Brain Injury Lecture Flashcards
what are some common complications associated with BI? (7)
- raised ICP
- heterotopic ossification
- decubiti
- DVT
- autonomic dysfunction
- infections and pulmonary problems
- amnesia
what is heterotopic ossification?
formation of bone in abnormal anatomical locations
what percentage of patients with BI or SCI develop HO?
5-20%
is it more common in males or females?
males > females
S/S of HO
- loss of ROM (common in hip)
- swelling
- heat
- erythema
- non-septic fever
what should be avoided with HO?
vigorous stretching
what is retrograde amnesia?
partial or total loss of the ability to recall events that have occurred DURING THE PERIOD IMMEDIATELY PRECEDING brain injury
what is post-traumatic Amnesia?
time lapse between ACCIDENT and the point at which the FUNCTIONS CONCERNED WITH MEMORY ARE RESTORED
what is anterograde amnesia?
decreased attention or inaccurate perception; inability to DEVELOP ONGOING SHORT TERM MEMORY (new memories after the BI)
what are the different presentations of amnesia?
- physical
- cognitive
- behavioral
- medical involvement
what is “comatose”
unconscious and unresponsive
what is “stuporous”
near unconscious with apparent mental inactivity and reduced ability to respond to stimulation
what is “obtunded”
opens their eyes; responds slowing to questions, somewhat confused, decreased interest in environment
what is “lethargic”
dull, sluggish, and appears half asleep
what is “alert”
vigilantly attentive
what is the primary predictor of outcomes?
length of coma
In relation to coma, what is the rancho level?
1
In relation to coma, what is the level of arousal?
eyes do not open
In relation to coma, what is the level of awareness of auditory/visual stimuli?
None
In relation to coma, what is the level of communication and emotion?
none
In relation to coma, what is the level of motor response?
no purposeful movement
in relation to vegetative state, what is the rancho level?
1 or 2
in relation to vegetative state, what is the level of arousal?
eyes open spontaneously, sleep-wake cycles resumes, and arousal sluggish and poorly sustained
in relation to vegetative state, what is the awareness of auditory/visual stimuli?
may move eyes to person/objects, may orient to sound
in relation to vegetative state,, what is the level of communication and emotion?
may moan, make sounds; cry/smile without apparent cause
in relation to vegetative state, what is the level of motor response?
withdrawals from noxious stimuli; non-purposeful repetitive movement
In relation to minimally conscious state, what is the rancho level?
2 or 3
In relation to minimally conscious state, what is the level of arousal?
eyes open spontaneously, normal to abnormal sleep wake cycle, and arousal obtunded to normal
In relation to minimally conscious state, what is the level of awareness of auditory/visual stimuli?
tracks objects; localizes sound
In relation to minimally conscious state, what is the level of communication and emotion?
communication ability; inconsistent - yes/no, gestures, basic emotions
In relation to minimally conscious state, what is the level of motor response?
localizes noxious stimuli, reaches for objects, automatic behaviors
in relation to confusional state, what is the rancho level?
4, 5, or 6
in relation to confusional state, what is the level of arousal?
fluctuation in level of responsiveness, may be excessively drowsy
in relation to confusional state,, what is the level of awareness of auditory/visual stimuli?
response to external stimuli may be accentuated
in relation to confusional state, what is the level of communication and emotion?
able to communicate but disoriented; impaired attention and memory
in relation to confusional state, what is the level of motor response?
purposeful motor responses
how common is dizziness associated with TBI?
15-78%
what percentage of patients experienced abnormal vestibular testing?
32-61%
what percentage of patient with post-traumatic dizziness showed at least one vestibular deficit?
88%
what percentage of patients with post-traumatic dizziness received a diagnosis of BPPV?
61%
what are some of the causes of dizziness associated with TBI?
- lesions of the peripheral vestibular system
- lesions of the central vestibular system
- non-vestibular causes
- conditions unrelated to trauma
what are some lesions of the peripheral vestibular system?
- BPPV
- perilymphatic fistula
- labyrinthine concussion
what are some lesions of the central vestibular system?
- brainstem concussion/ post-concussive syndrome
2. cerebellar contusion
what are some non-vestibular causes?
- cervicogenic dizziness
2. migraine
what are some conditions unrelated to trauma?
- prior history of migraine
- CNS disorders
- prior compensated peripheral vestibular lesion
why are we concerned about dizziness after TBI?
- underlying cause of TBI?
- complicate rehab for the sequelae of TBI
- mimic cognitive impairments seen with TBI
- cognitive impairments due to TBI may complicate vestibular rehab
special considerations: Musculoskeletal
limit types of exercises a patient can perform
special considerations: cognitive impairments
memory problems may influence follow through of exercises; confusion/decreased processing may increase space and motion discomfort = overwhelming to pt
special considerations: strategies
- reduce confusion
- improve motivation
- encourage consistency with performance
what are two “improvements” you can make with patients post TBI having dizziness
- improve attention
2. improve problem solving ability
what kind of learning should you encourage
declarative and procedural
what level of arousal would you like for these patients?
moderate to optimize learning
is progress slower for patients who have cognitive impairments?
yes
what are some s/s of TBI?
HA, fatigue/lack of energy, disruption of sleep patterns, dizziness, increase sensitivity to noise/light/distractions
what are examples of local brain damage?
contusions, lacerations, hematomas, and herniations
what are examples of diffuse brain damage?
axonal shearing, small hemorrhages
what are examples of secondary brain damage?
edema, hypoxia, hypotension, infection, salt/water imbalance, concussions or post traumatic epilepsy
what are examples of scalp injuries?
abrasion/contusion, hematoma/herniation, and scalp laceration
what are examples of skull fractures?
linear, comminuted, and compound
what are examples of intracranial injuries?
concussion, epidural/subdural hematomas, and ICP monitoring
what are examples of traumatic cerebro-vascular lesion?
aneurysms, and carotid-cavernous fistulas
what are examples of CN pathologies?
