Every minute a patient loses 1.9 million neurons which is why immediate treatment is critical to the outcome of the patient.12
The prognosis of ischemic stroke varies considerably based on several evaluating factors such as type, severity, extent of neurological deficits, complications, and treatment response. As such, outcomes may range from complete recovery to long-term complications and death.1 In general, the modified Rankin scale is used to determine the degree of dependence that a patient requires after suffering a stroke13:
0: No symptoms
1: Symptoms present but no significant disruption
2: Slight disability but able to look after one's own affairs
3: Moderate disability, requiring some help but are able to walk without assistance
4: Moderately severe disability, requiring assistance for bodily needs and walking
5: Severe disability, bedridden and incontinent
6: Dead
These class of drugs are administered through an IV into the blood and dissolves and prevents clots. It consists of drugs such as Alteplase (tPA) or Tenecteplase. Their general mechanism follows the structure:
Clot busters are best administered within ≤4.5 hours of stroke including time before arriving at hospital.
Situations where clot busters are not recommended:
If patient has an intracranial hemorrhage → clot busters worsen bleeding
If patient had recent surgery → clot busters can reopen wounds
If patient has severe uncontrolled hypertension → clot busters + high blood pressure can lead to an intracranial hemorrhage
There is inherent risk associated with the treatment of stroke via clot busters as it prevents clotting:
Hemorrhagic transformation occurs when prolonged ischemia leading to weaker vessels occurs and is followed by an influx of blood → rupture of vessels and hemorrhage in brain15
Dislodging of embolus to another part of brain
Allergic reactions
Kidney damage
Edema
This is a minimally invasive method which involves guiding a catheter to the site of occlusion to retrieve the clot via a stent or vacuum. Or a balloon can be used in the case of stenosis with no clot.
Catheter aspiration utilizes a specialized catheter which is attached to a vacuum that can aspirate the clot restoring blood flow.
Endovascular thrombectomy utilizes a stent, a mesh cylinder which expands, to trap the clot allowing it to be slowly pulled out through the catheter.
Situations where endovascular therapy is not recommended:
If patient has inaccessible vessel anatomy → risk of reaching area overweighs treatment cost
If patient has intracranial hemorrhage → treat bleeding first
If patient has large infarct core with small penumbra → risk overweighs treatment
Dislodging of embolus to another part of brain
Vessel perforation and dissection
Rehabilitation after stroke depends on the severity and type of symptoms the patient has after stroke. These treatments can be done in care centers, hospitals, or even home depending on patient needs. Inpatient care allows for intensive rehabilitation programs with specialized equipment, better for more severe cases, while homecare services allows for less intense rehabilitation with regular equipment, better for milder cases.
Rehabilitation depends on the brain's ability to perform cortical remapping and inherent neuroplasticity. This allows the brain to rewire functions that were damaged from ischemia. Many of these therapies can be combined for better effects.18
Motor-skill exercises
Improve muscle strength and coordination for tasks such as balance, swallowing, walking
Mobility training
Use of mobility aids like canes while relearning to walk
Constraint-induced therapy/forced-use therapy
Unaffected limb is restrained to force other affect limb to get practice with using affected limb
Range-of-motion therapy
Certain exercises/treatments in order to ease muscle tension or spasticity or in order to regain range of motion
Occupational therapy
Improve memory, processing, problem-solving, social skills, judgment and safety awareness
Speech therapy
Regain speaking, listening, writing, and comprehension skills
Psychological evaluation and treatment
Takes the form of counselling, support group, and emotional adjustment if psychological state is unstable
Can include antidepressants or other drugs to help
Electrical stimulation on muscles
Electric stimulation via electrodes allows muscles to contract which can help retrain muscles
Robotic technology
Assist limbs with making repetitive motions allowing the regaining of strength and function of limbs
Wireless technology
Motivation systems created to increase activity such as smart watches or similar devices
Noninvasive brain stimulation/Deep brain stimulation
Transcranial magnetic stimulation via electrodes on scalp for upper-limb paralysis and restoration of motor function
Biological therapy
Stem cells therapy to regrow damaged portions of brain, currently very preliminary and carries risk of cancer
VR integration
Motivation by interacting with many different environments from the comfort of home
Poststroke seizures can occur soon after ischemia onset or be delayed. Generally, two distinct subtypes are identified: early-onset and late-onset.
