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Flashcards from lecture notes on brain trauma and neurological disorders.
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Increased Intracranial Pressure (IICP)
May result from anything that takes up volume in the brain, e.g., tumor, edema, excess CSF, or hemorrhage.
Stage 1 of Intracranial Hypertension
Vasoconstriction and external compression of the venous system occur to decrease the ICP (may be asymptomatic).
Stage 2 of Intracranial Hypertension
Continuing swelling exceeds compensatory mechanisms; oxygenation is compromised, systemic vasoconstriction increases blood pressure to overcome decreased flow in the brain (confusion, drowsiness).
Stage 3 of Intracranial Hypertension
ICP equals arterial pressure, cerebral perfusion pressure falls, and hypoxia and hypercapnia of brain tissue occur (rapid deterioration: small sluggish pupils); all compensatory mechanisms have been used and dramatic rise in ICP over a very short period of time.
Stage 4 of Intracranial Hypertension
Brain tissue shifts (herniates) from a compartment of greater pressure to one of lesser pressure, impairing blood supply; ICP increases until it equals systolic arterial pressure, at which point cerebral blood flow ceases.
Cerebral Edema
An increase in the fluid content of brain tissue; occurs after trauma, infection, hemorrhage, tumor; distorts blood vessels, displaces brain tissue, causes herniation.
Hydrocephalus
Excess fluid in ventricles, subarachnoid space, or both, caused by too high production of CSF, obstructed flow through ventricles, or too low reabsorption of CSF.
3 Characteristics of Neuromotor Dysfunction
Alterations in muscle tone (flaccidity/hypotonia to rigidity/hypertonia, dystonia), alterations in movement (paresis/paralysis, hyperkinesia), and alterations in complex motor performance (disorders of posture, gait, expression).
Hypotonia
Flaccidity
Hypertonia
Rigidity
Dystonia
Sustained involuntary twisting movement of the hand and foot.
Paresis
Partial paralysis / weakness
Paralysis
Loss of motor neuron function so that a muscle group is unable to overcome gravity; occurs in both upper and lower motor neurons.
Hyperkinesia
Excessive movements e.g. tremors, tics - due to physical or chemical causes eg. insufficient dopamine
Decorticate
Upper extremities flexed at the elbows and held close to the body and lower extremities are externally rotated and extended; may occur with cerebral hemisphere damage.
Decerebrate
Increased tone in extensor muscles and trunk muscles, with clenched jaw and extended neck so head in neutral position, all four limbs rigidly extended; occurs with brain stem lesions.
Spastic Gait
Shuffle gait with leg extended and held stiff.
Hypermimesis
Inappropriate laughter or crying.
Dyspraxia/Apraxia
Inability performing tasks that require learned motor skills (speaking, writing, using tools, following instructions).
Closed brain trauma
Dura remains intact; may result in both focal brain injuries or diffuse axonal injuries
Open brain trauma
Break in the dura resulting in exposure of the cranial contents to the environment.
Contusions
Bruises in brain tissue; blood leaking from injured blood vessels; edema, infarction, necrosis, hemorrhage occur.
Coup injury
Impact against the object, causing direct trauma to the brain at the point of impact.
Contrecoup injury
Impact within skull, causing injury at area opposite to object, and shearing forces through the brain.
Extradural (epidural) hematomas
Injury causes bleeding between the dura mater and the skull due to arterial bleeding.
Subdural hematomas
Bleeding between the dura mater and the brain; acute develops rapidly, commonly within hours, chronic develops over weeks to months.
Intracerebral hematomas
Bleeding within the brain; penetrating injury or shearing forces traumatize small blood vessels; may be delayed, appearing 3-10 days after injury.
Penetrating brain trauma
Projectiles and debris from scalp and skull injury/fracture penetrate dura mater.
3 Mechanisms that produce brain damage
Focal brain injury (contusions - coup, contrecoup, hematomas), diffuse brain injury (DAI, concussion), secondary (cerebral edema, IICP, decreased cerebral perfusion pressure, ischemia, brain herniation), tertiary.
Focal brain injury
Specific, grossly observable brain lesions that occur in a precise location.
Diffuse brain injury
Concussion, result of shaking, rotational and twisting movements; involves a widespread area of the brain, with damage to axonal fibers; reduces the speed of informational processing.
