Cerebellar hemorrhage

• Structural Alterations Associated With Cardiovascular Autonomic Failure in Multiple System Atrophy
• Brain-Body Interactions in Ischemic Stroke: VNS Reprograms Microglia and FNS Enhances Cerebellar Neuroprotection
• Embolic Shower Pattern on Magnetic Resonance Imaging: An Atypical Presentation of Chikungunya Encephalitis
• A case report of a family with Primary familial brain calcification caused by a novel MYORG gene variants
• Isolated Aphasia From a Left Parietotemporal Infarct Secondary to a Patent Foramen Ovale: A Case Report
• Parent Artery Occlusion Using Multiple Short iED Coils and n-Butyl Cyanoacrylate via a Marathon Microcatheter for a Dissecting Aneurysm of the Distal Posterior Inferior Cerebellar Artery With Severe Flexion of the Caudal Loop: A Case Report
• Persistent trigeminal artery variant functioning as a duplicate superior cerebellar artery
• Fifty Years of Deciphering Stroke Pathophysiology

Cerebellar hemorrhage classification

Some common causes include:

Hypertension: High blood pressure is one of the leading causes of cerebellar hemorrhage. Chronic hypertension can weaken the blood vessel walls, making them more susceptible to rupture and bleeding.

Cerebral Amyloid Angiopathy (CAA): CAA is a condition characterized by the deposition of amyloid protein in the walls of small blood vessels in the brain, including the cerebellum. This can lead to vessel fragility and an increased risk of hemorrhage.

Arteriovenous Malformations (AVMs): AVMs are abnormal tangles of blood vessels that can rupture and cause bleeding in the brain, including the cerebellum.

Cerebral Aneurysms: Aneurysms are weakened areas in the walls of blood vessels that can balloon out and rupture, causing hemorrhage. Aneurysms can occur in the arteries supplying the cerebellum.

Head Trauma: Traumatic injury to the head can cause bleeding within the brain, including the cerebellum. This may result from falls, motor vehicle accidents, or other types of trauma.

Coagulopathy: Disorders of blood clotting, such as hemophilia or anticoagulant therapy, can increase the risk of spontaneous bleeding, including cerebellar hemorrhage.

Tumors: Both primary and metastatic brain tumors can cause cerebellar hemorrhage due to their disruption of normal blood vessel integrity.

Vascular Malformations: Other vascular abnormalities, such as cavernous malformations or venous angiomas, can predispose individuals to cerebellar hemorrhage.

Drug Abuse: Certain drugs, particularly stimulants like cocaine or methamphetamine, can increase blood pressure and the risk of cerebellar hemorrhage.

Infection: In rare cases, infections such as meningitis or brain abscesses can lead to cerebellar hemorrhage, often due to associated vascular inflammation and damage.

The underlying cause of cerebellar hemorrhage may influence treatment decisions and prognosis, making it important to identify the specific etiology whenever possible.

Clinical features can vary depending on the size and location of the hemorrhage, but they often include:

Severe headache: This is a common symptom and may be sudden and intense.

Nausea and vomiting: These symptoms can occur due to increased pressure within the brain.

Dizziness or vertigo: Patients may experience a sensation of spinning or imbalance.

Ataxia: This refers to a lack of muscle coordination, which can affect movements such as walking, reaching, and grasping objects.

Difficulty walking: Patients may have an unsteady gait or difficulty maintaining balance.

Weakness or paralysis: Depending on the extent of the hemorrhage and its effects on surrounding brain tissue, weakness or paralysis may occur, typically on one side of the body.

Head tilt or head tremor: These symptoms may occur due to involvement of the vestibular system, which helps maintain balance.

Decreased level of consciousness: In severe cases, patients may become lethargic, confused, or even comatose.

Speech difficulties: Some patients may experience slurred speech or difficulty articulating words.

Vision changes: Blurred vision, double vision (diplopia), or other visual disturbances may occur.

Diagnosing cerebellar hemorrhage typically involves a combination of clinical evaluation, imaging studies, and sometimes additional tests. Here's an overview of the diagnostic process:

Clinical Evaluation: A healthcare provider will begin by taking a detailed medical history and conducting a physical examination. They will assess the patient's symptoms, neurological function, and vital signs. Specific neurological tests may be performed to evaluate coordination, balance, strength, and sensation.

