of hypertension are typically attributed to hypertensive arteriopathy affecting small perforating vessels. 1, 2, 3 The putamen is the most frequent location within the basal ganglia (90% of cases). 5
Cerebral amyloid angiopathy (CAA) is the second most common cause of spontaneous intracerebral hemorrhage overall, though it predominantly affects lobar locations rather than deep structures. 3, 4 However, it should still be considered, particularly in elderly patients without hypertension.
Vascular Malformations
Arteriovenous malformations (AVMs) and dural arteriovenous fistulas can cause basal ganglia hemorrhage, particularly in younger patients. 2, 3, 4 These are more likely when:
- Age <70 years with lobar ICH
- Age <45 years with deep or posterior fossa ICH
- Age 45-70 years with deep ICH and no history of hypertension or small vessel disease 6
Cavernous malformations represent another vascular cause that can be identified on MRI with blood-sensitive sequences. 6
Moyamoya disease can present with hemorrhagic stroke in adults, with posterior circulation involvement associated with higher rates of recurrent hemorrhage. 7 The disease shows characteristic stenosis of the terminal internal carotid artery with abnormal vascular networks (moyamoya vessels) in the basal ganglia region.
Coagulopathy-Related Causes
Anticoagulation therapy (warfarin, direct oral anticoagulants) accounts for 12-14% of intracerebral hemorrhages, with this proportion increasing. 2
Antiplatelet agents and thrombocytopenia can contribute to hemorrhage risk.
Coagulation factor deficiencies (acquired or congenital) predispose to bleeding. 2
Other Important Causes
Cerebral venous thrombosis can cause hemorrhagic venous infarction. This should be suspected when there is:
- Unusual hemorrhage location
- Edema disproportionate to hemorrhage timing
- Abnormal signal in cerebral sinuses 2, 3
Tumors (primary CNS neoplasms or metastatic disease) can present with hemorrhage. 4
Sympathomimetic drugs (cocaine, amphetamines) are associated with intracerebral hemorrhage. 1, 3
Hemorrhagic transformation of ischemic infarct can occur, particularly in the basal ganglia territory. 4
Cerebral hyperperfusion syndrome following carotid revascularization. 4
Diagnostic Approach
Initial Imaging Strategy
CT without contrast is the gold standard for acute hemorrhage detection and should be performed emergently. 1, 2, 3
Vascular Imaging Indications
CTA or MRA should be performed to evaluate for underlying vascular lesions when: 3, 6
- Age <70 years with lobar hemorrhage
- Age <45 years with deep hemorrhage
- Age 45-70 years with deep hemorrhage WITHOUT hypertension or small vessel disease
- Unusual hematoma shape or location
- Subarachnoid hemorrhage component
- Edema disproportionate to timing
CT/MR venography should be added when venous thrombosis is suspected based on location or imaging characteristics. 2, 3
Catheter angiography remains the gold standard and has highest diagnostic yield in the populations listed above, particularly when CTA/MRA are negative or inconclusive. In one series, DSA identified vascular malformations in 10 of 89 patients with negative CTA and MRI/MRA. 4
MRI Role
MRI with gradient echo or T2 susceptibility-weighted sequences* should be performed (if not acutely, then as follow-up) to: 6
- Detect microbleeds or cortical superficial siderosis (suggesting CAA)
- Identify cavernous malformations
- Exclude underlying mass lesions (contrast-enhanced T1)
- Characterize chronic hemorrhagic lesions
Clinical Clues for Specific Etiologies
Hypertension: History of hypertension, single deep hemorrhage in putamen/thalamus/pons/cerebellum, presence of small vessel disease (white matter lesions, lacunar infarcts). 1, 6
Vascular malformation: Younger age, absence of hypertension, unusual location, enlarged vessels or calcifications at hemorrhage margins. 3, 6
CAA: Elderly, lobar location, multiple microbleeds on MRI, cortical superficial siderosis, no hypertension history. 3, 4
Moyamoya: Stenosis of terminal ICA, abnormal vascular networks in basal ganglia on imaging, posterior circulation involvement. 7
Common Pitfalls
Assuming all basal ganglia hemorrhages are hypertensive: While hypertension is most common, a substantial number have alternative etiologies, particularly in younger patients or those without hypertension history. 1
Inadequate vascular imaging in appropriate candidates: Missing vascular malformations because CTA/MRA alone were performed without follow-up catheter angiography when indicated. 4
Delayed MRI: Failing to obtain MRI to detect underlying lesions, microbleeds, or markers of specific vasculopathies. 6
Not considering venous thrombosis: Missing cerebral venous thrombosis when hemorrhage has atypical features. 2, 3