Stroke | Dr. Karim Ashraf Neurologist – Egypt

Stroke

## Definition of Stroke and TIA

Stroke is defined as an acute neurological dysfunction caused by an interruption of blood flow to part of the brain. This can be due to a blockage of a blood vessel (ischemic stroke) or bleeding into the brain tissue (hemorrhagic stroke). Transient ischemic attack (TIA) is a temporary episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. TIAs are often precursors to a full ischemic stroke. Karim Ashraf, MBBCh, MSc – MBA and MD/PHD, Contac now | WhatsApp.

## Incidence

Stroke is a leading cause of death and disability worldwide. Ischemic strokes account for 87% of all strokes, while hemorrhagic strokes make up the remaining 13%. The incidence of stroke increases with age, and the risk is higher in men compared to women, though women have a higher lifetime risk of stroke.

## Risk Factors

### Modifiable Risk Factors

• Hypertension: Elevated blood pressure is the most important modifiable risk factor for stroke. It damages the blood vessels and increases the risk of clot formation and rupture.
• Diabetes Mellitus: Poorly controlled diabetes increases the risk of stroke by causing damage to the blood vessels and promoting atherosclerosis.
• Dyslipidemia: Elevated levels of cholesterol and triglycerides contribute to the development of atherosclerosis, which can lead to stroke.
• Atrial Fibrillation: This heart rhythm disorder increases the risk of blood clots forming in the heart and subsequently traveling to the brain.
• Smoking: Smoking tobacco damages blood vessels and promotes the development of atherosclerosis, increasing the risk of stroke.
• Obesity: Excess body weight contributes to the development of hypertension, diabetes, and dyslipidemia, all of which are risk factors for stroke.
• Physical Inactivity: Lack of regular physical activity is associated with obesity, hypertension, and other risk factors for stroke.
• Excessive Alcohol Consumption: Heavy alcohol consumption contributes to hypertension and increases the risk of hemorrhagic stroke.

Karim Ashraf, MBBCh, MSc – MBA and MD/PHD, Contac now | WhatsApp.

### Unmodifiable Risk Factors

• Age
• Family history and genetics
• Race/ethnicity
• Prior history of stroke or TIA

## Types and Classification of Stroke

Ischemic Stroke Classification:

• Large-Artery Atherosclerosis: It occurs when atherosclerotic plaques in the large arteries, such as the carotid or vertebral arteries, cause narrowing or complete occlusion, leading to reduced blood flow.
• Cardioembolic Stroke: It results from blood clots that form in the heart, usually due to atrial fibrillation, and travel to the brain.
• Cryptogenic Stroke: It refers to cases where the cause of stroke remains unknown despite an extensive evaluation.
• Other Determined Etiologies: This category includes less common causes, such as arterial dissection, vasculitis, hypercoagulable states, and rare genetic disorders.

Ischemic stroke types:

• Thrombotic Stroke: It occurs when a blood clot forms within a brain artery, usually due to atherosclerosis and plaque build-up.
• Embolic Stroke: It occurs when a blood clot or other debris forms elsewhere in the body (such as the heart or large arteries) and travels to the brain, blocking a blood vessel.
• Lacunar Stroke: It involves the occlusion of a small penetrating brain artery, typically due to chronic hypertension and small vessel disease.

Hemorrhagic stroke types:

• Intracerebral Hemorrhage: It results from bleeding directly into the brain tissue, often caused by uncontrolled hypertension or ruptured brain blood vessels.
• Subarachnoid Hemorrhage: It occurs when there is bleeding into the space between the brain and the surrounding membranes, often caused by a ruptured cerebral aneurysm.

## Clinical Presentation

The clinical presentation of stroke depends on the location and extent of the brain injury. Common symptoms include:

• Sudden unilateral weakness or numbness
• Sudden difficulty speaking or understanding speech
• Sudden vision changes
• Sudden dizziness, loss of balance, or lack of coordination
• Sudden severe headache

**Cortical Stroke Syndromes**:

– Strokes affecting the cerebral cortex can lead to a wide range of neurological deficits depending on the specific area involved. – Damage to the primary motor cortex (precentral gyrus) can cause contralateral hemiparesis, with the face and arm being more affected than the leg. – Strokes in the primary somatosensory cortex (postcentral gyrus) can cause contralateral hemisensory loss. – Lesions in the language-dominant hemisphere (usually the left) can result in different types of aphasia, such as Broca’s aphasia (expressive) or Wernicke’s aphasia (receptive). – Strokes in the non-dominant hemisphere (usually the right) can cause spatial neglect, impaired visuospatial skills, and anosognosia (unawareness of the deficits). Karim Ashraf, MBBCh, MSc – MBA and MD/PHD, Contac now | WhatsApp.

