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Pathology-Motor Neurone Disease (MND)
I. Definition & Epidemiology:
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.
- 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.
- 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.
- 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.
- 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.
- 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 - Intracerebral Haemorrhage (ICH)
I. Definition:
I. Definition:
- Spontaneous (non-traumatic) bleeding into the brain tissue. Crucially, this differentiates it from other types of strokes.
- Accounts for approximately 20% of all strokes.
- Predominantly affects individuals in late middle age. Note the age range for highest risk.
- Hypertension (High Blood Pressure): This is the most frequent cause. Understand the strong link between uncontrolled hypertension and ICH.
- Less Common Causes: These are important to remember for differential diagnosis:
- Cerebral amyloid angiopathy (CAA)
- Ruptured arteriovenous malformation (AVM)
- Coagulation disorders (problems with blood clotting)
- Hypertension-related ICH: Mostly caused by the rupture of Charcot-Bouchard microaneurysms (small, weakened areas in blood vessels). Focus on understanding this key mechanism.
- Haematoma Formation: The resulting blood clot (hematoma) destroys brain tissue and rapidly increases intracranial pressure (ICP). This pressure increase is the primary cause of morbidity and mortality.
- Sudden Onset: The symptoms appear abruptly.
- Focal Neurological Deficits: Symptoms depend on the location of the bleed. Remember that the location dictates the specific neurological symptoms.
- Raised Intracranial Pressure (ICP) Symptoms: These are common and can include headache, vomiting, altered consciousness.
- Mortality Risk:
- Large hemorrhages can cause death rapidly due to high ICP and herniation (brain tissue displacement).
- Even small hemorrhages in vital brainstem areas (controlling breathing and heart rate) can be fatal.
- Haematoma: Visible blood clot replacing brain tissue.
- Mass Effect: The hematoma pushes on surrounding brain structures, causing midline shift and potentially herniation.
- Location:
- Hypertensive bleeds: Usually in basal ganglia, internal capsule, pons, or cerebellum.
- Other cause bleeds: More likely to be in the lobes (lobar). This helps in differential diagnosis.
- Early Stages: Blood clot surrounded by brain tissue with hypoxia (lack of oxygen) and edema (swelling).
- Later Stages: Reactive astrocytes (glial cells) proliferate, and the damaged area organizes similarly to an infarct (area of dead tissue from lack of blood supply).
- High Mortality Rate: >40% mortality due to the devastating effects of raised intracranial pressure. This highlights the seriousness of ICH.
- Relationship between hypertension and ICH: This is the cornerstone of understanding this condition.
- Pathophysiology of haematoma formation and its consequences: Understand the chain of events leading to increased ICP and potential death.
- Clinical presentation variations based on location: Different areas of the brain will cause different symptoms.
- Differential diagnosis based on location and etiology: Knowing the likely cause based on the location of the hemorrhage.
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Pathology - Subarachnoid Hemorrhage (SAH)
I. Definition & Epidemiology:
I. Definition & Epidemiology:
- Definition: Bleeding into the subarachnoid space (the space between the arachnoid mater and pia mater surrounding the brain).
- Incidence: Approximately 8 cases per 100,000 people annually.
- Age of Onset: Most common in adults aged 35-65.
- Primary Cause: Rupture of a berry aneurysm (a small, saccular aneurysm, usually at arterial bifurcations).
- Aneurysm Formation: Hypothesized to result from a congenital defect in the tunica media (middle layer) of cerebral vessels, exacerbated by later-life atherosclerosis and hypertension. Crucially, most berry aneurysms do not rupture.
- Location of Aneurysms: Most commonly found at the base of the brain, specifically:
- Anterior communicating artery (40%)
- Middle cerebral artery (34%)
- Internal carotid artery (20%)
- Posterior cerebral artery (4%)
- Rupture Mechanism: Rupture leads to extensive subarachnoid hemorrhage, potentially extending into the brain parenchyma (brain tissue itself).
- Cardinal Symptom: Sudden, severe headache, often described as a "thunderclap" headache or feeling like being hit on the back of the head.
- Precipitating Factors: Exertion or straining can trigger rupture.
- Severity: Can range from unconsciousness to immediate death in severe cases.
- Macroscopy: Blood is found in the subarachnoid space, frequently accumulating around the circle of Willis at the brain's base. The ruptured berry aneurysm may be visible after clot removal.
- Histopathology: The aneurysm wall lacks a muscular media layer; it consists of a thick fibrous intima (inner layer) and an outer adventitia (outer layer).