Mild concussion
No loss of consciousness but CSF pressure increases; confusion lasts for several minutes, retrograde amnesia.
Classic cerebral concussion
Loss of consciousness for up to 6 hr; confused state lasts for several hrs., headache, nausea, retrograde amnesia.
Mild DAI
6-24 hr coma; may display decerebrate or decorticate with extended periods of stupor/restlessness.
Moderate DAI
24hr coma; may display posturing with unconsciousness lasting days or weeks; on awakening, permanent deficit in memory, reasoning, language, etc.
Severe DAI
Emerge from coma in the first 3 months after injury; initial injury eventually results in compromised coordinated movements, verbal and written communication skills, inability to learn and reason.
Cerebrovascular disorders
Abnormality of the brain caused by a pathologic process in the blood vessel; results in ischemia/infarction/hemorrhage, leads to cerebrovascular accident or stroke.
Thrombotic Stroke
Occlusions formed by thrombi developing in arteries supplying the brain; develop as a result of atherosclerosis, after plaque ruptures and a clot is formed.
Transient ischemic attack (TIA)
A brief episode of neurologic dysfunction caused by a focal disturbance of brain with symptoms lasting less than 1 hr, no evidence of infarction and complete clinical recovery.
Embolic Stroke
Involves fragments that break from a thrombus formed outside the brain.
Hemorrhagic stroke
A mass of blood forms and grows to displace adjacent brain tissue; associated with increased systolic and diastolic pressures over several years.
Intracranial aneurysm
Size varies fr. 2mm-2/3cm, classified on the basis of shape; often asymptomatic; first indication is an acute subarachnoid hemorrhage and/or intracerebral hemorrhage.
Multiple Sclerosis
Acquired autoimmune inflammatory disorder, involves destruction of axonal myelin in the CNS, onset usually bet. 20-40 yrs/more common in women
Alzheimer Disease
Most common causes of severe cognitive dysfunction in older persons and the leading cause of dementia; plaques form between neurons and protein-containing tangles form inside neurons, damaging and killing neurons, disrupting nerve impulse transmission.
Types of Stroke
Thrombotic stroke, embolic stroke, hemorrhagic stroke
Structural Alterations in Arousal
Infections, neoplasms, trauma, metabolic disturbances.
Metabolic Alterations in Arousal
Hypoxia, drugs, electrolytes disturbances.
Glasgow Coma Scale
Method used for assessing level of consciousness in person w/ brain injury and numbered scores given to responses of eye opening, verbal utterances, and motor responses.
Evaluation of Arousal
Level of consciousness, patterns of breathing, pupillary changes, oculomotor responses, motor responses.
Persistent vegetative state (PVS)
Complete unawareness of self or the surrounding environment; sleep-wake cycles are present, brain stem reflexes are intact but bowel and bladder incontinence.
Locked-in syndrome
Complete paralysis of voluntary muscles except the eye movements; fully consciousness with intact cognitive function but can't communicate thru speech or body movements.
Outcomes of alterations in arousal
Brain death, cerebral death, PVS, minimally conscious state, locked-in syndrome.
Alterations in awareness
Include all cognitive functions; caused by destruction of tissue caused by hypoxia/ischemia or compression, or effects of toxins/chemicals.
Seizure
Sudden temporary change in motor, sensory, autonomic or psychic clinical manifestations and a temporary altered level of arousal; results from a sudden, explosive, disorderly discharge of cerebral neurons.
Agnosia
Inability to recognize the form/nature of objects; affects one sense; caused by any damage to a specific part of the brain.
Dysphasia
Inability to understand or use of symbols (written/verbal); caused by dysfunction in left cerebral hemisphere.
Aphasia
Inability to communicate.
Acute confusional states
Inability to concentrate on incoming sensory info.; highly distractible; caused by drug intoxication, nervous system disease, trauma, surgery, etc.
Dementia
Progressive failure of cerebral functions such as orienting, memory, language, judgment, and decision-making; accompanied by behavioral alterations.
3 injury states in cerebral blood flow
Inadequate cerebral perfusion, normal cerebral perfusion with an elevated intracranial pressure, excessive cerebral blood volume.