1. **Middle Cerebral Artery (MCA) Syndrome**:

– Contralateral hemiparesis (weakness) and hemisensory loss affecting the face, arm, and leg, typically more pronounced in the arm and face than in the leg. – Homonymous hemianopsia (loss of vision on the same side of both eyes). – Aphasia (language impairment) if the dominant hemisphere (usually left) is affected. – Neglect syndrome (unawareness or neglect of the affected side) if the non-dominant hemisphere (usually right) is affected.

2. **Anterior Cerebral Artery (ACA) Syndrome**:

– Contralateral leg weakness greater than arm weakness. – Sensory loss in the contralateral leg and foot. – Behavioral and cognitive changes, including apathy and personality changes. – Urinary incontinence if the frontal lobe and the motor areas controlling the bladder are affected.

3. **Posterior Cerebral Artery (PCA) Syndrome**:

– Homonymous hemianopsia (loss of vision on the same side of both eyes), usually affecting the contralateral visual field. – Visual agnosia or visual hallucinations. – Memory deficits. – Thalamic pain syndrome (burning or shooting pain) if the thalamus is involved.

4. **Vertebrobasilar Artery Syndrome**:

– Cranial nerve deficits, including diplopia (double vision), facial weakness, and difficulty swallowing. – Ataxia (uncoordinated movements) and gait disturbances. – Vertigo (spinning sensation) and dizziness. – Bilateral motor and sensory deficits affecting the limbs if the brainstem is involved.

**Subcortical Strokes**:

– Strokes affecting the subcortical structures, such as the basal ganglia, thalamus, and internal capsule, can present with more specific neurological syndromes. – Strokes affecting the internal capsule can cause contralateral hemiparesis, with the face and arm being more affected than the leg.

1. **Lacunar Syndrome**:

• Pure motor hemiparesis: Isolated weakness of the face, arm, and/or leg on one side.
• Pure sensory stroke: Isolated sensory loss affecting the face, arm, and/or leg on one side.
• Dysarthria-clumsy hand syndrome: Weakness and clumsiness of the hand and difficulty with articulation of speech.
• Ataxic hemiparesis: Combination of weakness and ataxia, affecting the arm and leg on the same side.

2. **Brainstem Stroke Syndromes**:

– Brainstem strokes can result in a variety of neurological deficits, depending on the specific location within the brainstem. – Wallenberg Syndrome (Lateral Medullary Syndrome):

• Ipsilateral cranial nerve deficits (e.g., Horner’s syndrome, dysphagia, dysarthria)
• Contralateral body sensory loss
• Ipsilateral cerebellar ataxia

– Benedikt Syndrome (Midbrain Syndrome):

• Contralateral hemiparesis
• Ipsilateral third nerve palsy
• Tremor or choreoathetosis of the contralateral limbs

– Pontine strokes can lead to crossed syndromes, with ipsilateral cranial nerve deficits and contralateral motor and sensory deficits.

3. **Thalamic Stroke Syndromes**:

– Thalamic Pain Syndrome (Dejerine-Roussy Syndrome):

• Contralateral body sensory loss, including pain and temperature
• Often associated with persistent, severe, and disabling pain

– Thalamic Astereognosis:

• Impaired ability to recognize the shape and texture of objects by touch.

4. **Basal Ganglia and Internal Capsule Strokes**:

– Pure Motor Hemiparesis:

• Contralateral weakness, typically more pronounced in the face and arm
• Lacunar Syndromes (e.g., pure motor, pure sensory, ataxic hemiparesis)

Karim Ashraf, MBBCh, MSc – MBA and MD/PHD, Contac now | WhatsApp.

**Cerebellar Stroke Syndromes**:

• Cerebellar strokes typically cause ipsilateral ataxia, nystagmus, and vertigo.
• Involvement of the cerebellar hemispheres can lead to dysmetria, intention tremor, and impaired coordination.
• Strokes affecting the vermis can cause gait ataxia and truncal instability.
• Cerebellar strokes can also increase intracranial pressure, leading to impaired consciousness and potentially brainstem compression.

