5.2 Stroke, Infection, Demyelination & Trauma

Ischemic vs Hemorrhagic Stroke Mechanisms

Ischemic stroke occurs when cerebral blood flow falls below the threshold needed for neuronal ATP production. Causes include large-artery atherosclerosis with in situ thrombosis, artery-to-artery embolism, cardioembolism (for example, atrial appendage thrombus concepts), small-vessel lipohyalinosis, and global hypoperfusion (watershed infarction). Neurons undergo ischemic cascade: energy failure → membrane depolarization → excitotoxic glutamate release → calcium overload → enzymatic damage, oxidative stress, and cell death. The ischemic core is irreversibly injured early; surrounding penumbra remains potentially viable if perfusion is restored—physiologic basis for time-sensitive reperfusion concepts on boards.

Hemorrhagic stroke results from vessel rupture into parenchyma (intracerebral hemorrhage) or other compartments. Chronic hypertension damages small penetrating arteries (Charcot–Bouchard microaneurysm concept) in putamen, thalamus, pons, and cerebellum. Cerebral amyloid angiopathy preferentially affects lobar vessels in older adults. Hemorrhage causes direct tissue destruction, mass effect, raised intracranial pressure, and secondary ischemia around the hematoma. Subarachnoid hemorrhage is arterial bleeding into CSF cisterns, most often from saccular aneurysm rupture at circle of Willis branch points.

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Arterial Territory Syndromes

MCA syndrome: contralateral face and arm weakness/sensory loss greater than leg; aphasia (dominant) or neglect (nondominant); may include contralateral visual field cut and conjugate gaze preference toward the lesion. Stem MCA occlusion can add deeper basal ganglia/internal capsule injury with denser deficits.

ACA syndrome: contralateral lower-extremity predominant weakness and sensory change; frontal behavioral changes, abulia, and grasp reflexes may appear; bilateral ACA disease can severely impair initiation and continence-related frontal networks.

PCA syndrome: contralateral homonymous hemianopia; alexia without agraphia can occur with dominant occipital plus splenium involvement (disconnection teaching); thalamic PCA branches may produce pure sensory stroke or sensorimotor mixtures.

Lacunar syndromes are small deep infarcts from lipohyalinosis of penetrators. Classic pure motor hemiparesis (posterior limb internal capsule or basis pontis), pure sensory stroke (thalamus), ataxic hemiparesis, and clumsy-hand dysarthria are localization patterns without cortical signs such as aphasia, neglect, or field cuts—useful negative findings in vignettes.

Watershed infarcts occur at borders between major arterial territories during severe hypotension, producing scattered or border-zone injury patterns rather than a single named cortical artery syndrome.

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Extra-axial Hemorrhage: Epidural, Subdural, SAH

Anatomy of meninges determines blood collection shape and time course.

Epidural hematoma typically follows temporal bone trauma lacerating the middle meningeal artery. Arterial blood strips dura from skull, forming a lens-shaped (biconvex) collection that does not cross suture lines (dura tightly adherent at sutures). Classic teaching sequence: loss of consciousness → lucid interval → secondary deterioration from herniation as the hematoma expands. Rapid deterioration reflects arterial pressure filling a confined space.

Subdural hematoma arises from tearing of bridging veins between cortex and dural sinuses. Venous blood spreads in the potential subdural space, forming a crescentic collection that can cross sutures but is limited by dural reflections (falx/tentorium). Acute subdural follows high-energy trauma; chronic subdural in elderly or atrophic brains may present days to weeks later as veins tear with minor trauma, with gradual confusion or focal signs as blood products accumulate and osmotically expand.

Subarachnoid hemorrhage (SAH) places blood in CSF pathways: sudden “thunderclap” headache, meningismus, photophobia, and risk of communicating hydrocephalus from impaired arachnoid granulation resorption. Aneurysms form at high-shear branch points (ACom, PCom, MCA bifurcation teaching sites). PCom aneurysm expansion can compress CN III—linking vascular anatomy to pupil-involving third-nerve palsy before or with rupture concepts.

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Meningitis, Encephalitis, Abscess: Organism Patterns and CSF

Meningitis is inflammation of the leptomeninges. Clinical cluster: fever, headache, nuchal rigidity, photophobia. Encephalitis emphasizes brain parenchymal dysfunction: altered mental status, seizures, focal neurologic deficits, personality change. Overlap (meningoencephalitis) is common.

