Question | Answer |
What is the incidence of traumatic brain injury (TBI)? | •2 million in the US each year sustain a TBI
•50,000 ppl per year die secondary to TBIs
•Rises with declining income and population density
•Death rate has declined over the past 25 years |
What are the three age peaks and populations most affected by TBI? | •1-2 years old (due to child abuse)
•15-24 years old (due to risk taking behavior)
oBiggest group
•Elderly (due to falls)
•Males are more likely to experience brain injury
•Males are more likely sustain severe injuries |
What is the most common etiology of TBI? | •Motor vehicle accidents
•Falls
•Assaults
•Sports and recreational activities
oFootball is biggest cause for boys
oSoccer is biggest cause for girls |
Differentiate between an open vs closed head trauma | •Open: skull fracture or laceration of brain
oUsually more severe
oAssociated w/ more severe contusions
•Closed: no skull fracture or laceration of brain
oLOC doest always occur
oCan occur w/ neck injury
oWorse if theres rotational injury
oNL neuro |
What constitutes secondary damage? | •further cellular damage from the effects of primary injuries. Secondary injuries may develop over a period of hours or days following the initial traumatic assault |
What is DAI and how is it diagnosed and categorized? | -Diffuse axonal injury
•Associated w/ rotational shearing effects
oHard to quantify
oReadily identifiable on CT scan as multiple punctate hemorrhages
•50% of all brain injuries
•Poor outcome
•White matter, corpus callosum & occasionally in the brai |
Coup Injury | •the result of a sudden, violent stop that causes the brain to accelerate forward and hit the side of the skull.
oInjury to the brain occurs on the same side as the impact
**brain is damaged as it rubs against the inner ridges of the skull |
Countrecoup Injury | •occurs when the brain accelerates forward, hits the side of the skull, and then bounces off the other side of the skull
o Injury to brain occurs on opposite side of impact
**brain is damaged as it rubs against the inner ridges of the skull |
What forces can produce a subdural hematoma? | •Tearing of the bridges veins between the brain surface and dural sinus
oAccumulation of blood in the dural space
-If great enough volume, brain cannot resorb the blood and results in a brain occupying lesion
•Falls can cause subdural hematomas |
What is produced when cortical bridging veins are disrupted? | Subdural Hematoma |
What vessels rupture in a subarachnoid hemorrhage? | •Vessels at the base of the brain
oBlood accumulates between the arachnoid layer and the pia layer |
Describe what happens when autoregulation of cerebral circulation is impaired in TBI. | • reduces the ability of injured brain to preserve an adequate blood flow in the face of hypertensive episodes |
What autonomic nervous system changes are related to TBI? | •Vascular changes
•If brain stem involvement: paralysis or death, less severe: changes in regularity of pulse and RR, temp. elevations, BP changes, excessive sweating, salivation, tearing of eyes, sebum secretion (oil on skin/hair) |
Decribe the vascular changes associated with the autonomic nervous system after a TBI | impaired autoregulation of circulation=> increase vascular volume=>acute hydrocephalus=> incr. volume in ventricles puts pressure on brain between ventricles and skull |
What symptoms are related to acceleration -deceleration injuries? | -contusions
-headache
-disability
-death
-decr. attn. span, perception & reasoning
-seizures
-irritability
-loss of consciousness
-stopped breathing (with rotation, brain stem resp. centers) |
What symptoms are indicative of post concussion syndrome? | •Headache
•Nausea
•Fatigue
•Disorientation
•Dizziness
•Personality changes
•Changes in emotional control |
Grade 1 Concussion | transient confusion, no loss of consciousness. Resolution of concussion symptoms or mental status abnormalities occurs in less than 15 mins |
Grade 2 Concussion | transient confusion, no loss of consciousness. Resolution of concussion symptoms or mental status abnormalities occurs in more than 15 mins |
Grade 3 Concussion | any loss of consciousness |
