Stroke Impact: Emotional Changes From Anterior Cranial Bleeds

The anterior cranial artery is a branch of the middle cerebral artery, which is the most common artery involved in acute stroke. The anterior cranial artery supplies blood to the medial frontal and parietal lobes, as well as the anterior portions of the basal ganglia and the anterior internal capsule. A hemorrhagic stroke in the anterior cranial artery can cause emotional changes, as it can lead to damage in the right anterior cingulate cortex, which is responsible for emotional awareness.

Intracerebral haemorrhage

Symptoms

ICH symptoms can vary depending on the severity, timeframe, and location of the bleed, but can include:

• Headache
• One-sided weakness
• Numbness
• Tingling
• Paralysis
• Speech problems
• Vision or hearing problems
• Memory loss
• Attention problems
• Coordination problems
• Balance problems
• Dizziness
• Nausea/vomiting
• Seizures
• Decreased level of consciousness
• Neck stiffness
• Fever
• Coma
• Loss of all sensory modalities
• Contralateral sensorimotor deficits
• Cranial nerve dysfunction
• Lethargy
• Bradycardia
• Cardiac arrest
• Dysphagia
• Cardiac arrhythmias
• Acute kidney injury
• Urinary tract infection
• Pneumonia
• Respiratory failure
• Respiratory distress
• Cardiac complications, such as myocardial infarction or atrial fibrillation

Diagnosis

ICH is typically diagnosed using a CT scan, which can show the extent of the bleed, surrounding oedema, mass effect, intraventricular clot extension, and raised intracranial pressure. MRI scans may also be used, particularly in the subacute phase of the bleed.

Treatment

ICH treatment ranges from medication to open surgery to actively evacuate the haematoma. Treatment depends on the type of ICH, and may include medication to control blood pressure, prevent seizures, and manage pain. Surgery may be required to remove the haematoma, particularly if it is greater than 3cm in size, or if there is a structural vascular lesion or lobar haemorrhage in a young patient.

Prognosis

ICH has a high mortality rate, with approximately 44% of those affected dying within a month. The prognosis depends on the size of the haematoma, location, and the patient's Glasgow Coma Scale (GCS) score on admission. At 30 days, the mortality rate can be as high as 50%, with most deaths occurring within the first 24 hours. Less than 20% of survivors are considered independent at 6 months following the acute haemorrhage.

Prevention

ICH prevention involves managing modifiable risk factors, such as:

• Hypertension
• Smoking
• Alcohol consumption
• Drug use
• High cholesterol
• Obesity
• Diabetes

Subarachnoid haemorrhage

A subarachnoid haemorrhage is a bleed located underneath one of the protective layers of the brain, known as the arachnoid layer. It is a type of haemorrhagic stroke, which is caused by a ruptured blood vessel. The other type of haemorrhagic stroke is intracerebral haemorrhage, which is bleeding within the brain tissue.

Another cause of subarachnoid haemorrhage is arteriovenous malformation (AVM), a condition where blood vessels within the brain cluster together and form abnormal connections. The abnormal formation is very weak and prone to bleeding.

Trauma, such as a blow to the head, can also cause subarachnoid haemorrhage by rupturing blood vessels within the brain.

• Rebleeding: The risk of rebleeding is highest in the few days after the first haemorrhage and carries a high risk of permanent disability or death.
• Communicating hydrocephalus: The arachnoid villi, responsible for cerebrospinal fluid (CSF) reabsorption, can become blocked, leading to abnormal enlargement of the brain cavities (ventricles).
• Cerebral oedema: Swelling of the brain due to lack of oxygen to brain tissue is a common side effect of any traumatic event involving brain tissue.
• Seizures: Abnormal signals sent from damaged brain cells can trigger temporary changes in sensation, behaviour, movement and consciousness.
• Cerebral vasospasm: Unidentified substances released after a subarachnoid haemorrhage can cause the blood vessels of the brain to spasm, decreasing blood supply to parts of the brain. This is the most significant cause of morbidity and mortality in patients surviving subarachnoid haemorrhage.