Age and context guide likely bacterial pathogens at the mechanism/epidemiology level taught on exams:

Viral meningitis (enteroviruses common) produces lymphocytic CSF with less dramatic glucose depression. Bacterial meningitis classically shows high neutrophils (PMNs), low glucose, high protein, high opening pressure, and organisms on Gram stain/culture when captured. Viral profiles: lymphocytic predominance, normal glucose, moderately high protein. Fungal/TB meningitis: lymphocytic (or mixed), low glucose, high protein, more subacute course. These CSF patterns are mechanism-adjacent readouts of immune response and pathogen metabolism of glucose.

HSV encephalitis preferentially involves temporal (and frontal) lobes because of proposed routes along olfactory pathways and limbic tropism—yielding seizures, behavioral change, aphasia, and hemorrhagic necrotizing temporal pathology on imaging concepts. Arboviral encephalitides follow vector ecology. HIV-related opportunistic CNS disease appears with declining cell-mediated immunity.

Brain abscess is a focal suppurative collection within parenchyma, often from contiguous spread (sinus/otogenic), hematogenous seeding (right-to-left shunt, chronic lung infection teaching), or trauma. Early cerebritis organizes into a capsule. Presentation is more mass-lesion/focal than diffuse meningitis; organisms reflect source (mixed oral anaerobes, staph after trauma, etc.).

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Demyelination: MS vs GBS vs PML

Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system with demyelination of axons myelinated by oligodendrocytes, relative axonal preservation early, and lesions separated in space and time. Periventricular white matter, optic nerves, brainstem, and spinal cord are frequent targets. Mechanistic themes: autoreactive lymphocytes, blood–brain barrier disruption, and oligodendrocyte injury; chronic stages add axonal loss. Optic neuritis, internuclear ophthalmoplegia (MLF demyelination), and partial cord syndromes are classic localizations. Oligoclonal bands in CSF reflect intrathecal antibody synthesis—a laboratory correlate, not a bedside treatment rule.

Guillain–Barré syndrome (GBS) is an acute inflammatory demyelinating polyradiculoneuropathy of the peripheral nervous system (Schwann cell myelin). Molecular mimicry after infection (classically Campylobacter jejuni for axonal variants in teaching) leads to immune attack on nerve roots and peripheral myelin. Areflexia, ascending weakness, and albuminocytologic dissociation (high CSF protein, few cells) are physiologic correlates of root inflammation and barrier breakdown without CNS pleocytosis. Autonomic instability and respiratory muscle weakness follow peripheral nerve involvement—not a brain plaque process.

Progressive multifocal leukoencephalopathy (PML) is demyelination from JC virus infection of oligodendrocytes in immunocompromised hosts (advanced HIV, certain immunosuppressants). It is infectious destruction of myelinating cells rather than classic autoimmune MS. Multifocal white-matter lesions without mass effect dominate the conceptual picture.

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Traumatic Brain Injury: Diffuse Axonal Injury

Primary traumatic brain injury mechanisms include focal contusion, laceration, hematoma, and diffuse axonal injury (DAI). DAI occurs with high-speed acceleration–deceleration or rotational forces that shear axons at interfaces of different tissue densities—classically gray–white junctions, corpus callosum, and dorsolateral brainstem. Axons may show retraction balls (axonal varicosities) as transport continues into disconnected stumps. Clinical severity ranges from concussion physiology (transient network dysfunction) to prolonged unconsciousness when deep white-matter and brainstem connections are extensively disrupted. Secondary injury cascades—ischemia, excitotoxicity, edema, raised ICP—amplify primary mechanical damage.

Epidural/subdural/SAH anatomy (above) are compartment-specific traumatic or nontraumatic bleeds; DAI is a microstructural axonal mechanism even when gross hematoma is absent. Coup–contrecoup contusions reflect brain impact against inner skull tables opposite or at the site of blow, especially orbitofrontal and temporal poles.

Integrating Stroke, Infection, and Demyelination Vignettes

Ask four questions: (1) Vascular territory or small-vessel lacunar pattern? (2) Which meningeal/parenchymal compartment holds the blood or pus? (3) CNS versus PNS myelin, and autoimmune versus viral oligodendrocyte infection? (4) Focal mass effect versus diffuse axonal shear? Mechanism-first answers match CBSE style far better than memorized drug doses or stroke-scale cutoffs.