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Basal Ganglia Hemorrhage
CT scan illustrating a basal ganglia hemorrhage (BGH) on the left side of the brain
CT scan illustrating a basal ganglia hemorrhage (BGH) on the left side of the brain
SpecialtyNeurosurgery
SymptomsSudden severe headache, Weakness or paralysis on one side of the body, Difficulty in speaking or understanding speech[1], Movement disorder[2], Decreased level of consciousness[3]
CausesHypertension[4], Ruptured aneurysm, Arteriovenous malformation (AVM)[5], Cerebral amyloid angiopathy[6]
Diagnostic methodCT Scan[7], MRI[8]
TreatmentBlood pressure management, Rehabilitation[9]

Basal ganglia hemorrhage (BGH) is a type of intracerebral hemorrhage (ICH) that involves bleeding within the basal ganglia, a region deep within the brain responsible for motor control, cognition, and behavior.[10] Chronic, uncontrolled hypertension is the most common cause; other potential causes may include malformations of the blood vessels, certain concurrent diseases, and injuries to the head.[11] Symptoms can be diverse, which depends on the hemorrhage's size and its location within the basal ganglia. Still, common symptoms include movement disorders and impaired consciousness.[3]

To confirm the presence of hemorrhage, computed tomography (CT) scans and magnetic resonance imaging (MRI) are usually conducted.[7][8] Meanwhile, further laboratory tests on individuals’ blood samples might also be performed to evaluate potential risk factors.[12] Management of the conditions in individuals with BGH involves controlling blood pressure, reversing anticoagulation medication, and reducing intracranial pressure (ICP).[13][14]

BGH, classified as an ICH subtype, is generally more prevalent in Asian populations, also affecting more males than females.[4] Although bilateral BGH (occurring at both sides of the brain) is rarer than unilateral BGH (occurring only at one side of the brain), bilateral BGH has a relatively greater mortality than unilateral BGH.[4]

Signs and Symptoms

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Schematic of the ascending reticular activating system, which plays a role in sensory processing, motor control, and consciousness. BGH can disrupt this pathway, leading to sensory deficits, movement disorders, and altered awareness

BGH typically manifests unilaterally, affecting one side of the body. While less frequent, bilateral involvement can result in more pronounced and severe symptoms, with the specific presentation influenced by the location and size of the hemorrhage, as well as any associated complications. These hemorrhages can lead to neurological deficits, impacting consciousness, motor function, and reflexes.

One of the most significant concerns, particularly with bilateral hemorrhages, is altered consciousness. Damage to the ascending reticular activating system in the brain disrupts arousal and awareness, potentially leading to reduced alertness, unconsciousness, or even coma.[3] Motor dysfunction is also common in unilateral and bilateral hemorrhage, presenting as movement disorders involving slowness of movement, tremor, and involuntary muscle contractions.[2]

In addition to impaired consciousness, BGHs can disrupt nearby neuroanatomical structures, resulting in speech dysfunction, such as repetition or the inability to name objects.[1] Such injuries can also lead to difficulty in swallowing, or functional damage to the digestive tract, such as the soft palate, tongue, or the esophagus.[15] Respiratory abnormalities may also occur, leading to irregular breathing rhythms, impaired cough reflex, and decreased responsiveness to blood carbon dioxide levels changes. Hence, individuals with BGH may require additional mechanical ventilation.[16] Collateral symptoms may also include cognitive and behavioral changes, such as executive dysfunction, attention deficits or memory impairment.[17]

Causes

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Causes of BGH can be non-traumatic or traumatic.

Non-traumatic Causes

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Brain blood vessel damage (a-f) from amyloid buildup in cerebral amyloid angiopathy. Images show mild (Grade 1), moderate (Grade 2), and severe (Grade 3) damage from left to right.

Non-traumatic causes account for the majority of cases, and are frequently linked to chronic medical conditions. Chronically elevated and poorly managed blood pressure weakens the arterial walls within the basal ganglia, increasing the risk of hemorrhage.[4] Despite its low occurrence, cerebral amyloid angiopathy at the basal ganglia can also be a potential cause, particularly in elderly individuals.[6] Other possible non-traumatic reasons include arteriovenous malformations (AVM), manifested as abnormal tangles of blood vessels, which are associated with an elevated risk of hemorrhage.[5] Apart from existing medical conditions, substance abuse, especially alcohol, can also promote the occurrence of bleeding in the basal ganglia.[4]

Traumatic Causes

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Traumatic BGH, while less common than non-traumatic causes, results from head injuries, surgical intervention in the brain, or even lightning strike under rare circumstances.[4] Such injuries directly damage blood vessels within the basal ganglia, consequently causing blood leakage. A hematoma then forms as the blood clots, whether the bleeding is immediate or develops over time. The magnitude of the applied force, along with any accompanying injuries, dictates the severity of the resulting hemorrhage. In some cases, even relatively minor head trauma triggers a hemorrhage in individuals with predisposing vascular abnormalities or other risk factors.