Early-onset:
The estimated rate of early-onset poststroke seizures range from 2% to 33%. Acute ischemia leads to an increased concentration of glutamate (see module 2). Surviving neurons may be exposed to glutamate, causing recurrent epileptiform-type neuronal discharges - synchronized, bursts of electrical activity by neurons that can cause seizures.
Late-onset (at least 2 weeks after stroke):
The estimated rate of late-onset poststroke seizures range from 3% to 67%. Acute ischemia triggers gliosis (scarring process of glial cells after damage) and subsequent development of a meningocerebral cicatrix (glial scars merging with connective tissues). This causes changes in membrane properties, deafferentation (interruption of nerve impulse from body to CNS), selective neuronal loss, and collateral sprouting (neurons growing branches in damaged areas). Sufficient changes may result in hyperexcitability and neuronal synchrony, leading to seizures.
Treatment20:
Conventional anticonvulsants.
Spasticity involves muscle tightness, stiffness, and spasms. The prevalence of spasticity ranges from 30% to 80% in stroke survivors. Occurrence typically peaks at 1 to 3 months after stroke. Ischemic stroke causes damage to the upper motor neurons and disrupts communication between the brain and spinal cord. This causes a loss of descending inhibitory influences from CNS, leading to excessive muscle activation and spasticity.
Treatment20:
Combination of physiotherapy and pharmacological treatment.
Surgical treatment is rarely used as a last resort.
Cerebral edema, or swelling caused by fluid accumulation, typically peaks between 3 to 5 days after ischemic stroke. Ischemic stroke causes the abrogation of oxidative phosphorylation. Once ATP reserves are depleted, active transport ion pumps begin to fail and cause an influx of extracellular ions. Intracellular osmolarity then drives the inflow of water, causing cellular swelling and cytotoxic edema.
Cytotoxic edema affects cells in both gray and white matter, which works along with other factors (see module 2) to break down the blood brain barrier. This process leads to vasogenic edema, allowing protein-rich fluid to leak into the brain.
If untreated, cerebral edema can lead to rapid clinical deterioration and death.1
Treatment1
Ventriculostomy - drainage of excess fluids from a ventricle in the brain.
If severe, decompressive suboccipital craniectomy is recommended. A portion of the skull is removed to relieve pressure from the brain.
Dysphagia:
Dysphagia affects more than 50% of stroke survivors. Most patients recover swallowing function within 7 days, and only 11-13% of patients remain dysphagic after 6 months.23 Ischemic stroke causes the loss of CNS control over swallowing networks, similar to spasticity.24 This results in the lack of coordination and dysfunction of swallowing.
A serious complication of dysphagia is aspiration pneumonia. Dysphagia may cause the dysfunction of pharyngeal muscles, which impairs airway protective mechanisms.24Patients may inhale foreign objects into the lungs, causing systemic infections and acute respiratory failures. Post-stroke aspiration pneumonia accounts for 60% of stroke-associated deaths worldwide.24
Treatment:
Various treatment methods, such as feeding tubes1 and tongue exercises23, are available depending on the severity of dysphagia.
Poststroke Depression:
The estimated risk of poststroke depression ranges from 18-33%.1 Risk factors includes female sex, history of psychiatric illness, large and multiple strokes, strokes involving frontal lobes, and poor social support.25
Poststroke depression remains underdiagnosed and undertreated. The mechanisms of this complication and the best screening tools also remains unclear due to its multifactorial and complex nature.25
Treatments20:
Antidepressants and nonpharmacological therapy.
Approximately 25% of stroke patients experience urinary incontinence after discharge from hospital. The exact mechanisms of urinary incontinence post ischemic strokes are unknown.
Management:
Exclusion of exacerbating/precipitating features, such as urinary tract infections, certain drugs, and fecal impaction (stool stuck in rectum).
Use of anticholinergic medications.
Catheter - thin tubes inserted into the body to drain fluids.
A. Tortuous vasculature
B. Small saveable area of brain tissue
C. Allergies
D. Intracranial hemorrhage
A. Surviving neurons may be exposed and trigger early-onset seizures
B. It can complicate into aspiration pneumonia
C. Surviving neurons may be exposed and trigger late-onset seizures
D. It requires the patient to use a catheter
A. Severe Disability
B. Moderate Disability
C. Moderate Severe Disability
D. Dead
Answer Key
C
A
C