Alterations in Neural Function Flashcards
what is increased intracranial pressure? Causes? Symptoms?
-increase in pressure in brain
common causes:
-inflammation (infection, inflammatory response to injury)
-mass (tumor)
-bleeding (hemorrhagic stroke)
-aneurysm (takes up space, may bleed)
common symptoms:
-headache
-blurred vision
-altered LOC
-NV
-behavioral changes
-weakness
-difficulty speaking
-seizures
what is traumatic brain injury? what are the types?
-Injury to brain from trauma
-Leading cause of death and disability in U.S. for persons under 24.
- Most r/t transportation-related accidents, falls, firearms & sports
Types of TBI
Focal injuries: (coup) localized to site of impact.
Polar injuries: (coup contrecoup) d/t acceleration-deceleration movement of brain within skull, resulting in double injury (usually opposite focal injury).
Diffuse injury: D/t movement of brain within skull, resulting in widespread axonal injury.
Concussion:
Mild TBI; most common injury of military personnel & athletes
-Alteration in or loss of consciousness (< 30 minutes)
-No evidence of brain damage on CT
-HA, nausea, vomiting, dizziness, fatigue, blurred vision, cognitive & emotional disturbances
Contusion: CT or MRI reveals area of brain tissue damage (necrosis, laceration, bruising)
what is an intracranial hematoma? what can cause the injury? etiology?
Localized collection of blood within the cranium.
Break in blood vessel in cranium causes hemorrhage and inflammation.
Expands slowly or rapidly; compresses brain & causes increased ICP
Mechanisms of injury:
-blunt (closed, non-penetrating)
-penetrating (open)
-compression
Types of intracranial bleeds: epidural, subdural, or intracerebral.
Etiologies: MVA, falls, violence, sports injuries, drugs, traumatic birth injury.
what is an epidural hematoma? CM? Diagnosis? Tx?
Collection of blood between dura & skull.
Usually arterial injury thus rapid onset of symptoms.
Associated with skull fracture; often temporal bone.
Manifestations: primary injury is minor, may suffer only brief period of disturbed consciousness followed by period of normal cognition (lucid interval), then LOC rapidly deteriorates
Diagnosis: CT scan
Treatment: surgery to remove hematoma
what is a subdural hematoma? Dx? Tx?
-Collection of blood between dura & outer layer of arachnoid membrane.
-Involves bridging veins, thus symptom onset slower.
-Chronic prone to re-bleeding.
Acute: symptomatic within 24-72 hrs.
Subacute: increased ICP (HA, N/V, blurred vision) 2-10 days later
Diagnosis: CT, MRI
Treatment: remove tissue and clot
what is a subarachnoid hemorrhage?
-Collection of blood between arachnoid membrane and pia mater.
-D/t rupture of bridging veins that pass through subarachnoid space.
-More commonly associated with rupture of cerebral aneurysms or arteriovenous malformations; arterial in origin.
-Blood spreads throughout CSF, causing meningeal irritation, hydrocephalus, headache, vasospasms, ischemia.
what is secondary injury?
-Initiated by TBI.
-Result from ischemia, increased ICP & altered vascular regulation.
-Ischemic & hypoxic events, edema & other processes that lead to IICP and may affect pt outcomes to a greater extent than the primary injury.
-Ruptured vessels may re-bleed or spasm, and CSF drainage can become clogged.
-Concomitant trauma may complicate brain injury.
what is cerebrovascular disease and stroke? what are the types?
Sudden onset of neurologic dysfunction d/t cardiovascular disease
-Abnormality in cerebral perfusion results in localized area of brain infarction.
-Third leading cause of death in U.S.
-Most common form of stroke is ischemic.
Types:
ISCHEMIC
-Thrombotic: atherosclerosis,
-Embolic: A-fib, valve disease, hypercoagulable states
HEMORRHAGIC
-structural anomalies
-hypertension
what are transient ischemic attacks? Cause? Warning signs? Tx?
Mimic a stroke for few secs to few hrs without permanent damage.
-Caused by temporary interference in cerebral blood flow.
Important warning sign for possible stroke.
-Neurologic symptoms can last mins. up to 24 hrs
-Symptoms resolve without lasting neurologic dysfunction
Tx: daily ASA; carotid endarterectomy, angioplasty
what is ischemic stroke?
