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Pathology F10
TBI
| 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 |
Created by:
CWestrick
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