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Oncology- Palliative Surgery
I. Core Principles of Palliative Surgery
  • Timing is Crucial: The decision to operate is paramount. The adage "Good surgeons know how to operate; better ones when to operate; the best when not to operate" highlights the importance of considering a patient's life expectancy and overall condition. Multidisciplinary team discussions are essential.
  • Individualized Approach: The optimal procedure varies widely depending on the patient's specific circumstances and tumor characteristics.
II. Specific Palliative Procedures
A. Bowel Obstruction
  • Causes: Most commonly arises from colon cancer, due to resectable tumors or advanced pelvic masses. Ovarian cancer can also cause obstruction.
  • Management:
    • Resectable tumors: Surgical resection is ideal.
    • Inoperable tumors:
      • Colostomy/Ileostomy: Decompresses the bowel.
      • Endoscopic stent placement (left-sided tumors): A less invasive option, but carries a 4% perforation and 12% migration risk.
    • Ovarian cancer: Debulking surgery (often combined with chemotherapy) may provide good long-term palliation in suitable patients.
    • Multiple obstruction sites: Often difficult to manage surgically; internal bypass or proximal stoma may be options, but surgery isn't always feasible.
B. Fistulae
  • Causes: Direct tumor invasion or post-radiotherapy complications (especially with pelvic tumors).
  • Types: Rectovaginal, enterovaginal, colovesical, vesicovaginal, enteroenteric, enterocutaneous.
  • Management: Preoperative assessment is crucial. If definitive surgery isn't possible, a proximal end stoma is the preferred treatment to minimize distress. Endoscopic covered stents can be used for colovesical fistulae.
C. Jaundice
  • Management:
    • Endoscopic Stenting (ERCP): Primary method for periampullary lesions. Percutaneous transhepatic cholangiography (PTC) may be necessary for hilar cholangiocarcinomas, sometimes in conjunction with ERCP. Metallic stents are preferred for survival >3 months.
    • Operative Options (Hepatojejunostomy/Choledochojejunostomy): Less common due to endoscopic stenting, but regaining popularity via laparoscopic techniques due to shorter hospital stays and reduced morbidity compared to endoscopic stenting. Segment III biliary enteric bypass for selected inoperable hilar tumors. Requires hepato-pancreato-biliary (HPB) MDT discussion.
D. Ascites
  • Management: Sodium restriction, diuresis, serial paracentesis are first-line treatments.
  • Refractory Cases: Peritoneal drain or a peritoneal-venous shunt (Le Veen or Denver) may provide relief, particularly for ovarian or breast cancer. Less effective for GI malignancies. Assess for loculated ascites and mucinous tumors (risk of rapid shunt occlusion).
E. Pain
  • Management: Requires collaboration with palliative care. Surgical options include:
    • Debulking: For large, slow-growing tumors in fit patients.
    • Fracture Stabilization: Prophylactic pinning for bone metastases affecting >50% of the cortex.
    • Neurosurgical Approaches (rare): Cordotomy is rarely used now due to advancements in analgesia.
    • Thoracoscopic Splanchnectomy (rare): For intractable pancreatic cancer pain, largely replaced by EUS-guided coeliac plexus blocks.
F. Gastrointestinal Bleeding
  • Management: Endoscopic and radiological techniques (injection sclerotherapy, laser coagulation, arteriographic embolization) are initial treatments. Surgery is considered only if other methods fail and life expectancy is ≥3 months.
G. Cytoreductive Surgery
  • Partial resection: Appropriate when complete removal of disease is not possible, particularly in ovarian cancer, to improve outcomes with subsequent chemotherapy.
H. Palliative Resection of Primary Tumor
  • Breast Cancer: Resection may improve quality of life (QoL) by preventing fungation or uncontrolled axillary metastases, especially in patients with bone metastases (median survival >2 years).
  • Gastric Cancer: Considered for outlet obstruction or persistent anemia despite transfusions.
  • Colorectal Cancer: May be considered even with inoperable liver metastases to reduce bleeding, perforation, or obstruction risk.
I. Minimally Invasive Techniques: Laparoscopic surgery is increasingly used for many palliative procedures, reducing morbidity and improving QoL.
III. Key Terms
  • Palliation: Relieving symptoms and improving quality of life without aiming for a cure.
  • Debulking: Surgical removal of as much of a tumor as possible.
  • ERCP (Endoscopic Retrograde Cholangiopancreatography): Endoscopic procedure to visualize and treat biliary and pancreatic ducts.
  • PTC (Percutaneous Transhepatic Cholangiography): A procedure to visualize the biliary system via a needle inserted through the skin and liver.
  • MDT (Multidisciplinary Team): A team of specialists (surgeons, oncologists, radiologists, etc.) working together to plan patient care.
  • Co-morbidities: The presence of one or more additional diseases or conditions in a patient.​
  • QoL (Quality of Life): A subjective assessment of a patient’s overall well-being.
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Pathology- Dementia with Lewy Bodies (DLB)