CN 2,3,6,7,8 commonly injured
how is the prognosis of the recovery stages measured?
- Glasgow Coma Scale
2. Rancho Los Amigos Cognitive Scale
Brain infection can be from: (4)
- bacterial
- parasitic
- fungal
- viral
All of the 4 microorganisms do what?
attack the CNS
how do the microorganisms get to the brain?
- most hematogenously (through blood)
2. through PNS (rabies, herpes)
How are brain infections categorized?
by location and cause
what are the 3 common locations infections are found within the brain?
- abscesses (enclosed infections)
- meningitis (infection of meninges)
- encephalitis (inflammation of brain/SC)
In relation to an abscess, how do organisms reach brain tissue?
staph or pseudomonas – secondary to inflammatory process elsewhere - lungs, heart, sinuses, ear mastoiditis
what part of the brain tissue does an abscess involve?
white matter, most often reaches frontal and parietal lobes through superior sagittal sinus
An abscess is a ____________ infections that ______________ _________.
generalized; increased ICP
Due to the increased ICP, what are some s/s of an abscess?
HA, convulsions, hemiparesis, incoordination, and ataxia if the cerebellum is involved
what are the 4 kinds of meningitis?
- leptomeninges
- bacterial
- viral
- chronic
what does leptomeninges involve?
pia + arachnoid mater (dura mater usually doesn’t get infected)
what is the process of leptomeninges?
infection spread through CSF with inflammatory process of pia mater, arachnoid mater, and superificial CNS tissues - includes SAS
how does infection spread with leptomeninges?
organisms cross blood brain barriers and blood CSF barriers; or with trauma to torn meninges from a contaminated wound
why is CSF an ideal growth medium
contains no antibodies and few cells
what is leptomeningitis usually classified as?
bacterial or viral meningitis
For bacterial meningitis, what are the age specific agents?
neonate - e.coli
childhood - h influenza
adolescent - n meningitides
adult - s pneumoniae
what is the process of bacterial meningitis?
inflamed congested pia-arachnoid mater with PMN exudate - obstructs ventricular foramina – increased ICP
what is a symptom of bacterial meningitis?
decreased blood sugar levels
what are some s/s of bacterial meningitis?
HA, vomiting, fever, altered consciousness, convulsions, irritability, and nuchal rigidity
what is a test to confirm nuchal rigidity (can’t move the neck)
+ Brudzinski Neck Sign (neck flexion causes hip/knee flexion
if bacterial meningitis is left untreated, what happens
death
what are the s/s of viral (aseptic) meningitis?
similar to bacterial but not life-threatening
what is an adjective used to describe viral meningitis?
fulminating (occurs suddenly)
who does viral meningitis affect?
children and young adults
what are the blood sugar levels like for viral meningitis?
normal
what is the process of viral meningitis?
viral contamination of CSF with an increase in lymphocytes (acute viral lymphocytic meningitis)
what are some agents for viral meningitis?
mumps, ECHO, lymphocytic choriomeningitis, and coxsackie B
what are some agents for chronic meningitis?
mycobacterium tuberculosis (lung TB), preponema pallidum (syphillis)
what is the process of chronic meningitis?
gelatinous exudate in meninges, increased lymphocytes/plasma cells/macrophages/fibroblasts
what happens if chronic meningitis is in the SAS
hydrocephalus
what are some s/s of hydrocephalus?
gait disturbances, incontinence, altered mental status
what are some s/s of chronic meningitis?
HA, vomiting, mental confusion, weight loss, fatigue, night sweats, chest pain, malaise
what is the medical management of meningitis?
antimicrobial antibiotics for bacteria; treat viral infections symptomatically - antivirals if caught soon
what is the process of encephalitis?
viral invasion of brain ans SC cells (neurons and glia)
what does encephalitis cause?
edema and inflammation of the brain/SC destroying white matter
what does ICP lead to?
transtentorial herniation (tentorium spearates cortex from cerebellum)
S/S of encephalitis
HA, fever, nuchal rigidity, vomiting, malaise – coma, CN palsies (III), hemiplegia
what does encephalitis stand for?
inflammation of the brain
what does encephalomeningitis mean?
inflammation of the brain and SC
what does encephalomyeloneuropathy?
inflammation of the brain, SC, and PNS
what does acute viral encephalisis affect?
frontal/temporal lobe gray matter
what is the most fatal type of encephalitis?
acute viral encephalitis
what is acute viral encephalitis a combination of?
herpes simplex I and II, CNS primary infection
what is parainfectious encephalitis a combination of?
rubella measles, paramyxovirus mumps, and varicella zoster chicken pox
what is acute toxic encephalitis?
arbovirus arthropod-borne systemic infection
what diseases are associated with acute toxic encephalitis?
lyme disease, west nile virus
what is the progress of the slow virus encephalitis?
incubation periods, fatal within months - progressive dementia
what does slow virus encephalitis look like in the brain?
“spongiform” bubbles and holes in brain cortex, resembles degenerative disease
what are the s/s of the slow virus encephalitis?
personality abnormalities, visual and spatial orientation/coordiation problems – leads to dementia with myoclonus
what is creutzfeldt Jacob Disease caused by?
prion
what is the etiology of CJD
familial, sporadic, and iatrogenic
does CJD show symptoms immediately?
no, it takes decades for the s/s to show
what are the s/s in the beginning for CJD
altered mental status, gait disturbances, no safety awareness, poor behavioral reactions, no memory
when should CJD be considered?
when patient develops rapid dementia and myoclonus
patients with CJD die when?
within 6 months-1 year