The diagnosis of subarachnoid haemorrhage involves several tests, including:

• CT scan: This can identify the extent of the haemorrhage, pinpoint the location of the bleed, and detect complications such as communicating hydrocephalus.
• Lumbar puncture: CSF is removed with a needle and examined for the presence of blood.
• Intra-arterial digital subtraction angiography (IADSA) or cerebral angiography: This radiological procedure is commonly used to locate the cause of an aneurysmal subarachnoid haemorrhage.
• MRI scan: This non-invasive scan uses strong magnetic fields to visualise brain blood vessels and their abnormalities.

Treatment for subarachnoid haemorrhage can be surgical or conservative, depending on the cause and severity of the haemorrhage. Surgical techniques include clipping, where the ruptured aneurysm is located and surgically clipped, and endovascular coiling, where minute coils are introduced into the aneurysm to cause clotting and prevent further bleeding.

The long-term complications of subarachnoid haemorrhage include:

• Epilepsy: This is when the normal working of the brain is interrupted, causing repeated fits or seizures.
• Cognitive dysfunction: Most people experience difficulties with one or more brain functions, such as memory and concentration.
• Emotional problems: Depression, anxiety disorder, and post-traumatic stress disorder (PTSD) are common long-term complications.

Hypertension

The treatment of hypertension is crucial in preventing hemorrhagic stroke. Antihypertensive medications are used to lower blood pressure gradually, with a target of 150/90 mmHg. Intensive blood pressure reduction has been found to attenuate hematoma growth. However, it is important to gradually lower blood pressure to avoid further ischemic injury to the brain tissue.

In addition to hypertension, other modifiable risk factors for hemorrhagic stroke include smoking, obesity, alcohol consumption, diet, hyperlipidemia, physical inactivity, diabetes, and cardiac causes such as cardiomyopathy, heart failure, and atrial fibrillation.

Cerebral amyloid angiopathy

CAA can lead to emotional changes, including emotional dysregulation, impulse dyscontrol, and apathy. A study found that the most frequent neuropsychiatric symptoms in CAA were depression/dysphoria, irritability/lability, agitation/aggression, apathy/indifference, and anxiety. These symptoms were more common in CAA patients than in healthy controls, and the number and severity of symptoms were similar to those observed in patients with mild cognitive impairment. Higher white matter hyperintensity volume was associated with more frequent and severe symptoms, suggesting that white matter damage may underlie some of these emotional changes.

CAA can be diagnosed based on clinical and radiological findings, but a high index of suspicion is needed to ensure appropriate investigations are requested. There is currently no specific treatment for CAA, but controlling blood pressure is beneficial in reducing haematoma expansion in the acute phase.

Cerebral microbleeds

The detection of MBs is made possible by the paramagnetic properties of blood degradation products, particularly hemosiderin, which can be visualised using specific magnetic resonance imaging (MRI) sequences such as T2*-gradient recalled echo (GRE) imaging and susceptibility-weighted imaging (SWI). The implementation of these MRI sequences has allowed for the identification of MBs as a common finding across different populations.

The clinical and prognostic significance of MBs is still a subject of ongoing research. However, they have been associated with an increased risk of intracerebral hemorrhage (ICH) and cognitive impairment. MBs have also been linked to specific underlying vasculopathies, such as cerebral amyloid angiopathy and hypertensive vasculopathy, depending on their topographic distribution.

The presence of MBs may influence the approach to anti-thrombotic therapy, as they appear to indicate a hemorrhage-prone state of the brain. While there are no formal contraindications, some data suggest that MBs are an independent risk factor for warfarin-related ICH, and even anti-platelet agents have been associated with an increased risk of ICH in subjects with a high number of MBs. Therefore, the presence of MBs should be carefully considered when making decisions regarding anti-thrombotic therapy.

Frequently asked questions