I. Definition & Epidemiology

  • Definition: DLB is a neurodegenerative disease. Clinically, it presents as dementia. Histopathologically (microscopically), it's characterized by the presence of Lewy bodies in brain neurons (both cortical and subcortical).
  • Epidemiology:
    • Second most common cause of dementia.
    • Prevalence: ~5% in individuals >85 years old.
    • Slightly more prevalent in men.

II. Etiology & Pathogenesis

  • Etiology (Cause): Unknown.
  • Pathogenesis (Mechanism): The accumulation of Lewy bodies within neurons is believed to cause neuronal damage and subsequent cell loss, leading to the clinical manifestations of DLB.

III. Clinical Presentation & Differentiation from Alzheimer's Disease (AD)

  • Presentation: Progressively worsening dementia, similar to Alzheimer's Disease (AD).
  • Key Distinguishing Features from AD: This is crucial for diagnosis! DLB presents with:
    • Fluctuating cognition: Mental clarity varies significantly throughout the day or week.
    • Recurrent visual hallucinations: Patients experience vivid, often repetitive, visual hallucinations.
    • Parkinsonism: Features of Parkinson's disease, such as tremors, rigidity, and slow movement, may be present.

IV. Macroscopic & Microscopic Findings (Pathology)

  • Macroscopy (Gross Examination):
    • Cerebral atrophy (brain shrinkage), particularly in the temporal and parietal lobes.
    • Loss of pigment in the substantia nigra (a brain region crucial for movement control).
  • Histopathology (Microscopic Examination):
    • Lewy bodies: Intracytoplasmic (within the cell's cytoplasm) inclusions composed of α-synuclein, ubiquitin, and parkin. These are the hallmark of DLB.
    • AD-like changes: Amyloid plaques and neurofibrillary tangles (characteristic of Alzheimer's) are often present but areas typically severely affected in AD (like the hippocampus) are usually spared in DLB. This is a critical differentiator.

V. Prognosis

  • Highly variable, but the average survival after diagnosis is 5-7 years.

VI. Summary Table for Comparison with Alzheimer's Disease

Feature

Dementia with Lewy Bodies (DLB)

Alzheimer's Disease (AD)

Hallmark Feature

Lewy bodies (α-synuclein, ubiquitin, parkin)

Amyloid plaques and neurofibrillary tangles (tau protein)