How quickly can axon swelling develop after brain injury? | Within 12 hours of injury. (Wallerian degeneration) |
What neuroanatomical injuries are related to acceleration-deceleration? | •Bruising & bleeding from shear forces, Frontal & Ant. Temporal lobes (hippocampus= memory)
•Focal lesions caused by this type of trauma can affect language as well as difficulties w/ attention span, perception & reasoning
-pt may experience seizures |
A coma lasts no longer than __ ______. | 4 weeks |
What are the various levels of consciousness | Coma
Persistent vegetative state
Vegetative state
Locked-in syndrome |
Coma | lowest level of conciousness, won’t obey commands, no words, won’t open eyes, unresponsive |
Persistent vegetative state | reduced level of consciousness, postcomatose unawareness, characterized by wakeful, reduced responsiveness w/ no evident cerebral cortical fxn. This includes eye opening with sleep-wake cycles and tracking of the eyes, controlled at a subcortical level. |
Vegetative state | preserved arousal mechanisms assoc. w/ a complete lack of self/environmental awareness. Open eyes spontaneously, w/o visual tracking or gaze fixation. No purposeful movement, remains mute. |
Locked-in syndrome | quadriplegia in the setting of preserved awareness and arousal. (injury to ventral pons) Spares vertical eye movements and can be seen w/ disordered breathing patterns assoc. w/ injury to brain stem resp. centers |
What are executive functions? | c• collection of brain processes that are responsible for planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions, and selecting relevant sensory information |
Retrograde | inability to recall events that occurred before trauma. Tends to improve during recovery. Incr. length of coma= Incr. extent of RA. Inability to convert short term to long term. |
Anterograde | inability to form new memories. Common after TBI. Manifests as decr. Attention, inaccurate perception (don’t recognize that they have injury) |
PTA | time lapse between injury and the return of fxnal memory. A type of anterograde amnesia. General state of disorientation. Automatic activities (things they knew how to do before the accident) may improve but no carryover of tasks requiring new learning |
How can pain affect physical recovery after TBI? | -persistent distraction
-decr ability to concentrate
-affect ability to sleep
-emotional rxns (anxiety/depression)
-myofascial pain w/ trigger pts/ stiffness/ weakness
-deep burning pain then persistent, invol, irreg mvmnts of ft
-fibromyalgia
-suf |
Olfactory Nerve damage & TBI | usually temporary damage, well protected |
Optic Nerve damage & TBI | can result in monocular blindness, dialated pupil w/ absent direct pupil response and brisk consensual response to light |
Oculomotor, trochlear, abducens & TBI | maintains gaze stability and scanning |
Trigeminal Nerve damage & TBI | anesthesia of portion of nose, eyebrow, forehead. Sensory deficits may extend to cheek, upper lip, gums, teeth & hard palate, eyelids can be opened easily, absent corneal reflex |
Abducens Nerve damage & TBI | failure of eye to abduct when the head is passively turned away from the side of the lesion, abnormal wandering movements |
Facial Nerve damage & TBI | facial n. palsy, loss of tear production, saliva secretion and taste in ant. 2/3 of tongue, and loss of stapedius m. fxn may be noted. Mm. controlling expressions b/c weak |
Vestibular Nerve damage & TBI | dizziness, vertigo, hearing loss |
Glosspharyngeal, vagus, spinal accessory and hypoglossal damage & TBI | cardiac irregularities, excessive salivation, loss of sensation and gag reflex of palate, loss of taste on post. 1/3 of tongue, hoarse voice, dysphagia and deviation of tongue to side of the lesion |
What is HO and what joints are at greatest risk in the TBI population? | •Heterotopic ossification- found in proximal & intermediate joints (i.e. Hip and elbow)
oCalcium metabolism disrupted, producing bone in a muscle secondary to trauma.
oLack of ROM, heat, bony endfeel
ocan give meds to stop osteoblasts or surgery remo |
What signs assist in localizing brainstem damage and determining the depth of coma? | Reflexes: Pupils, oculocephalic, vestibule-oculocephalic, corneal, cough, gag |