- Tripartite Outcome: Prognosis is generally categorized into thirds:
- ⅓ Immediate Death: Due to tonsillar herniation (brain stem compression) from massive intracranial pressure increase.
- ⅓ Unconscious with High Risk: High risk of mortality or permanent neurological deficits.
- ⅓ Good Outcome: Provided there is no re-bleeding.
- Congenital Weakness: The underlying congenital defect in the arterial wall is crucial to understanding aneurysm formation.
- Atherosclerosis & Hypertension: These conditions exacerbate the congenital weakness, increasing rupture risk.
- Location Matters: The specific location of aneurysms dictates potential neurological consequences based on affected arteries.
- Rapid Onset: The sudden, severe headache is a hallmark symptom reflecting the acute nature of the hemorrhage.
- Variable Outcome: The significant variability in outcomes highlights the severity and unpredictable nature of SAH.
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Pathology-Meningitis
I. Definition:
I. Definition:
- Infection of the subarachnoid space (the area between the brain and the protective membranes).
- Viral Meningitis: Approximately 11 cases per 100,000 people per year.
- Bacterial Meningitis: Approximately 3 cases per 100,000 people per year. Note the significantly lower incidence compared to viral meningitis.
- Viral Meningitis: Most commonly caused by echoviruses and coxsackieviruses. No organism is cultured from CSF.
- Bacterial Meningitis:
- Most common causes: Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus).
- Neonates (newborns): Escherichia coli and Group B streptococci are significant causes.
- CSF culture and/or blood cultures will yield the causative organism.
- Bacterial Meningitis: Bacteria typically enter the bloodstream from the nasal cavity (often following a viral upper respiratory infection). Their capsules provide resistance to phagocytosis (immune cell engulfment) and complement (part of the immune system). Bacteria exploit weaknesses in the blood-brain barrier (e.g., the choroid plexus) to access the subarachnoid space. Rapid bacterial multiplication in the cerebrospinal fluid (CSF) triggers an acute inflammatory response within the meninges.
- Viral Meningitis: The pathogenic mechanisms are less detailed in the provided text, but it implies a similar entry point via the bloodstream but without the bacterial capsule-related resistance to immune response.
- Common Symptoms (both viral and bacterial): Headache, fever, neck stiffness (meningismus), photophobia (light sensitivity).
- Severity: Bacterial meningitis typically presents with more severe symptoms than viral meningitis.
- Lumbar Puncture (Spinal Tap): CSF analysis is crucial.
- Viral Meningitis: CSF will show a predominance of lymphocytes (a type of white blood cell).
- Bacterial Meningitis: CSF will show a predominance of neutrophils (another type of white blood cell).
- Gram Staining (Bacterial Meningitis): Helps identify the bacteria present in the CSF, aiding in rapid diagnosis and treatment.
- Culture (Bacterial Meningitis): CSF and/or blood cultures are used to grow and identify the specific bacteria.
- Viral Meningitis: Generally mild, with complete recovery expected.
- Bacterial Meningitis: Much more serious; potentially life-threatening if not treated promptly with appropriate antibiotics. Severe cases can lead to permanent neurological complications including hearing loss, learning disabilities, paralysis, and epilepsy.
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Pathology- Cerebral Infections
I. Encephalitis
A. Definition: Infection of the brain parenchyma (functional tissue of the brain).
B. Etiology: Primarily viral, most commonly Herpes Simplex Virus (HSV).
C. Pathogenesis: HSV encephalitis typically results from reactivation of latent HSV in the trigeminal ganglion, leading to infection of the temporal lobe.
D. Presentation: * Confusion * Behavioral changes * Altered consciousness * Seizures (severe cases) * Key diagnostic clue: Simultaneous perioral (around the mouth) involvement.
E. Diagnosis: * Imaging: Brain imaging (e.g., MRI) may show temporal lobe abnormalities. * Laboratory: Polymerase chain reaction (PCR) on cerebrospinal fluid (CSF) to identify HSV DNA. * Histology: Necrotizing inflammation with characteristic herpetic intranuclear inclusions in neurons and glial cells (post-mortem).
F. Treatment: Urgent antiviral treatment is essential.
II. Cerebral Abscess
A. Definition: Localized brain infection with tissue destruction.
B. Etiology: Primarily bacterial, often mixed infections.
C. Pathogenesis: * Direct spread: From paranasal sinuses, middle ear, or teeth. * Hematogenous spread: From septic emboli (e.g., infective endocarditis).
