Related Subjects:
|Subarachnoid Haemorrhage
|Perimesencephalic Subarachnoid haemorrhage
|Haemorrhagic stroke
|Cerebellar Haemorrhage
|Putaminal Haemorrhage
|Thalamic Haemorrhage
|ICH Classification and Severity Scores
π§ Putaminal Haemorrhage is a common form of deep primary intracerebral haemorrhage, usually related to long-standing hypertension.
It occurs within the putamen (part of the basal ganglia), which is central to motor control.
Accounts for ~30β40% of all ICH cases and carries significant morbidity and mortality.
π Epidemiology
- Incidence: 30β40% of intracerebral haemorrhages.
- Age: Predominantly >60 years.
- Sex: More common in males.
- Geography: Higher prevalence in Asian populations.
𧬠Pathophysiology
- Rupture of deep penetrating arteries (lenticulostriates) due to chronic hypertension.
- Expanding clot raises ICP and compresses adjacent structures.
- Damage to the internal capsule β profound motor and sensory deficits.
β οΈ Causes
- Chronic hypertension (most common)
- Cerebral amyloid angiopathy (elderly)
- Anticoagulation / coagulopathy
- Brain tumours or metastases
- Substance misuse (esp. cocaine, amphetamines)
- Vascular malformations (rare)
π§Ύ Clinical Correlation with Location
- Anterior putamen:
- Left: aphasia, abulia, contralateral weakness.
- Right: behavioural changes, poor insight, aggression.
- Mid-putamen:
- Compression of adjacent structures.
- Left: global aphasia.
- Right: neglect syndrome.
- Posterior putamen: contralateral hemianopia, sensory loss, limb ataxia.
- Medial bleeds: risk of rupture into ventricles β hydrocephalus, coma.
π©Ί Clinical Presentation
- Sudden severe headache, nausea, vomiting.
- Focal neurological deficits (motor/sensory loss, speech disturbance).
- Altered consciousness β coma in severe cases.
- Raised ICP signs: papilloedema, bradycardia, hypertension, irregular breathing (Cushingβs triad).
β οΈ Complications
- Expansion of bleed β brainstem compression, herniation.
- Obstructive hydrocephalus.
- Seizures.
- Infection risk with CSF drains.
- Long-term disability (motor + cognitive).
π¬ Investigations
- CT head (non-contrast): first-line to identify bleed size, site, ventricular extension.
- MRI: for underlying lesions or delayed imaging.
- CTA / DSA: if vascular malformation suspected.
- Bloods: FBC, coagulation, U&E.
- ECG: monitor for arrhythmias due to raised ICP/stress.
π Management
- Stabilisation: ABCs, BP control (target SBP <140 mmHg).
- Reverse anticoagulation: e.g. Octaplex / Beriplex for warfarin.
- Medical therapy: antihypertensives, ICP control (mannitol, hypertonic saline), anticonvulsants if seizures.
- Surgery:
- Ventriculostomy for hydrocephalus.
- Clot evacuation in selected cases.
- Rehabilitation: MDT input β physio, OT, speech therapy, neuropsychology.
π Prognosis
- Mortality: high with large bleeds or intraventricular extension.
- Outcome depends on bleed size, GCS at presentation, and comorbidities.
- Survivors often left with significant neurological disability.
π‘οΈ Prevention
- Strict hypertension control (lifestyle + medication).
- Avoid unnecessary anticoagulation in high-risk patients.
- Substance misuse counselling.
- Regular follow-up for vascular risk factors.
π§ͺ Recent Advances
- Minimally invasive clot evacuation techniques (MIS, stereotactic aspiration).
- Neuroprotective agents in clinical trials.
- Advanced CT/MRI for prognostication and surgical planning.
π Clinical Guidelines
- Target systolic BP <140 mmHg (AHA/ESO guidelines).
- Immediate anticoagulant reversal if on warfarin/DOACs.
- Seizure prophylaxis considered if cortical involvement.
π References
- Hemphill JC et al. (2015). Guidelines for management of spontaneous ICH. Stroke.
- Broderick JP et al. (1993). Baseline NIHSS predicts outcome after ICH. Stroke.
π Additional Resources
πΌοΈ Images
Figure 1: Anatomy of the putamen within the basal ganglia.
Figure 2: Common haemorrhage sites within the putamen.