-Sudden occlusion of a cerebral artery secondary to thrombus (arteriosclerosis) or embolus (atrial fibrillation).
-O2 to neurons is reduced, Na+ pump & neurotransmitters fail leading to cerebral edema, vasospasm & reduced cerebral perfusion.
-If anoxia lasts longer than 10 minutes = irreversible damage
what is hemorrhagic stroke?
-Occurs with long standing HTN
-Large hemorrhage results in significant ICP
-Degree of secondary injury & associated morbidity & mortality much higher in hemorrhagic stroke than ischemic stroke
what is stroke sequelae?
Motor and Sensory Deficits
Motor: Flaccidity/paralysis; function recovery occurs with onset of spasticity
-Contralateral to side of brain where stroke occurred
Sensory: Same areas as motor, contralateral field blindness
Language Deficits
-Aphasia d/t cerebral damage; can involve all language modalities
-Broca aphasia (verbal motor/expressive): Poor articulation & sparse vocabulary
-Wernicke aphasia (sensory, acoustic, receptive): Impaired auditory comprehension and speech that is fluent but does not make sense
Cognitive Deficits
-Area of brain affected dictates presence & severity.
-Impairment in language, spatial relationship skills, short-term memory, concentration, reasoning & judgment
what is a cerebral aneurysm?
-weakened vessel that leads to dilation & ballooning
-Congenital defect of layer of artery weakens to arterial pressure, allowing dilated portion to fill with blood & eventually burst causing subarachnoid hemorrhage.
-Most found in Circle of Willis.
-Typical presentation is severe HA.
-HTN, acute ETOH intoxication, & recreational drug use implicated.
what is an arteriovenous malformation?
-Tangle of enlarged vessels that can burst
-Pts. typically present with seizure & neurological dysfunction.
-May enlarge & compress adjacent structures or rupture.
-D/t high vascular pressure AVM’s are vulnerable to hemorrhage
what is meningitis? CM?
Bacteria reach CNS via blood stream or extension from cranial structures like ears & sinuses.
Viral: Self-limiting with complete recovery (herpes).
Bacterial: Leaves residual effects (Neisseria meningitis, streptococcus, haemophilus).
- Often follows upper respiratory infection.
-Pathogen crosses BBB & migrates in CNS causing inflammation with increased CSF which increases ICP.
Manifestations; Fever, vomiting, nuchal rigidity (neck stiffness), signs of IICP, septic emboli
what is encephalitis? CM?
-Inflammation of brain commonly caused by West Nile virus, western equine encephalitis, and herpes simplex
-Transfer usually by mosquito from animals to humans.
-Causes inflammation & lysis of cells.
Manifestations: cerebral edema, headache, fever, confusion, convulsions, weakness and rash.
what is brain abscess?
Localized collection of pus within brain parenchyma.
-Presents as space-occupying lesion with changes in LOC & typically signs of infectious etiology.
-Associated with penetrating wounds, mastoiditis, sinusitis, or blood-borne dissemination from a distant site.
-Organisms include: streptococcus, staphylococci, and anaerobes.
what is seizure disorder/epilepsy? etiology? What are the types?
Abnormal or excessive cortical electrical discharges manifested by disturbances of skeletal motor function, sensation, autonomic function, behavior, or consciousness.
-Neurons become abnormally hyperactive & hypersensitive to changes in their environment.
-Epilepsy or seizure disorder refers to recurrent seizures
Etiologies: Genetic, acquired from pathologic conditions, head injury, infections, space-occupying lesions, metabolic—electrolyte imbalance, hypoxia, acidosis, renal failure, drugs
Non synchronized neuronal activity, with groups of neurons inhibited & excited during transfer of info between different brain areas.
Type depends on location & pattern of spread.
Generalized seizures: Involve entire brain from onset of seizure.
Focal/Partial seizures: Abnormal electrical activity is restricted to one brain hemisphere.
Status epilepticus: Continuing series of seizures without a period of recovery between episodes & can be life-threatening.
what is cerebral palsy? etiology?
-Common disorder of childhood.
-Damage to motor control centers of brain.
-Classified on basis of neurologic signs and symptoms.
-Types include: spasticity (hypertonia), dyskinesia (involuntary movement and fine motor coordination), ataxic (gait disturbances), hypotonic (low muscle tone) and mixed.
