Disorders of Brain Function Flashcards
Differentiate cerebral hypoxia from cerebral ischemia and focal from global ischemia.
- Focal Cerebral Ischemia = short term
- Typical causes: thrombus/embolism
- “zone of penumbra” without infarction - Global Ischemia = Loss of Consciousness
- Release of “excitatory” amino acid neurotransmitters
- Disruption of calcium balance
- Formation of free radicals (instability with free electron floating around)
- Mitochondrial injury
- ATP malfunction = “power failure” = edema
If not restored quickly, permanent damage!
Characterize the role of excitatory amino acids as a common pathway for neurologic disorders.
- Neuron injury results in release and activation of mediators that overstimulate cell receptors
- Amino acids (e.g. glutamate), catecholamine’s, free radicals etc. - Glutamate attaches and opens calcium channels leading to “calcium cascade” into cells
- Protein breakdown
- Free radical formation
- DNA fragmentation
- Mitochondrial injury
- Cell death
Compare cytotoxic and vasogenic cerebral edema
- Vasogenic
- Leaking of water/proteins into Interstitial space
- Causes: hemorrhage, meningitis, injury, tumors
- White matter more so (not as dense as gray)
- Result: herniation, focal defects, increased intracranial pressure, altered LOC - Cytotoxic
- Increased intracellular fluid
- Causes: water intoxication, impaired K+/Na+ pump
- Result: cell rupture with damage to surrounding tissue, - increased intracellular fluid
State the determinants of increased intracranial pressure and describe the typical symptoms associated with this condition.
Compartment syndrome in the skull
- Intracranial pressure greater than arterial blood pressure
- Arteries collapse; blood flow to brain cut off
Compliance = change in volume change in pressure - Tissue: tumor, edema, bleed
- Blood: vasodilation, obstruction of outflow
- CSF: increased production, decreased absorption, obstruction
Compare the causes, manifestations, and usual treatment of communicating and noncommunicating hydrocephalus
- Increased CSF volume enlarges ventricles and compresses brain tissue
1. Non-communicating/Obstructive - Congenital malformations, tumors, inflammation, hemorrhage = CSF blockage
2. Communicating - Impaired reabsorption of CSF via arachnoid villi d/t infection, scarring, blockage by lyzed rbcs post repair of bleed
- Increased production of CSF (rare)
Manifestations
- Fontanel bulging fetus/newborn
- Signs of increased ICP in all ages
- Optic nerve atrophy/blindness
Differentiate primary and secondary brain injuries due to head trauma.
1. Primary/Direct injuries—due to impact Microscopic damage: diffuse axonal injury Contusions Coup (place of impact) Contrecoup (injury that occurs as a result of brain moving due to impact) 2. Secondary injuries—due to: Ischemia Hemoorage Infection Increased intracranial pressure
Describe the mechanism of brain damage in coup-contrecoup injuries.
- a coup injury occurs under the site of impact with an object
- a contrecoup injury occurs on the side opposite the area that was hit
Describe the symptoms associated with mild, moderate, and severe traumatic head injuries.
- Mild
- Concussion (immediate & possible post-concussion syndrome)
- Limited symptoms to momentary LOC, residual amnesia - Moderate
- Small hemorrhages, edema
- LOC, cognitive/motor deficits, hemiparesis, nerve palsies - Severe
- Shearing, pressure = axon/vessel/tissue damage
- Extensive damage with secondary manifestations- Hemiplegia, signs of elevated ICP, coma
Differentiate among the location, manifestations, and morbidity of epidural, subdural, and intracerebral hematoma.