Cognition

Fluctuating

Progressive decline, typically more gradual

Visual Hallucinations

Frequent, recurrent

Less common

Parkinsonism

Often present

Usually absent

Hippocampus

Usually spared

Severely affected
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Pathology- Creutzfeldt-Jakob Disease (CJD)
I. Definition & Epidemiology:
  • Definition: CJD is a rare, fatal spongiform encephalopathy caused by the accumulation of misfolded prion protein (PrP) resistant to normal cellular breakdown. It's the most common human prion disease.
  • Epidemiology: Extremely rare, with an annual incidence of approximately 1 per 1,000,000.
II. Etiology (Causes):
  • Sporadic CJD: Spontaneous, random misfolding of normal PrP into the abnormal PrP form. The exact mechanism remains unclear.
  • Familial CJD: Inherited mutations in the PRNP gene increase the likelihood of PrP misfolding.
  • Variant CJD (vCJD): Believed to be transmitted via consumption of beef contaminated with PrPSc from cattle with bovine spongiform encephalopathy (BSE, "mad cow disease").
III. Pathogenesis (Disease Mechanism):
  • Misfolded Protein Propagation: The presence of abnormal PrPSc acts as a template, causing normal PrPC to misfold into the abnormal form.
  • Exponential Growth & Cell Death: This process leads to an exponential increase in PrPSc, ultimately causing neuronal cell death and the characteristic brain damage.
IV. Clinical Presentation:
  • Sporadic CJD: Typically affects middle-aged and elderly individuals. Onset is marked by rapidly progressing neurological symptoms.
  • Variant CJD (vCJD): Affects younger individuals (<30 years old). initially presents with psychiatric symptoms, followed by cerebellar ataxia (problems coordination and balance) dementia. < />pan>Key difference from sporadic CJD.
V. Histopathology (Microscopic Findings):
  • Sporadic CJD & vCJD: Both show spongiform changes (vacuolation of grey matter), neuronal loss (death of nerve cells), and gliosis (scarring in the brain).
  • Variant CJD (vCJD only): The presence of numerous "florid plaques" composed of amyloid forms of PrPSc is a key distinguishing neuropathological feature. These are absent in other CJD forms.
VI. Prognosis:
  • Currently, no effective treatment exists for CJD. The disease is invariably fatal.​

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Pathology-Motor Neurone Disease (MND)
I. Definition & Epidemiology:
  • Definition: MND is a group of neurodegenerative diseases causing selective loss of motor neurons. This means the nerve cells that control voluntary muscle movement are progressively destroyed.
  • Epidemiology:
    • Rare disease: Annual incidence 1-5 per 100,000.
    • Slight male predominance.
    • Typical onset: 50-70 years old.
II. Aetiology (Causes):
  • Mostly Idiopathic: In most cases (90%), the cause is unknown.
  • Familial (Inherited): Approximately 10% of cases are inherited, showing a genetic component.
  • Genetic Links: Several genes associated with familial MND have been identified, including SOD1, TDP-43, and FUS.
III. Pathogenesis (Disease Mechanisms):
  • Poorly Understood: The precise mechanisms driving MND remain largely unclear, even with insights from familial cases.
  • RNA Metabolism Dysfunction: A leading hypothesis points to defects in RNA metabolism as a crucial factor in motor neuron degeneration. This is based on the properties of TDP-43 and FUS proteins.
  • TDP-43 & FUS: Both are RNA/DNA-binding proteins with similar structures. Their dysfunction is strongly implicated in MND development.
IV. Clinical Presentation:
  • Muscular Symptoms: Asymmetrical muscle weakness and wasting (atrophy), muscle twitching (fasciculations), and muscle stiffness (spasticity) in limbs are common early signs.
  • Bulbar Symptoms: Difficulty with swallowing (dysphagia), chewing, speaking (dysarthria), coughing, and breathing (dyspnea) are characteristic as the disease progresses and affects the muscles controlling these functions.
  • Cognitive Changes: Cognitive impairment can also occur in some cases.
V. Macroscopic & Microscopic Findings:
  • Macroscopy (Gross Examination): The anterior roots of the spinal cord (which carry motor neuron axons) are atrophied (shrunken).
  • Histopathology (Microscopic Examination):
    • Selective loss of motor neurons in the motor cortex (brain) and anterior horns of the spinal cord is the defining feature.
    • In sporadic (non-inherited) MND, remaining motor neurons often contain abnormal protein inclusions that include ubiquitin and TDP-43.
VI. Prognosis:
  • Progressive & Fatal: MND is typically progressive, leading to death within a few years.
  • Cause of Death: Aspiration pneumonia (lung infection from inhaling food or saliva due to swallowing difficulties) is a frequent cause of death.




