Pathology of the Central Nervous System
The pathology of the central nervous system (CNS) examines diseases affecting the brain, spinal cord, and associated structures. It investigates structural and functional changes, including how neurons and glial cells respond to injury. Key areas include understanding normal CNS components, cellular reactions to damage, and critical conditions such as increased intracranial pressure, cerebral edema, hydrocephalus, and various types of brain herniations, all vital for neurological health.
Key Takeaways
CNS pathology studies diseases impacting the brain and spinal cord.
Neurons and neuroglia exhibit distinct responses to various injuries.
Increased intracranial pressure is a critical, life-threatening neurological condition.
Cerebral edema and hydrocephalus involve abnormal fluid accumulation in the brain.
Brain herniations are severe displacements of brain tissue with dire consequences.
What constitutes the normal structure of the Central Nervous System?
The Central Nervous System (CNS) comprises two main tissue types. Neuroectodermal tissues form core functional units: neurons (nerve cells) and supportive neuroglia. Mesodermal tissues provide structural integrity and immune defense, including microglia, protective meninges (dura mater, leptomeninges), blood vessels, and mesenchymal cells. Understanding these components is crucial.
- Neuroectodermal Tissues: Neurons (nerve cells) and neuroglia.
- Mesodermal Tissues: Microglia, dura mater, leptomeninges, blood vessels, mesenchymal cells.
How do neurons react to injury in the Central Nervous System?
Neurons in the CNS react distinctly to injury based on its nature. Acute injury, like ischemia, rapidly causes 'red neurons' within 12-24 hours, indicating irreversible cell death. Chronic or subacute injuries lead to gradual neuronal degeneration, cell loss, and reactive gliosis. Axonal reaction (central chromatolysis) is a regenerative response to axonal damage.
- Acute Neuronal Injury: 'Red neurons' (shrinkage, pyknosis, Nissl loss, eosinophilia).
- Chronic/Subacute Injury: Degeneration, neuronal loss, gliosis.
- Axonal Reaction: Cell body enlargement, nucleus displacement, nucleolus enlargement, Nissl dispersion.
What are the roles and responses of neuroglia in CNS pathology?
Neuroglia are non-neuronal cells vital for supporting neurons, playing diverse roles in CNS pathology. Astrocytes provide structural support, maintain the blood-brain barrier, and respond to injury via gliosis. Oligodendrocytes form and maintain myelin, crucial for nerve impulse transmission. Ependymal cells line ventricles, influencing CSF composition. Microglia, the CNS's immune cells, become mobile and phagocytic.
- Astrocytes: Support neurons, blood-brain barrier, gliosis, Rosenthal fibers.
- Oligodendrocytes: Myelin formation/maintenance; myelin disorders.
- Ependymal Cells: Line ventricles, influence CSF.
- Microglia: CNS macrophages, mobile, proliferate ('rod cells'), form nodules, neuronophagia.
What are the significant unique features in Central Nervous System pathology?
The Central Nervous System has unique features influencing its pathology. It is highly susceptible to increased intracranial pressure due to its rigid enclosure, and extremely vulnerable to ischemia and hypoxia, causing rapid cell damage. The lesion's precise location often dictates clinical outcome. Crucially, the CNS has limited regenerative capacity; injury results in gliosis (glial scarring) rather than fibrous tissue.
- Susceptible to increased ICP, ischemia, hypoxia.
- Lesion site more critical than nature.
- Selective vulnerability of structures.
- Heals via gliosis, no regeneration/fibrosis.
What causes and manifests as increased intracranial pressure?
Increased intracranial pressure (ICP) occurs when pressure within the skull exceeds 7-15 mmHg, threatening brain function. Causes include cerebral edema, fluid accumulation, and space-occupying lesions like infarctions, hemorrhages, infections, or tumors. Head trauma and hydrocephalus also contribute. Clinical manifestations are diverse: papilledema, visual disturbances, nausea, vomiting, headaches, neck stiffness, and mental status changes.
- Normal ICP ranges from 7-15 mmHg.
- Causes: Cerebral edema, infarction, hemorrhage, infections, tumors, trauma, hydrocephalus.
- Manifestations: Papilledema, visual disturbances, nausea, vomiting, headache, neck stiffness, mental status changes.
What is cerebral edema and what are its types?
Cerebral edema is abnormal fluid accumulation within brain parenchyma, causing swelling and potentially increased intracranial pressure. This compromises brain function by compressing structures and impairing blood flow. Two primary types exist: Vasogenic edema results from blood-brain barrier disruption. Cytotoxic edema involves direct cell injury, leading to intracellular fluid accumulation.
- Accumulation of excess fluid in brain parenchyma.
- Types: Vasogenic (blood-brain barrier disruption), Cytotoxic (cell membrane injury).
What is hydrocephalus and what are its causes and types?
Hydrocephalus is excessive cerebrospinal fluid (CSF) accumulation within the brain's ventricular system, causing enlargement. This results from rare CSF overproduction or, more commonly, impaired flow or resorption. Noncommunicating hydrocephalus involves an obstruction within the ventricular system. Communicating hydrocephalus occurs when CSF flow is normal, but its absorption is impaired. Ex vacuo hydrocephalus is compensatory ventricular dilatation.
- Excessive CSF in the ventricular system.
- Causes: Overproduction or impaired flow/resorption.
- Types: Noncommunicating (obstruction), Communicating (impaired resorption), Ex vacuo (compensatory dilatation).
What are the different types of brain herniations and their consequences?
Brain herniations are life-threatening conditions where increased intracranial pressure displaces brain tissue, compressing vital structures. Subfalcine (cingulate) herniation involves the cingulate gyrus under the falx cerebri, potentially compressing anterior cerebral artery branches. Transtentorial (uncinate) herniation sees the medial temporal lobe pushing through the tentorium, leading to third cranial nerve, posterior cerebral artery, and cerebral peduncle compression. Tonsillar herniation, where cerebellar tonsils descend through the foramen magnum, is dangerous as it compresses the brainstem, compromising respiratory and cardiac centers.
- Subfalcine: Cingulate gyrus under falx cerebri, compresses anterior cerebral artery.
- Transtentorial: Medial temporal lobe through tentorium, compresses 3rd nerve, PCA, cerebral peduncle; Duret hemorrhage.
- Tonsillar: Cerebellar tonsils through foramen magnum, compresses brainstem (respiratory/cardiac).
Frequently Asked Questions
What are the primary components of normal CNS structure?
The CNS comprises neuroectodermal tissues like neurons and neuroglia, and mesodermal tissues including microglia, meninges (dura mater, leptomeninges), blood vessels, and mesenchymal cells.
How do neurons respond to acute injury?
Acute neuronal injury, often seen as 'red neurons,' involves cell body shrinkage, nuclear pyknosis, loss of Nissl substance, and intense cytoplasmic eosinophilia, indicating cell death within hours.
What is the main function of oligodendrocytes?
Oligodendrocytes are crucial for forming and maintaining myelin, the insulating sheath around nerve fibers. Disorders affecting these cells can lead to demyelinating diseases.
Why is increased intracranial pressure significant in CNS pathology?
Increased intracranial pressure is critical because the skull is a rigid box. Elevated pressure can compress brain tissue, impair blood flow, and lead to severe neurological deficits or fatal herniations.
What is the difference between communicating and noncommunicating hydrocephalus?
Noncommunicating hydrocephalus results from an obstruction within the ventricular system, preventing CSF flow. Communicating hydrocephalus occurs when CSF flow is open, but its resorption into the bloodstream is impaired.