- Hematoma - Epidural
- Meningeal artery tear
- Rapid bleeding; unconsciousness may be followed by brief lucid period
- Ipsilateral pupil dilation, contralateral hemiparesis d/t uncal herniation
- Treatment prior to LOC has good prognosis - Hematoma- Subdural
- Venous tear between dura & arachnoid
- Slower bleeding
- Acute (within 24 hours)
- Increased ICP, decerebrate posturing, LOC, high mortality rate
- Subacute (2-10 days)
- Periods of improvement prior to rapid deterioration
- Chronic (weeks)
- Slow bleed, decreased LOC, drowsiness, confusion, apathy, h/a - Hematoma- Intracerebral
- Usually frontal or temporal lobes
- Risk: age, alcoholism
- Symptoms dependent on size & location
- Increased ICP
- herniation
Discuss Doll’s eyes response, decorticate and decerebrate posturing, and Cheyne-Stokes breathing as they relate to diffuse brain injury.
- Doll’s eyes response: (vestibulo-ocular reflex)
- Indicates brain stem damage
- Possible tentorial herniation - Decorticate posturing
- Damage to one or both corticospinal tracts involving the “red nucleus” in midbrain - Decerebrate posturing
- Indicated brain stem damage below level of red nucleus
- Upper & lower extremity extension
- Head arched back
- Can be one side or both or just arms - Cheyne-Stokes
Differentiate the pathologies and risk factors of ischemic and hemorrhagic stroke.
- Ischemic Stroke (interruption in blood flow)
- Age, gender, race, familial, HTN, smoking, DM, sickle cell disease, atrial fibrillation, CAD
- Obesity, physical inactivity, alcohol, drug use, - - - hypercoagulability disorders, oral contraceptives, - hormone replacement therapy - Hemorrhagic Stroke (bleed into brain tissue)
- HTN, aneurysms, AV malformations, head injury, blood dyscrasias
Explain the significance of transient ischemic attacks, the ischemic penumbra, and watershed zones of infarction and how these conditions relate to ischemic stroke.
Transient: - Focal cerebral ischemia - “zone of penumbra” without infarction - Reverses prior to ischemia - Similar risk factors and symptoms as stroke but symptoms last < 1 hour with fully recovery Increases risk of stroke
Describe the progression of motor deficits and problems with speech and language that occur as a result of stroke.
- Usually unilateral and focal
- Weakness/numbness (face, arm, leg)
- Vision loss
- Aphasia (language disorder)
- Dysarthria (motor speech disorder)
- Ataxia (muscle coordination disorder)
Cite the most common causes, manifestations, and possible complications of subarachnoid hemorrhage.
- Risk factors of aneurysm
- AV malformations of brain
- Atherosclerosis
- Polycystic kidney
- Coaractation of aorta - Risk factors of rupture
- Age
- Smoking
- HTN
- Alcoholism
- Size of aneurysm
- Conditions that increase ICP - Pre-rupture
Sudden-onset headache with n&v, dizziness
Hemorrhage
- Sudden severe h/a, N&V, nuchal ridigity, photophobia, vision and motor problems, loss of consciousness
Complications post-op
- re-bleeding, vasospasm, hydrocephalus
Describe the alterations in vasculature that occur with arteriovenous malformations.
- Tangle of abnormal arteries and veins linked by fistulas
- Possibly due to lack of capillary formation invitro
- Structurally unstable with high pressure flow from - arteries to veins
- Ischemic symptoms
- Symptoms may not show until > 40 yrs of age
- Hemorrhage usually slower process
- Surgical removal
Compare the pathophysiology and manifestations of acute bacterial and viral meningitis
Acute Bacterial Meningitis:
- Inflammation of pia, arachnoid and subarachnoid space
- Contagious: direct contact (blood/mucous)
- Carriers
- 10% permanent damage (ear, sight, etc.)
- 10% fatal
- Neisseria meningitidis or Streptococcus pneumoniae
- Group B streptococci (neonates)
Acute Bacterial Meningitis Risk Factors
ABM risk Factors:
- Basilar skull fracture
- Otitis media
- Sinusitis/mastoiditis
- Neurosurgery
- Sepsis
- Living in close quarters/aged/infants
Acute Bacterial Meningitis patho:
ABM patho:
- Bacteria replicate & lyze in CSF
- Endotoxins/debris result in inflammatory process
- Neutrophils/albumin etc. allowed into CSF
- Thrombi, scarring, blockage