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Pathology- Huntington's Disease
I. Definition & Epidemiology:
  • Definition: HD is an inherited, neurodegenerative disorder resulting from a mutation in the HTT gene. This mutation leads to the production of a dysfunctional huntingtin protein.​
  • Epidemiology:
    • Prevalence: 5-10 per 100,000 globally, with geographical variation.
    • Onset: Typically 35-45 years, but can occur at any age.
    • Sex: Affects men and women equally.
    • Inheritance: Autosomal dominant (only one affected copy of the gene is needed to develop the disease).
II. Genetics:
  • HTT Gene: Contains a CAG trinucleotide repeat sequence.
    • Normal HTT: Less than 36 CAG repeats.
    • Mutant HTT: More than 36 CAG repeats. The number of repeats directly correlates with disease severity and age of onset (more repeats = earlier onset, greater severity).
  • Anticipation: The number of CAG repeats tends to increase in subsequent generations, leading to earlier onset and more severe disease in offspring. This phenomenon is known as anticipation.
III. Pathogenesis:
  • Huntingtin Protein (HTT): The protein encoded by the HTT gene has various cellular functions and is expressed throughout the body, but is most concentrated in the brain and testes.
  • Mechanism of Disease: Mutated huntingtin protein is cytotoxic (toxic to cells), particularly affecting neurons in the caudate nucleus and putamen (basal ganglia structures crucial for movement control).
IV. Clinical Presentation:
  • Early Symptoms: Uncontrolled, jerky, involuntary movements (chorea).
  • Progressive Disease: Over time, HD leads to progressive motor, neuropsychiatric (mood disorders, cognitive issues), and cognitive decline, ultimately culminating in dementia.
V. Macroscopic & Microscopic Findings:
  • Macroscopy: Significant atrophy (shrinking) of the caudate nucleus and putamen. Cortical atrophy may also be present.
  • Histopathology: Marked neuronal loss in the caudate nucleus. Surviving neurons contain excessive amounts of the mutated huntingtin protein.
VI. Prognosis:
  • Survival: Average survival is approximately 20 years from symptom onset, but varies depending on the number of CAG repeats (more repeats = shorter survival).
  • Cause of Death: Often pneumonia or cardiac failure due to mutated huntingtin expression in cardiac muscle.
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Pathology-Parkinson's Disease
I. Definition & Epidemiology:
  • Definition: Parkinson's disease is a neurodegenerative disorder. Clinically, it's characterized by parkinsonism (a group of motor symptoms); histologically (microscopically), it's defined by neuronal loss in the brain and the presence of Lewy bodies (abnormal protein aggregates) concentrated in the substantia nigra. Crucially, parkinsonism itself is not diagnostic of Parkinson's Disease.
  • Epidemiology: Primarily affects the elderly. Prevalence is approximately 1% in individuals over 60 years old.
II. Aetiology (Causes):
  • Mostly Unknown: The cause of most Parkinson's cases remains unclear.
  • Genetic Factors (Rare Cases): Rarely, inherited mutations in the PARK1 gene (chromosome 4), which codes for α-synuclein (a protein component of Lewy bodies), are implicated.
III. Pathogenesis (Disease Mechanism):
  • Dopamine Deficiency: Neurons in the substantia nigra project to the putamen and globus pallidus (basal ganglia structures crucial for movement). These neurons release dopamine, a neurotransmitter essential for controlling movement. In Parkinson's, dopamine release is significantly reduced.
  • Movement Disorder: The lack of dopamine leads to the characteristic movement disorders.
IV. Presentation (Symptoms):
  • Parkinsonism: The classic triad of symptoms includes:
    • Tremor: Involuntary shaking.
    • Rigidity: Stiffness and resistance to movement.
    • Bradykinesia: Slowness of movement.
  • Important Note: Parkinsonism can result from various causes (drugs, toxins, infections, trauma) and isn't solely indicative of Parkinson's disease.
V. Macroscopic & Microscopic Findings:
  • Macroscopy (Gross Examination): Shows pallor (loss of color) in the substantia nigra and locus ceruleus (brain regions).
  • Histopathology (Microscopic Examination): Reveals:
    • Loss of pigmented neurons in the substantia nigra.
    • Presence of Lewy bodies within remaining neurons.
VI. Prognosis & Treatment:
  • Treatment: Dopamine-replacement therapies can alleviate parkinsonism symptoms. However, these treatments do not slow or stop the disease's progression.
  • Variable Progression: The rate of disease progression varies significantly between individuals.
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Pathology-Alzheimer's Disease
I. Definition & Epidemiology:
  • Definition: Alzheimer's disease (AD) is a neurodegenerative disorder clinically characterized by dementia and histopathologically by neuronal loss in the cerebral cortex, accompanied by amyloid plaques and neurofibrillary tangles. Crucially, it's the most common cause of dementia.
  • Epidemiology:
    • Incidence dramatically increases with age (5% >65 years old, 20% >80 years old).
    • Represents a significant socioeconomic burden on healthcare systems.
II. Aetiology & Pathogenesis:
