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Pathology F10


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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