It’s important to note that these syndromes provide a general framework, but individual presentations may vary. The clinical picture can also be influenced by factors such as the size of the stroke, collateral circulation, and any pre-existing neurological conditions. Prompt recognition of stroke symptoms and appropriate medical intervention are crucial for optimizing outcomes and minimizing long-term disability.

Some additional details on the clinical presentation and localization of different types of strokes:

1. **Watershed Infarcts**:

– Watershed infarcts occur in the border zones between the major cerebral artery territories. – They can result from hypoperfusion, such as during low-flow states or severe stenosis of the major cerebral vessels. – Clinical presentation depends on the specific watershed area affected: – Anterior watershed infarcts: Affect the border zone between the anterior and middle cerebral arteries, leading to cognitive impairment, aphasia, and contralateral hemiparesis. – Posterior watershed infarcts: Involve the border zone between the middle and posterior cerebral arteries, causing visual field deficits and visuospatial impairments. – Hemispheric watershed infarcts: Affect the border zone between the anterior and posterior circulations, resulting in cognitive, language, and motor deficits.

2. **Venous Sinus and Cerebral Venous Thrombosis**:

– Thrombosis of the cerebral venous sinuses or cerebral veins can cause a distinct clinical presentation. – Symptoms may include headache, altered mental status, seizures, and focal neurological deficits, depending on the specific veins or sinuses involved. – Superior sagittal sinus thrombosis can lead to bilateral parasagittal infarcts and increased intracranial pressure. – Lateral sinus thrombosis can cause papilledema, cranial nerve palsies, and ipsilateral cerebellar or brainstem dysfunction.

3. **Spinal Cord Strokes**:

– Strokes affecting the spinal cord are less common than cerebral strokes, but can still have significant clinical implications.

• Anterior spinal artery syndrome: Characterized by loss of motor function and pain/temperature sensation below the level of the lesion, with preservation of proprioception and vibration sense.
• Posterior spinal artery syndrome: Causes loss of proprioception and vibration sense, with relative sparing of motor function and pain/temperature sensation.
• Central cord syndrome: Results in greater upper extremity weakness compared to the lower extremities, often with bladder and bowel dysfunction.

4. **Transient Ischemic Attacks (TIAs)**:

– TIAs are characterized by the sudden onset of focal neurological deficits that resolve within 24 hours, typically within minutes to hours. – The clinical presentation of a TIA is like that of a stroke, but the neurological deficits are transient and do not result in permanent tissue damage. – TIAs are considered a medical emergency, as they can be a precursor to a more severe, potentially disabling stroke. – Prompt recognition and appropriate management of TIAs are crucial to prevent the development of a full-blown stroke.

## Diagnostic Evaluation

The initial evaluation of a suspected stroke includes:

• History and physical examination
• Neuroimaging: Computed tomography (CT) scan of the brain is the most common initial imaging study to evaluate stroke. Magnetic resonance imaging (MRI) can provide more detailed information.
• Vascular Imaging: Carotid ultrasound, CT angiography, or MR angiography can assess the blood vessels and identify any blockages or abnormalities.
• Cardiac Evaluation: Electrocardiography (ECG) is essential to identify cardiac arrhythmias, such as atrial fibrillation, which increases the risk of stroke. Echocardiography examines the heart’s structure and function.
• Laboratory Tests: Coagulation studies, including prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR), help evaluate the blood’s ability to clot.

## Stroke Scales

Several stroke scales are used to assess stroke severity, risk, and prognosis, including:

• NIHSS (National Institutes of Health Stroke Scale): Evaluates neurological deficits and stroke severity.
• ABCD2 (Age, Blood pressure, Clinical features, Duration, Diabetes): Predicts the risk of stroke after a TIA.
• CHADS2 (Congestive heart failure, Hypertension, Age, Diabetes, Stroke/TIA): Estimates the risk of stroke in patients with atrial fibrillation.

## Stroke Mimics and Complications

It is important to recognize that certain conditions, such as seizures, migraine, and brain tumors, hypoglycemia can mimic the symptoms of a stroke. Additionally, potential complications of stroke include:

• Increased intracranial pressure and Cerebral edema
• Pneumonia
• Deep vein thrombosis
• Urinary tract infections
• Depression and cognitive impairment

## Acute Treatment The primary goal of acute stroke treatment is to restore blood flow to the affected brain tissue as quickly as possible. This can be achieved using:

• Thrombolytic agents, such as recombinant tissue plasminogen activator (rt-PA) or tenecteplase, which can dissolve the blood clot causing the ischemic stroke. They are administered intravenously within a specific time window after symptom onset.

key details regarding the dosage of recombinant tissue plasminogen activator (rtPA) for the treatment of acute ischemic stroke:

• Standard Dose:

The standard dose of intravenous rtPA for the treatment of acute ischemic stroke is 0.9 mg/kg of body weight. The maximum dose is 90 mg. 10% of the total dose is given as an initial bolus, and the remaining 90% is infused over 60 minutes.