D. Presentation: Symptoms of an infected intracranial mass: * Headache * Nausea * Vomiting * Fever * Seizures * Focal neurological signs (depending on abscess location).
E. Diagnosis: Primarily through CT scan.
F. Treatment: Surgical drainage and prolonged antibiotic therapy.
G. Prognosis: High mortality (20%) and significant morbidity (50% of survivors have persistent neurological deficits or epilepsy).
III. Progressive Multifocal Leukoencephalopathy (PML)
A. Definition: Demyelinating disease of the central nervous system white matter.
B. Etiology: JC virus (polyomavirus).
C. Risk Factors: Virtually exclusive to immunocompromised individuals (e.g., HIV/AIDS, transplant recipients).
D. Pathogenesis: JC virus infection leads to multiple foci of demyelination in the white matter, which can coalesce.
E. Histology: Viral inclusions in the nuclei of astrocytes, macrophages, and oligodendrocytes within demyelinated areas.
F. Diagnosis: * Clinical presentation: Neurological symptoms. * Imaging: Characteristic MRI findings. * Laboratory: Detection of JC virus DNA in CSF.
G. Prognosis: High mortality (up to 50% within 3 months).
I. Encephalitis
A. Definition: Infection of the brain parenchyma (functional tissue of the brain).
B. Etiology: Primarily viral, most commonly Herpes Simplex Virus (HSV).
C. Pathogenesis: HSV encephalitis typically results from reactivation of latent HSV in the trigeminal ganglion, leading to infection of the temporal lobe.
D. Presentation: * Confusion * Behavioral changes * Altered consciousness * Seizures (severe cases) * Key diagnostic clue: Simultaneous perioral (around the mouth) involvement.
E. Diagnosis: * Imaging: Brain imaging (e.g., MRI) may show temporal lobe abnormalities. * Laboratory: Polymerase chain reaction (PCR) on cerebrospinal fluid (CSF) to identify HSV DNA. * Histology: Necrotizing inflammation with characteristic herpetic intranuclear inclusions in neurons and glial cells (post-mortem).
F. Treatment: Urgent antiviral treatment is essential.
II. Cerebral Abscess
A. Definition: Localized brain infection with tissue destruction.
B. Etiology: Primarily bacterial, often mixed infections.
C. Pathogenesis: * Direct spread: From paranasal sinuses, middle ear, or teeth. * Hematogenous spread: From septic emboli (e.g., infective endocarditis).
D. Presentation: Symptoms of an infected intracranial mass: * Headache * Nausea * Vomiting * Fever * Seizures * Focal neurological signs (depending on abscess location).
E. Diagnosis: Primarily through CT scan.
F. Treatment: Surgical drainage and prolonged antibiotic therapy.
G. Prognosis: High mortality (20%) and significant morbidity (50% of survivors have persistent neurological deficits or epilepsy).
III. Progressive Multifocal Leukoencephalopathy (PML)
A. Definition: Demyelinating disease of the central nervous system white matter.
B. Etiology: JC virus (polyomavirus).
C. Risk Factors: Virtually exclusive to immunocompromised individuals (e.g., HIV/AIDS, transplant recipients).
D. Pathogenesis: JC virus infection leads to multiple foci of demyelination in the white matter, which can coalesce.
E. Histology: Viral inclusions in the nuclei of astrocytes, macrophages, and oligodendrocytes within demyelinated areas.
F. Diagnosis: * Clinical presentation: Neurological symptoms. * Imaging: Characteristic MRI findings. * Laboratory: Detection of JC virus DNA in CSF.
G. Prognosis: High mortality (up to 50% within 3 months).
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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:
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.
- 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.
- 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.
- 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).
- Most patients experience progressive disease.
- Significant complications due to disability: pneumonia, urinary tract infections, pressure sores. Think disability leads to secondary complications.
- 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-Alzheimer's Disease
I. Definition & Epidemiology:
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.
- 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.
- 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.
- 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.
- Death typically occurs approximately 10 years post-diagnosis, often due to complications like pneumonia.
- 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-Parkinson's Disease
I. Definition & Epidemiology:
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.
- 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.
- 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.
- 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.
- 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.
- 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- Huntington's Disease
I. Definition & Epidemiology:
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).
- 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.
- 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).
- 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.
- 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.
- 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 - Cerebral Infarction
I. Definition & Epidemiology
VI. Histopathology (Microscopic Changes)
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.
- 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.
- 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.
- 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.
- 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.
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.
- 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.
