Chapter 44: Acute Disorders of Brain Function (Exam 3)

What is primary brain injury?

Direct injury caused by the initial insult.

What is secondary brain injury?

Progressive damage caused by the body's response to the initial insult.

What key factor influences neuronal survival after brain injury?

The degree of ATP depletion.

What is ischemia?

Inadequate arterial blood flow to meet brain tissue's metabolic needs.

What is hypoxia?

Reduced oxygen at the tissue level that can impair aerobic ATP production.

Why is brain tissue sensitive to oxygen deprivation?

It has high ATP requirements and limited capacity for anaerobic metabolism.

How does oxygen deprivation cause cellular acidosis?

Anaerobic metabolism produces lactate and hydrogen ions, lowering cellular pH.

What happens to ion gradients during cellular energy failure?

They deteriorate because of inadequate ATP.

How does excess glutamate contribute to brain injury?

It overstimulates neurons, causing excessive calcium entry and cellular injury.

How can NMDA receptor activation worsen brain injury?

It stimulates nitric oxide production, which can increase damaging reactive nitrogen species.

What is reperfusion injury?

Cell damage when oxygen returns and reactive oxygen species are produced.

How can free radicals damage brain cells?

They damage cell membranes through lipid peroxidation and promote inflammation.

What is abnormal autoregulation after brain injury?

Failure to match cerebral blood flow and oxygen supply to tissue demand.

What three components determine intracranial pressure (ICP)?

Brain tissue, cerebrospinal fluid (CSF), and blood.

What does the Monro-Kellie hypothesis state?

An increase in one intracranial component can be offset by a decrease in the other two.

What can increased ICP cause?

Compression of neural tissue and blood vessels, and possible brain herniation.

What is brain herniation?

Protrusion of brain tissue through an opening in the supporting dura.

How is increased ICP evaluated?

Brain CT or MRI and measurement of ICP and cerebral perfusion pressure.

How may increased ICP be treated?

Removing a mass or CSF and using osmotic diuretics.

What is the most sensitive indicator of altered brain function?

A change in level of consciousness (LOC).

What tool is used to assess LOC after acute brain injury?

The Glasgow Coma Scale (GCS).

How is mild traumatic brain injury classified by GCS?

GCS 13–15.

How is moderate traumatic brain injury classified by GCS?

GCS 9–12.

How is severe traumatic brain injury classified by GCS?

GCS 8 or below.

What is a focal brain injury?

An injury localized to the site of impact.

What is a polar brain injury?

Acceleration-deceleration causes injury at two locations in the brain.

What is a diffuse brain injury?

Movement of the brain within the skull causes widespread axonal injury.

What is a brain contusion?

An observable brain lesion typically caused by impact.

Which vessel is associated with an epidural hematoma?

The middle meningeal artery.

Which vessels are associated with a subdural hematoma?

Bridging veins.

What are possible manifestations of an epidural hematoma?

Headache, nausea, vomiting, seizures, and a possible lucid interval.

What are possible manifestations of a subdural hematoma?

Increased ICP and focal neurologic deficits.

Why is secondary injury important in traumatic brain injury?

Ischemia, hypoxia, edema, increased ICP, and altered vascular regulation can worsen outcomes.

What are key priorities in traumatic brain injury treatment?

Cardiopulmonary stabilization, imaging, and maintaining normal temperature, PaCO2, glucose, and intravascular volume.

What are the three major cerebrovascular disorders?

Transient ischemic attack (TIA), ischemic stroke, and hemorrhagic stroke.

What is a stroke?

Sudden neurologic dysfunction caused by cerebrovascular disease resulting in brain infarction.

What are major stroke risk factors?

Hypertension, diabetes mellitus, hyperlipidemia, and smoking.

What causes an ischemic stroke?

Occlusion of a cerebral artery by a thrombus or embolus.

What is a thrombotic stroke?

A stroke caused by a thrombus forming in an artery supplying the brain or within intracranial vessels.

What is an embolic stroke?

A stroke caused by a traveling clot fragment formed elsewhere, often associated with cardiac dysfunction or dysrhythmia.

What is the goal of early ischemic stroke treatment?

Salvage the penumbra, minimize infarct size, and preserve neurologic function.

What time window do the slides identify for thrombolytic treatment to be maximally effective?

Within 3 hours of symptom onset.

What is a hemorrhagic stroke?

Bleeding within the brain parenchyma.

What is a major risk factor for hemorrhagic stroke?