• Time Window for rtPA Administration:

The approved time window for the administration of intravenous rtPA is within 4.5 hours of symptom onset. Treatment should be initiated as soon as possible, as the benefits of rtPA decrease with time. In selected patients with wake-up strokes or unknown time of onset, rtPA may be considered if the patient is deemed to be within the 4.5-hour window based on imaging criteria.

• Contraindications and Cautions:

Absolute contraindications include active internal bleeding, history of intracranial hemorrhage, and recent (within 3 months) ischemic stroke or serious head trauma. Relative contraindications include recent major surgery or serious trauma, uncontrolled hypertension, and recent use of oral anticoagulants. In the presence of contraindications or cautions, the risks and benefits of rtPA administration should be carefully considered and discussed with the patient or their family.

• Monitoring and Management:

Patients receiving rtPA require close monitoring, including frequent blood pressure measurements and neurological assessments. If significant bleeding or other complications occur, the infusion of rtPA should be immediately discontinued, and appropriate management strategies should be initiated.

• Mechanical Thrombectomy: In some cases, a procedure called mechanical thrombectomy may be performed to physically remove the clot using specialized devices.

In some cases, neurosurgical intervention may be necessary, such as decompressive craniectomy to relieve intracranial pressure in cases of severe stroke or hemorrhage. Karim Ashraf, MBBCh, MSc – MBA and MD/PHD, Contac now | WhatsApp. ## Secondary Prevention After the acute phase, the focus shifts to secondary prevention of recurrent stroke. This includes:

• Antiplatelet Therapy: Aspirin is the most used antiplatelet medication for secondary stroke prevention. Other options include clopidogrel, ticagrelor, and dipyridamole.
• Anticoagulation: Patients with atrial fibrillation or other high-risk conditions may require anticoagulant medications, such as warfarin or direct oral anticoagulants (DOACs), to prevent blood clot formation.
• Risk Factor Management: Controlling hypertension, managing diabetes, and optimizing lipid levels through lifestyle modifications and medications are essential for reducing the risk of recurrent stroke.

## Rehabilitation

Stroke rehabilitation is a crucial component of the recovery process. It typically involves a multidisciplinary team, including physical therapists, occupational therapists, speech-language pathologists, and other healthcare professionals. The rehabilitation plan is tailored to the individual’s needs and may include:

• Physical therapy to improve mobility, strength, and balance.
• Occupational therapy to regain independence in activities of daily living.
• Speech therapy to address language, swallowing, and communication difficulties.
• Noninvasive Brain Stimulation (tDCS – rTMS) to improve neuroplasticity.

Brain Hemorrhage and Hematoma

### Causes

Brain hemorrhage, also known as intracranial hemorrhage, can occur due to a variety of factors. The most common causes include:

1. **Hypertension**: Uncontrolled high blood pressure can weaken the walls of blood vessels in the brain, leading to rupture and bleeding.
2. **Trauma**: Head injuries, such as those sustained in falls or motor vehicle accidents, can cause blood vessels to rupture and bleed into the brain.
3. **Vascular malformations**: Abnormal blood vessel formations in the brain can be prone to rupturing and bleeding.
4. **Anticoagulant medications**: Drugs that thin the blood, such as warfarin or direct-acting oral anticoagulants (DOACs), can increase the risk of brain hemorrhage.
5. **Underlying medical conditions**: Conditions like arteriovenous malformations, brain tumors, and certain blood disorders can predispose individuals to brain hemorrhage.

### Clinical Picture

The clinical presentation of brain hemorrhage can vary depending on the location and severity of the bleeding. Common symptoms include:

1. **Sudden, severe headache**: Often described as the “worst headache of the patient’s life.”
2. **Altered level of consciousness**: Ranging from confusion to coma, depending on the extent of the hemorrhage.
3. **Neurological deficits**: Symptoms such as weakness, numbness, or paralysis on one side of the body, visual disturbances, or speech difficulties.
4. **Nausea and vomiting**: Often due to increased intracranial pressure.
5. **Seizures**: Can occur, particularly in cases of lobar or intraventricular hemorrhage.

