Deep right capsuloganglionic high-flow arteriovenous malformation presenting with intracerebral hemorrhage in an adolescent: A comprehensive case report

Sripreethi1*, Jayamenon2

1Nurse Educator, Kauvery Hospital, Heart city, Trichy, Tamil Nadu

2Nursing superintendent, Kauvery Hospital, Heart city, Trichy, Tamil Nadu

*Correspondence

Abstract

Intracranial arteriovenous malformations (AVMs) are congenital vascular anomalies that frequently present with intracerebral hemorrhage in young individuals. Deep-seated AVMs involving the capsuloganglionic region are associated with significant neurological morbidity due to involvement of eloquent motor pathways.  We report a 17-year-old female who initially presented with acute left hemiparesis secondary to right basal ganglionic hemorrhage. Imaging confirmed a deep capsuloganglionic AVM. She underwent right front temporoparietal (FTP) craniotomy with hematoma evacuation. Six months later, she was admitted for diagnostic cerebral angiography (DSA), which revealed a deep right gangliocapsular high-flow AVM with predominant deep venous drainage (Spetzler–Martin Grade IV).  This case highlights diagnostic challenges, surgical considerations, angiographic characteristics, and long-term management implications of deep AVMs in adolescents.

Keywords: Arteriovenous malformation; Capsuloganglionic AVM; Intracerebral hemorrhage; DSA; Spetzler–Martin Grade IV; Hemiparesis

Introduction

Cerebral AVMs account for approximately 1–2% of all strokes and are a major cause of hemorrhagic stroke in young patients. Deep AVMs involving basal ganglia and internal capsule represent high surgical risk due to proximity to motor tracts.  Spetzler–Martin grading is essential for operative planning and risk stratification.

Case presentation

Patient profile

  • Age: 17 years
  • Gender: Female
  • No significant past comorbidities

History of present illness:

Six months prior, the patient developed sudden onset weakness of the left upper and lower limbs associated with giddiness. There were no trauma or seizures. Evaluation revealed intracerebral hemorrhage in the right basal ganglion region secondary to AV malformation. She underwent: Right FTP craniotomy with hematoma evacuation and tapping. Postoperatively, she had residual mild left hemiparesis and was advised for cerebral angiographic evaluation.

Clinical examination (Current Admission)

On admission to DSA:

Conscious and oriented

GCSE4V5M6
BP110/60 mmHg
PR76 bpm
RSNormal vesicular breath sounds
CVSS1 S2 heard
AbdomenSoft

Neurological findings

  • Residual left hemiparesis
  • Right upper and lower limb power: 5/5
  • Left upper and lower limb: Mild weakness

Radiological Investigations

CT Brain (Initial Episode)

  • Acute hematoma (3.6 × 2.5 cm) in right basal ganglion
  • Effacement of right lateral ventricle

MRI Brain

  • Acute intraparenchymal hematoma in right capsuloganglionic region
  • Mild compression of right lateral ventricle
  • Midline shift: 5 mm
  • Suspicion of AVM

CT Angiogram

  • Large AV malformation in right capsuloganglionic region
  • Cerebral Angiogram (DSA Findings)
  • Performed via right transfemoral route under local anesthesia.

Angiographic findings

  • Compact AVM nidus in deep right cerebral region involving gangliocapsular area
  • Nidus size: 4.3 × 3.3 × 3.8 cm

Predominant feeders

  • Hypertrophied right lenticulostriate arteries (from MCA M1 segment)
  • Additional supply from right PCA
  • Early venous opacification (high-flow shunt)
  • Deep venous drainage predominance
  • No intranidal aneurysm
  • No major arterial stenosis

Final angiographic impression:

  • Deep right gangliocapsular high-flow AVM with predominant deep venous drainage
  • Spetzler–Martin Grade IV

Laboratory Investigations

Complete Blood Count

Total WBC7220 cells/cumm
Neutrophils49%
Lymphocytes29.5%
Monocytes7.8%
Eosinophils13% (mildly elevated)
Basophils0.7%
Absolute Neutrophil Count3540 cells/µL
Platelet Count2,30,000 /cumm
MPV10.0

Clinical Chemistry

Urea17 mg/dL
Creatinine0.7 mg/dL
Sodium134 mmol/L (borderline low)
Potassium3.9 mmol/L
Chloride101 mmol/L
Bicarbonate26 mEq/L

Renal function and electrolytes were within acceptable limits.

Procedure Monitoring (DSA)

HR72–76 bpm
BP120/80 mmHg
SpO₂99%
RR20/min
Aldrete Score post-procedure10/10

Advice

  • Right lower limb immobilization for 6 hours
  • Monitor for groin hematoma

Final Diagnosis

Deep right gangliocapsular high-flow arteriovenous malformation with prior intracerebral hemorrhage.  Residual left hemiparesis.  Spetzler–Martin Grade IV

Discussion

  • Deep capsuloganglionic AVMs are rare but clinically significant due to:
  • Involvement of internal capsule
  • High hemorrhage risk
  • Predominant deep venous drainage
  • Complex arterial feeders
  • High-flow AVMs demonstrate early venous opacification, as seen in this case.
  • Spetzler–Martin Grade IV indicates:
  • Large size (>3 cm)
  • Deep venous drainage
  • Eloquent brain location
  • Such lesions have increased surgical morbidity. Management options include:
  • Microsurgical Excision
  • Endovascular embolization
  • Stereotactic radiosurgery
  • Multimodal approach
  • Given prior hemorrhage, long-term definitive treatment planning is essential.
  • Clinical Significance.

Case highlights

AVM is a cause of stroke in adolescents. Importance of angiographic grading.  Role of early surgical evacuation in hemorrhagic cases. Need for multidisciplinary neurosurgical planning.

Conclusion

Deep right capsuloganglionic AVM presenting with intracerebral hemorrhage in adolescence requires early recognition, careful surgical intervention, and comprehensive angiographic evaluation. Spetzler–Martin Grade IV lesions demand individualized treatment planning due to high operative risk. Long-term neurological outcome depends on hemorrhage control, vascular architecture, and timely intervention.

References

  1. Lawton MT, Rutledge WC, Kim H, Stapf C, Whitehead KJ, Li DY, et al. Brain arteriovenous malformations. Nat Rev Dis Primers. 2015;1:15008.
  2. Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg. 1986;65(4):476–83.
  3. Mohr JP, Parides MK, Stapf C, Moquete E, Moy CS, Overbey JR, et al. Medical management with or without interventional therapy for unruptured brain arteriovenous malformations (ARUBA): a multicentre, non-blinded, randomised trial. Lancet. 2014;383(9917):614–21.
  4. Stapf C, Mast H, Sciacca RR, Choi JH, Khaw AV, Connolly ES, et al. The New York Islands AVM Study: determinants of hemorrhagic presentation. Stroke. 2006;37(10):2499–503.
  5. da Costa L, Wallace MC, ter Brugge KG, O’Kelly C, Willinsky RA, Tymianski M. The natural history and predictive features of hemorrhage from brain arteriovenous malformations. Stroke. 2009;40(1):100–5.
  6. Al-Shahi R, Fang JS, Lewis SC, Warlow CP. Incidence and prognosis of arteriovenous malformations of the brain in adults. Brain. 2000;123(Pt 3):482–9.
  7. Derdeyn CP, Zipfel GJ, Albuquerque FC, Cooke DL, Feldmann E, Sheehan JP, et al. Management of brain arteriovenous malformations: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2017;48(8):e200–24.
  8. Gross BA, Du R. Natural history of cerebral arteriovenous malformations: a meta-analysis. J Neurosurg. 2013;118(2):437–43.
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