  • Aetiology (Cause): The cause is unknown in most cases. A small percentage are familial, linked to genetic mutations in the amyloid precursor protein (APP) gene on chromosome 21.
  • Pathogenesis (Mechanism):
    • AD is considered a "proteinopathy," focusing on the abnormal accumulation of amyloid-beta (Aβ) and tau proteins.
    • Aβ peptides are derived from APP through secretase enzymes.
    • The exact mechanism by which Aβ and tau accumulation leads to neuronal loss remains unclear—this is a key area of ongoing research.
III. Clinical Presentation:
  • Early Stages: Begins with memory loss, especially recent memory and new learning difficulties. Progressive decline in daily activities (finances, shopping).
  • Middle Stages: Loss of motor skills impacts dressing, cooking, and cleaning.
  • Late Stages: Agitation, restlessness, wandering, and disinhibition emerge, causing distress for family and caregivers. Eventually, speech loss, immobility, and incontinence occur.
IV. Macroscopic & Microscopic Findings:
  • Macroscopy (Gross Anatomy):
    • Reduced brain weight (often <1000g).< />pan>
    • Cortical atrophy, particularly in the temporal lobe and hippocampus.
  • Histopathology (Microscopic Anatomy):
    • Key Features: Abundant neuritic plaques and neurofibrillary tangles in the cerebral cortex, alongside neuronal and synaptic loss.
    • Neuritic Plaques: Spherical collections of distorted neuronal processes around a central amyloid core, primarily composed of Aβ protein.
    • Neurofibrillary Tangles: Intracellular accumulations of paired helical filaments within neurons; mainly composed of tau protein.
V. Prognosis:
  • Death typically occurs approximately 10 years post-diagnosis, often due to complications like pneumonia.
Key Concepts to Master:
  • Amyloid-beta (Aβ) plaques: Extracellular deposits, key hallmark of AD.
  • Neurofibrillary tangles: Intracellular accumulations of tau protein, another hallmark of AD.
  • APP (Amyloid Precursor Protein): A protein implicated in familial forms of AD.
  • Tau protein: A microtubule-associated protein whose abnormal accumulation contributes to neurofibrillary tangles.
  • Proteinopathy: A disease caused by misfolded or aggregated proteins.
  • The relationship between Aβ and tau accumulation and neuronal death needs further study.
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Pathology- Multiple Sclerosis (MS)
This guide summarizes key information on Multiple Sclerosis to aid understanding and effective study.
I. Definition & Epidemiology:
  • Definition: MS is a relapsing-remitting, demyelinating disease of the Central Nervous System (CNS). Neurological disturbances affect different CNS areas at different times. Think intermittent attacks in different locations.
  • Epidemiology:
    • Peak onset: 20-30 years old.
    • Slightly more common in females.
    • Significant geographical variation: higher incidence at higher latitudes (farther from the equator), near absence near the equator. This hints at environmental factors.
II. Aetiology & Pathogenesis:
  • Aetiology (Cause): Unknown. Leading hypothesis: immune-mediated demyelination triggered by a childhood infection in genetically susceptible individuals. Think infection + genetics = trigger.
  • Pathogenesis (Mechanism):
    • Demyelination episodes cause acute neurological deficits (symptoms) developing over days and lasting weeks.
    • Early stages: Complete recovery is typical.
    • Progression: Slower recovery, residual deficits, axonal death, and permanent disability due to extensive axonal loss. Think initial recovery, then progressive damage.
III. Clinical Presentation: (Note the association between location of demyelination and symptoms)
  • Optic Nerve: Blurred vision, loss of color vision.
  • Cerebellum: Vertigo, incoordination.
  • Brainstem: Eye movement disorders.
  • Spinal Cord: Patchy numbness/tingling, progressing to paraplegia (paralysis of lower limbs), incontinence, and sexual dysfunction.
IV. Macroscopic & Microscopic Findings:
  • Macroscopy (Gross Examination): Well-circumscribed grey plaques in CNS white matter. Common locations: optic nerves, periventricular white matter, brainstem, cervical spinal cord. Think visible lesions in specific areas.
  • Histopathology (Microscopic Examination):
    • Active plaques: Inflammatory infiltrate, myelin sheath destruction.
    • Established plaques: Complete myelin loss, reduced oligodendrocytes (myelin-producing cells), relatively normal or slightly reduced axon numbers (initially).
V. Prognosis:
  • Most patients experience progressive disease.
  • Significant complications due to disability: pneumonia, urinary tract infections, pressure sores. Think disability leads to secondary complications.
Key Concepts to Remember:
  • Relapsing-remitting: Periods of attacks followed by periods of remission (partial or complete recovery).
  • Demyelination: Damage to the myelin sheath surrounding nerve fibers, impairing signal transmission.
  • Geographical variation: Strong evidence for environmental influence.
  • Progressive axonal loss: The ultimate cause of permanent disability.
  • Location-specific symptoms: The location of the demyelination dictates the presenting symptoms.
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Pathology - Head Injury