Etiologies: Prenatal infections, birth trauma, exposure to poisons, and reduced oxygen supply to the brain.
what is hydrocephalus? what are the types?
Abnormal accumulation of CSF in cerebral ventricular system associated with congenital neural tube defects. May occur in adults from lesions or hemorrhage.
Three Types:
-Normal pressure: d/t increase in volume of CSF without change in pressure
-Obstructive: d/t obstruction to flow of CSF
-Communicating: abnormal absorption of fluid.
what is multiple sclerosis? etiology? patho? CM? tx?
Slowly progressive demyelinating disease of CNS
Etiology: Unknown. Autoimmune & environmental factors suspected.
Patho: Destruction of myelin sheath interrupts conduction of nerve impulses.
-Causes inflammation & sclerosis of myelin sheaths
-Demyelization can occur throughout CNS, often affects optic & oculomotor nerves & spinal nerve tracts.
Manifestations: double/blurred vision, weakness, poor coordination, sensory deficits; bowel & bladder control loss; memory impairment.
-Exacerbations/remissions; heat, infxn trauma, stress.
TX: Steroids for acute exacerbations. Immune-modifying rxs may slow symptom progression
what is spina bifida? dx? CM? tx?
Incomplete closure of neural tube
Spina bifida occulta: Not visible
Spina bifida cystica: External protrusion of saclike structure
Dx: prenatally (ultrasound and α-fetoprotein testing)
Clinical manifestations: saclike cyst filled with CSF, spinal cord, and/or meninges; permanent neurologic damage resulting in motor weakness or paralysis & sensory deficit below level of spinal defect
Tx: surgery, C-section, folic acid before & during pregnancy
what is amyotrophic lateral sclerosis (Lou Gehrig’s Disease)? etiology? CM? dx/ tx?
Degenerative dse of upper & lower motor neurons of cerebral cortex, brain stem & spinal cord resulting in total paralysis. Demyelination occurs.
-More common in men, between 40-60 years.
-Fatal in 3-5 yrs.
Etiology: idiopathic, viral infections, metabolic disorders, autoimmune.
Clinical manifestations: weakness, atrophy, cramps, stiffness, irregular twitching of muscles, hyperreflexia in weak, atrophied extremity
Dx: Based on clinical S/S, nerve conduction studies, MRI, & labs
Tx: comfort measures, no cure
what is spinal cord injury? What are the types?
-Consequence of trauma-falls, MVA, sports injury.
-Compression, transection, or contusion. Further damage from hemorrhage, edema & ischemia.
-Types of injury: hyperflexion, hyperextension, compression.
TYPES:
1. Spinal Shock
-Immediately follows injury: temporary loss of reflexes & muscle flaccidity below level of injury.
-Lasts 2 days to several mos.
-Associated with hypotension & bradycardia.
-Resolves when reflexes return & flaccidity replaced by spasticity
2. Neurogenic Shock
-Peripheral vasodilatation after injury
-Hypotension & circulatory collapse can occur; high cord injuries affect respiratory muscles, leading to ventilatory failure.
3. Autonomic Dysreflexia
-Occurs with injury at or above T6
-Abnormal, overreaction of the ANS to stimulation
-Acute reflexive response to sympathetic activation below level of injury.
-Manifestations: HTN, HA, bradycardia, flushing above the level of injury & clammy skin below level of injury.
what is Guillain-Barre syndrome? etiology? patho? CM?
Inflammatory demyelinating disease of peripheral nervous system or a lower motor neuron disorder.
-Also known as Acute Idiopathic Polyneuropathy
Etiology: Idiopathic, often follows viral infection. May be auto immune.
Pathogenesis: Antibody formation damages peripheral nerve myelin, impulses are slowed.
Manifestations: Sudden ascending muscle weakness beginning in lower extremities & moving upward.
-Spontaneous recovery usually occurs
-Remyelination occurs in descending order over periods of months.
what is Bell’s Palsy? etiology? CM?
Paralysis of muscles on one side of face, idiopathic
Etiology: virus, self-limiting.
Clinical manifestations: Develop rapidly over 24-48 hrs., unilateral facial weakness, droop & diminished eye blink & lacrimation (tears) & hyperacusis (sensitivity to sounds)
-May last days to wks.