Pathophysiology

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BGH results from a primary brain injury, specifically the rupture of a blood vessel within the basal ganglia, which can then initiate a cascade of secondary brain injuries.

Primary Brain Injury

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When a blood vessel within the basal ganglia ruptures, the infiltration of blood exerts pressure on the surrounding brain tissue, an effect known as "mass effect."[18] Disrupting the normal function of adjacent neurons and neural pathways, this direct compression of adjacent neural structures results in a series of complications that range from motor impairments and sensory alterations to cognitive dysfunction. Primary injuries often trigger secondary brain injuries.

Secondary Brain Injury

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A schematic showing the anatomical structure of the blood-brain barrier.

Beyond the immediate compression exerted, secondary injuries further exacerbate the damage. Edema frequently develops around the bleeding site, not only intensifying the compression of brain tissue and elevating ICP, but also contributing to further neuronal dysfunction.[19] Furthermore, the hemorrhage can trigger excitotoxicity that leads to the death of nearby neurons.[20] Inflammation also plays a significant role in secondary injury. While intended to be protective, it may inadvertently harm healthy brain tissues. By disrupting the blood-brain barrier, which normally safeguards the brain from harmful substances, inflammatory cells and damaging molecules gain entry into the brain, potentially extending the damage beyond the initial site of hemorrhage.[21]

Diagnosis

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The diagnosis of BGH relies on a combination of clinical assessments, neuroimaging, and laboratory investigations.

Initial Assessment

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The initial assessment of an individual suspected of having a BGH begins with a thorough neurological examination. This examination focuses on evaluating individuals' cranial nerve function, motor and sensory function, level of consciousness, and reflexes. Simultaneously, vital signs, including respiratory rate, blood oxygen saturation, blood pressure, and heart rate, are assessed to not only ensure immediate stabilization but also tailor subsequent management of the individual. These tests usually involve reputable scoring systems, such as the Glasgow Coma Scale, or the National Institutes of Health Stroke Scale.[22] Aiming to determine the severity of the condition, such assessments should be performed without sedation.[22]

Neuroimaging

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An MRI showing the anatomy of the basal ganglia (BG). Regions of interest are indicated by colored circles: globus pallidus (blue), putamen (red), nucleus accumbens (grey), and caudate nucleus (orange).

Neuroimaging is critical in confirming the diagnosis of BGH and excluding other potential causes of neurological deficits. CT scans are favored due to their speed, widespread availability, and high sensitivity for detecting acute hemorrhage, rapidly identifying the presence, location, and size of the hematoma.[7]

MRI also provides superior sensitivity for detecting smaller hemorrhages, revealing underlying structural abnormalities such as AVM or tumors that may have predisposed the individual to the hemorrhage. In cases where a vascular malformation or aneurysm is suspected, angiography, which may involve CT angiography or magnetic resonance angiography, can be employed to visualize the cerebral vasculature in detail.[8]


Laboratory Tests

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Laboratory tests not only aid in the evaluation of potential contributing factors, but also in the exclusion of other underlying conditions. A complete blood count test is performed to identify any abnormalities, such as anemia or thrombocytopenia.[12] Besides, coagulation studies, including partial thromboplastin time, thrombin time, and prothrombin time, are conducted to identify any underlying abnormalities in the ability to form blood clots that may have contributed to the hemorrhage.[23] Moreover, a toxicology screen may be considered if there is any suspicion of drug use as a potential precipitating factor in the hemorrhagic event.