Imaging Studies:

CT Scan: Computed tomography (CT) scanning is often the initial imaging study used to diagnose cerebellar hemorrhage. It can quickly detect the presence of bleeding in the brain and provide information about the location, size, and extent of the hemorrhage.

MRI Scan: Magnetic resonance imaging (MRI) may be performed to obtain more detailed images of the brain and to assess the surrounding structures. MRI is particularly useful for evaluating the impact of the hemorrhage on adjacent brain tissue and for detecting underlying conditions that may have contributed to the bleeding. Additional Tests:

Angiography: In some cases, cerebral angiography may be performed to evaluate the blood vessels in the brain and identify any abnormalities or vascular malformations that could have contributed to the hemorrhage

see Cerebellar hemorrhage treatment.

see Cerebellar hemorrhage outcome.

Han et al. presented a SCH management protocol in our institute and analyzed the clinical and radiological findings in 41 SCH patients. The outcomes of each method (surgery and conservative treatment) were compared among patients with initial Glasgow Coma Scale (GCS) score of 9-13 and hematoma volume greater than 10 mL.

Two (4.9%), 16 (39%), and 23 (56.1%) patients had an initial GCS score of 3-8, with 3-8, 9-13, and 14-15, respectively. Initial GCS score showed significant correlation with Glasgow Outcome Scale (GOS) score (p = 0.005). The mean largest hematoma diameter was 3.2 ± 1.5 cm, and the mean volume was 11.0 ± 11.5 mL. Both of them showed significant inverse correlation with GOS score (p < 0.001). Among patients with an initial GCS score of 9-13 and hematoma volumes greater than 10 mL, 3 (50%) had good outcome and 3 (50%) had poor outcome in the surgical, and all of those in the conservative treatment group had poor outcomes. The outcome distribution differed significantly in the surgical and conservative groups (p = 0.030).

Initial GCS score and largest hematoma diameter and volume on brain computed tomography are important determinants of outcome in SCH patients. The surgery group showed better outcome than the conservative treatment group among those with an intermediate neurological status and large hematomas ¹⁾.

One hundred and one consecutive patients with hypertensive cerebellar hemorrhage were analyzed to determine the criteria for surgery. New criteria based on the patient's Glasgow Coma Scale score at admission and the maximum diameter of the hematoma, as disclosed by computed tomography, are proposed from a retrospective analysis of 52 earlier cases. The criteria are as follows: 1) patients with Glasgow Coma Scale scores of 14 or 15 and with a hematoma of less than 40 mm in maximum diameter are treated conservatively; 2) for the patients with Glasgow Coma Scale scores of 13 or less at admission or with a hematoma measuring 40 mm or more, hematoma evacuation with decompressive suboccipital craniectomy should be a treatment of choice; and 3) for the patient whose brain stem reflexes are entirely lost with flaccid tetraplegia or whose general condition is poor, intensive therapy is not indicated. The validity of these criteria was tested and confirmed in 49 recent cases ²⁾.

Clinical features and the operative results of hypertensive cerebellar hemorrhage (18 cases) were compared with those of hemorrhage caused by small angiomas (7 cases). Hypertensive hemorrhage occured most frequently in the seventh decades. Two thirds of the patients developed brainstem compression syndrome within a week from onset. One third remained awake or drowsy throughout their clinical course. Surgical removal of a hematoma was carried out in 13 patients with four deaths. Of note, two comatose patients regained consciousness after surgery, and were discharged with residual ataxia. Rupture of a small angioma occurred in younger patients. Their clinical course was sub-acute or chronic associated with focal cerebellar dysfunction. All seven surgically treated patients subsequently regained independent function. CT findings have been found helpful not only for diagnosis but also in defining appropriate therapy. Hematomas larger than 3 cm in diameter produced signs of rapidly progressing compression of the brainstem. Thereby, regardless of the cause of bleeding, emergency removal of a clot is indicated even in awake patients. Hematomas of 2 to 3 cm produced brainstem compression or prolonged cerebellar dysfunction, and occasionally require surgical decompression. Hematomas smaller than 2 cm can be managed conservatively, since they were absorbed spontaneously in three weeks without residual functional disturbances. However, in case of a young patient exploration should be performed for a probable “cryptic” angioma ³⁾.