Severe, chronic hypertension.

Where do many hemorrhagic strokes described in the slides occur?

The basal ganglia or thalamus.

How is hemorrhagic stroke managed?

Controlled blood pressure reduction and monitoring and management of increased ICP.

How is acute stroke evaluated?

Brain CT determines the type and location of the stroke.

What motor changes may occur after a stroke?

Initial flaccidity or paralysis; spasticity may develop during recovery.

What rehabilitation may be needed after stroke?

Physical, occupational, speech, and neurocognitive therapies, plus range-of-motion exercises.

What sensory problems may occur after stroke?

Sensory disturbances in areas affected by motor paralysis, sometimes including visual impairment.

What is aphasia?

An integrative language disorder associated with damage to the dominant cerebral hemisphere.

What cognitive deficits may occur after stroke?

Language impairment, spatial relationship difficulties, short-term memory problems, and poor judgment.

What is a cerebral aneurysm?

Dilation or ballooning of an artery segment due to vessel-wall weakness.

What can happen if a cerebral aneurysm ruptures?

It can cause subarachnoid hemorrhage.

How may a cerebral aneurysm be treated?

Surgical clipping or embolization.

How can organisms reach the CNS?

Through the bloodstream, direct extension, peripheral or cranial nerves, or maternal-fetal exchange.

What is the usual cause of meningitis versus encephalitis?

Meningitis is generally bacterial; encephalitis is generally viral.

Which bacteria are commonly associated with meningitis?

Streptococcus pneumoniae and Neisseria meningitidis; Haemophilus influenzae is also noted.

What CSF findings are typical of bacterial meningitis?

Neutrophil-predominant WBCs, increased protein, and decreased glucose.

What are classic clinical features of meningitis?

Headache, fever, stiff neck, cerebral dysfunction, and possible rapid decline in consciousness.

How is bacterial meningitis treated?

Supportive care, IV antibiotics targeting the pathogen, and management of complications.

What can meningitis-related inflammatory exudate cause?

Obstructive hydrocephalus.

What is encephalitis?

Inflammation of the brain, commonly caused by viruses.

Which viruses are associated with encephalitis in the slides?

West Nile virus, western equine encephalitis, and herpes simplex virus.

What are common manifestations of encephalitis?

Malaise, headache, nausea, vomiting, fever, muscle pain, or rash.

What CSF findings are typical of viral encephalitis?

Normal or mildly elevated WBC count, slightly increased protein, and normal glucose.

How is viral encephalitis generally treated?

Supportive and symptomatic treatment.

What is a cerebral abscess?

A localized collection of pus within the brain parenchyma.

How can a cerebral abscess develop?

Through local spread from infections such as sinusitis or mastoiditis, or through the bloodstream.

How may a cerebral abscess present?

As a space-occupying lesion with altered consciousness and signs of infection.

How is a cerebral abscess treated?

Drainage and/or excision plus IV antibiotic therapy.

How are LOC and cranial nerve reflexes used in brain-injury assessment?

LOC/GCS assesses overall brain function and injury severity; cranial nerve reflexes help assess brainstem function.

What are common manifestations of traumatic brain injury and intracranial hemorrhage?

Decreased LOC, cranial nerve dysfunction, muscle weakness, increased ICP symptoms, and coma.

How do stroke prevention strategies differ by cause?

Thrombotic: reduce atherosclerosis and platelet aggregation; embolic: anticoagulation when appropriate for atrial fibrillation; hemorrhagic: control hypertension.

Why do ischemic stroke symptoms vary by artery affected?

Each artery supplies a different brain territory with different physical and cognitive functions.

What are common long-term stroke sequelae?

Motor, sensory, language, and cognitive deficits.

How are long-term stroke deficits managed?

Rehabilitation, including speech, occupational, neurocognitive, and physical therapies.

What is the usual presentation of a ruptured cerebral aneurysm or AVM described in the key questions?

Subarachnoid hemorrhage with severe headache, meningismus, nausea/vomiting, photophobia, and possible seizure.

How does bacterial meningitis differ from viral encephalitis in CSF findings?

Bacterial meningitis: neutrophils, high protein, low glucose. Viral encephalitis: normal or mildly elevated WBCs, slightly high protein, normal glucose.

How does treatment differ between bacterial meningitis and viral encephalitis?

Bacterial meningitis requires IV antibiotics and supportive care; viral encephalitis is generally treated supportively and symptomatically.