### Investigations

Prompt diagnosis is crucial for the management of brain hemorrhage. The following investigations are typically performed:

1. **Neuroimaging**: Computed tomography (CT) scan of the head is the initial imaging modality of choice, as it can quickly detect the presence and location of the hemorrhage.
2. **Magnetic resonance imaging (MRI)**: MRI may be used for further characterization of the hemorrhage and to detect any underlying vascular abnormalities.
3. **Angiography**: Cerebral angiography may be performed to identify the source of the bleeding, such as an arteriovenous malformation or an aneurysm.
4. **Lumbar puncture**: In some cases, a lumbar puncture may be performed to rule out other causes of the patient’s symptoms, such as subarachnoid hemorrhage.

### Distinguishing Features between Brain Stroke and Hemorrhage

It is important to differentiate between brain hemorrhage and ischemic stroke, as the management and prognosis can differ significantly.

1. **Onset of symptoms**: Hemorrhage often presents with a sudden, severe headache, whereas ischemic stroke symptoms may develop more gradually.
2. **Level of consciousness**: Patients with brain hemorrhage are more likely to present with a decreased level of consciousness or altered mental status, compared to those with ischemic stroke.
3. **Neurological deficits**: Hemorrhage may be associated with more focal neurological deficits, such as hemiparesis or aphasia, whereas ischemic stroke can present with a wider range of neurological symptoms.
4. **Neuroimaging**: CT scan or MRI can clearly differentiate between the presence of bleeding (hemorrhage) and lack of blood flow (ischemic stroke).

### Management

The general management of patients with brain hemorrhage and hematomas includes:

1. **Airway, breathing, and circulation (ABC)**: Ensuring the patient’s airway is patent, providing respiratory support if necessary, and maintaining hemodynamic stability.
2. **Blood pressure control**: Lowering blood pressure to prevent further bleeding and limiting the expansion of the hematoma.
3. **Reversal of anticoagulation**: If the patient is on anticoagulant medications, reversal of the anticoagulant effect may be necessary.
4. **Intracranial pressure management**: Measures to reduce intracranial pressure, such as administration of osmotic diuretics or surgical decompression, may be required.
5. **Surgical intervention**: In some cases, surgical evacuation of the hematoma may be necessary, particularly for large, life-threatening hemorrhages.
6. **Supportive care**: Monitoring and management of complications, such as seizures, hydrocephalus, or cerebral vasospasm.

The specific management approach will depend on the type, location, and severity of the brain hemorrhage, as well as the underlying cause and the patient’s overall clinical condition.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a specific type of brain hemorrhage that occurs when bleeding occurs within the subarachnoid space, the area between the arachnoid membrane and the pia mater surrounding the brain.

#### Causes of Subarachnoid Hemorrhage

The most common cause of subarachnoid hemorrhage is the rupture of an intracranial aneurysm, a weakened or balloon-like area in the wall of a brain artery. Other less common causes include:

• Arteriovenous malformations
• Trauma
• Bleeding disorders
• Tumors

#### Clinical Presentation of Subarachnoid Hemorrhage

Patients with subarachnoid hemorrhage often present with the sudden onset of a severe, “thunderclap” headache, which is frequently described as the “worst headache of their life.” Other common symptoms include:

• Nausea and vomiting
• Altered level of consciousness, ranging from confusion to coma
• Neck stiffness or pain
• Photophobia (sensitivity to light)
• Focal neurological deficits, such as cranial nerve palsies

#### Diagnosis of Subarachnoid Hemorrhage

– Noncontrast CT scan of the head is the initial imaging modality of choice, as it can quickly detect the presence of blood in the subarachnoid space. – If the initial CT scan is normal but clinical suspicion remains high, a lumbar puncture may be performed to analyze the cerebrospinal fluid for the presence of red blood cells or xanthochromia (yellow discoloration). – Cerebral angiography may be required to identify the source of the bleeding, such as an aneurysm or arteriovenous malformation

#### Management of Subarachnoid Hemorrhage

1. Securing the ruptured aneurysm or other vascular malformation to prevent rebleeding.
2. Maintaining adequate cerebral perfusion and oxygenation.
3. Preventing and managing complications, such as cerebral vasospasm, hydrocephalus, and delayed cerebral ischemia.

Treatment options may include surgical clipping, endovascular coiling, or a combination of both, depending on the location and characteristics of the aneurysm or vascular malformation. Unlocking the Secrets of the Brain: Explore the Power of EEG with Dr. Karim Ashraf

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