I. Epidemiology & Severity

  • Incidence: Approximately 50,000 severe head injuries occur annually in the UK.
  • Mortality: Accounts for roughly 20% of deaths in young adults (5-45 years).
  • Disability: Significant disability is common among survivors.

II. Types of Head Injuries

A. Skull Fracture:

  • Mechanism: Occurs at the impact site in severe head injuries.
  • Significance: Indicates serious injury and increases the risk of intracranial damage (contusions, hematomas).
  • Base of Skull Fractures: Can lead to cranial nerve palsies or cerebrospinal fluid (CSF) leakage from the nose or ear.

B. Cerebral Contusions:

  • Mechanism: Brain bruising caused by sudden movement within the skull, resulting in impact against the skull.
  • Location: Typically occurs at the impact site ("coup" lesion) and opposite ("contrecoup" lesion).
  • Consequences: Bleeding into brain tissue (parenchyma) and cerebral edema increase intracranial pressure.

C. Extradural Hematoma (Epidural Hematoma):

  • Mechanism: Bleeding between the dura mater and the skull.
  • Cause: Often due to middle meningeal artery rupture from temporal bone fracture.
  • Progression: Slow initial blood accumulation due to the dura's adherence to the skull. Patients may initially appear well, then rapidly deteriorate as the hematoma expands.

D. Subdural Hematoma:

  • Mechanism: Bleeding between the dura and arachnoid mater.
  • Cause: Tearing of bridging veins draining into the cerebral venous sinuses.
  • Spread: Blood spreads widely, enveloping the affected hemisphere.
  • Clinical Presentation: Common in the elderly after minor trauma; may present with confusion.

E. Traumatic Axonal Injury (TAI):

  • Mechanism: Typically caused by sudden acceleration-deceleration forces.
  • Diffuse Axonal Injury (DAI): The most severe form, leading to immediate unconsciousness and high mortality.
  • Histology: Shows widespread axonal swelling, increased microglia, and eventual fiber tract degeneration.