Treatment

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Medical Management

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Effective blood pressure management is a critical component of medical care, aiming to prevent further hematoma enlargement. Careful attention is given to avoiding both hypertension and hypotension, as both can adversely impact the individual’s health.[24]

In individuals receiving anticoagulant medications, prompt evaluation for potential anticoagulation reversal is essential. This often involves administering appropriate reversal agents, such as the utilization of vitamin K to reverse the effects of warfarin, guided by laboratory values and clinical assessment.[25]

Furthermore, monitoring for elevated ICP prompts consideration for interventions to mitigate its effects. Interventions usually include: elevating the head of the bed to facilitate venous drainage, and administering osmotic agents like mannitol or hypertonic saline to reduce cerebral edema.[13][14] Additionally, sedation may also be considered to reduce cerebral metabolic demands and, consequently, ICP.[26]

In the cases of hydrocephalus or if elevated ICP is unresponsive to the aforementioned measures, the placement of an external ventricular drain (EVD) to drain cerebrospinal fluid (CSF) will be considered. EVD placement allows for continuous ICP monitoring and CSF diversion, providing a means to control ICP and improving neurological outcomes.[27]

The use of seizure prophylaxis with anticonvulsant medications is carefully considered on a case-by-case basis. Prophylaxis is particularly relevant in individuals with a history of seizures, those exhibiting clinical seizure activity, or those with electrographic evidence of seizures on electroencephalography.[28]

Surgical Management

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While traditional craniotomy is an option (B), minimally invasive techniques are increasingly utilized. It also shows preoperative planning (A), a preoperative CT scan (C) of the hematoma, and a postoperative CT scan (D) after hematoma removal.

Surgical intervention may be considered in certain cases of BGH. Hematoma evacuation may be an option for individuals with large hematomas, significant mass effect, or hydrocephalus.[29] Surgical approaches vary, including traditional craniotomy, and minimally invasive techniques, which are considered more promising.[11]

Rehabilitation

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A structured rehabilitation program, including speech therapy, occupational therapy, and physical therapy, is often prescribed for individuals with BGH, aiming to help them regain motor skills, improve independence in daily living activities, and address communication difficulties, contributing to overall recovery.[9]




Epidemiology

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Incidence and Prevalence

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ICH, including BGH, represents a significant portion of all stroke cases, accounting for approximately 10-20%.[30] Particularly, the basal ganglia are a prevalent site for ICH.[31]

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The average age of individuals with BGH was 51 years, mainly affecting males rather than females. Besides, males diagnosed with BGH also tend to be younger than females.[4]

Hypertension prevalence by age and ethnicity. South Asian groups show higher prevalence across age groups.

Geographic Variations

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Epidemiological studies have revealed geographic variations in the incidence of ICH, with a greater incidence reported in Asian populations compared to Western populations. These differences may be attributed to variations in genetic factors, dietary habits, and the prevalence of hypertension across different regions.[4]

Mortality and Prognosis

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BGH is associated with substantial morbidity and mortality rates. The 30-day mortality rate for ICH is typically around 40%.[11][32] Meanwhile, bilateral BGH and unilateral BGH have a 30-day mortality of 25% and 16% respectively.[11] Factors linked to poorer outcomes include large hematoma size, and the presence of intraventricular hemorrhage.

Special Populations

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Due to the specific challenges they present, the elderly and children with BGH often require individualized management strategies.

Geriatrics

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BGH disproportionately affects the elderly, owing to the increased prevalence of risk factors such as cerebral amyloid angiopathy, hypertension, vascular wall defects and anticoagulant medication. [33][34][35]

Management of BGH in the population requires thorough consideration of potential drug interactions, comorbidities, and age-related physiological changes, with comorbidities being the key factor that complicates BGH treatment.[34]

Typical treatment approaches for BGH include managing hypertension, limiting alcohol consumption, and monitoring anticoagulants.[36]

Pediatrics

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BGH is rare in children, but when it occurs, it carries a high risk of death or long-term disability.[35] Moreover, it is often associated with underlying conditions such as inherited metabolic disorders, hypoxic-ischemic brain injury, neurotoxicity, or infections.[37][38] As the clinical presentation, diagnosis, and management of BGH in children may be different from those in adults, it is crucial to thoroughly identify the underlying causes.[39] Thus, treatment and resulting neurological outcomes are highly individualized, taking into account the causes and influencing factors of BGH in children.

References

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  31. ^ Lobo, Kaike; Santos, Cláudia; Campos, Pedro; Oliveira, Larah; da Silva, Vithor Ely Bortolin (2025-01-15). "Neuroendoscopic surgery versus craniotomy for basal ganglia hemorrhage: a systematic review and meta-analysis of randomized controlled trials". Neurosurgical Review. 48 (1): 50. doi:10.1007/s10143-025-03213-w. ISSN 1437-2320.
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