III. Key Differences & Summary Table

Injury Type

Location

Mechanism

Clinical Presentation

Skull Fracture

Skull

Direct impact

Varies depending on location; may indicate further injury

Cerebral Contusion

Brain surface

Coup & Contrecoup injury

Varies depending on severity; may cause increased ICP

Extradural Hematoma

Between dura & skull

Middle meningeal artery rupture

Lucid interval followed by rapid deterioration

Subdural Hematoma

Between dura & arachnoid

Bridging vein rupture

Often subtle initially, especially in the elderly

Traumatic Axonal Injury

Widespread brain tissue

Acceleration-deceleration forces

Immediate unconsciousness (in DAI), often fatal

ICP: Intracranial Pressure

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Pathology - Cerebral Infarction
I. Definition & Epidemiology
  • Definition: Cerebral infarction is ischemic (lack of blood flow) necrosis (tissue death) of a brain region. This is crucial to understand
  • the fundamental nature of the condition.
  • Epidemiology: It's the most common type of stroke (~80%), predominantly affecting the elderly. Remember this high prevalence and its association with age.
II. Aetiology (Causes)
  • Thromboembolism: The majority of cases result from blood clots (thromboemboli) originating in the internal carotid artery or the left side of the heart. These clots travel to and block a cerebral artery. Understand the source of the emboli is key here.
  • In situ thrombosis: A smaller percentage arises from clots forming directly within a cerebral artery, often due to atherosclerosis (hardening of the arteries). Distinguish between emboli and in situ thrombosis.
III. Pathogenesis (Mechanism)
  • Artery Occlusion: Sustained blockage of a cerebral artery leads to ischemia and subsequent necrosis in the brain area supplied by that artery. The longer the occlusion, the greater the damage.
IV. Presentation (Symptoms)
  • Rapid Onset: Cerebral infarction presents with a sudden onset of neurological symptoms specific to the affected artery's distribution. This is a hallmark of stroke.
  • Middle Cerebral Artery Involvement: Most infarctions affect the middle cerebral artery, resulting in contralateral (opposite side) hemiplegia (paralysis) or hemiparesis (weakness), homonymous hemianopia (loss of half of the visual field in both eyes), and dysphasia (language impairment). Memorize these common symptoms and their locations.
  • Transient Ischemic Attacks (TIAs): TIAs are brief episodes of focal neurological symptoms (less than 24 hours) that serve as significant warning signs for future infarction. Recognize TIAs as crucial predictors.
V. Macroscopic Changes (Visible with the Naked Eye)
  • 24 hours: The infarcted area softens, and the grey-white matter boundary becomes indistinct. Cerebral edema (brain swelling) and midline shift may occur.
  • 48 hours - 10 days: The infarct becomes gelatinous, and the distinction between infarct and normal tissue clarifies.
  • 10 days - 3 weeks: Liquefaction (conversion to liquid) and cystic changes (cavity formation) develop.
  • Hemorrhagic Infarct: Reperfusion (restoration of blood flow) can sometimes lead to bleeding into the infarcted area.
Remember the temporal progression of macroscopic changes.
VI. Histopathology (Microscopic Changes)
  • First 48 hours: Ischemic neuronal changes (shrunken, eosinophilic neurons) and neutrophil (white blood cell) infiltration are observed.
  • Later Stages: Mononuclear cells (other white blood cells) remove myelin debris, and astrocytes (glial cells) proliferate as the infarct heals.
VII. Prognosis & Complications
  • Mortality: High initial mortality (20% at 1 month), followed by a 10% annual mortality rate.
  • Complications: Pneumonia, depression, contractures (muscle shortening), constipation, bedsores, and significant emotional impact on the family are common. Remember the range of potential complications.
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Facts about medicine and its subtopic such as anatomy, physiology, biochemistry, pharmacology, medicine, pediatrics, psychiatry, obstetrics and gynecology and surgery.