Week 3 & 4 Flashcards
glasgow coma score
Eye opening, verbal response, motor response; total score is 3-15
• Mild – 13-15 with negative CT/MRI findings
• Moderate – 9-12 or 13-15 with positive radiological findings (i.e. fracture)
• Severe – 3-8
1 mmHg PaCO2 increase CBF by ___
3%
1*C rise in temp increases CMRO2 (cerebral metabolic rate of O2) by ___
7%
does concussion cause structural abnormality
no
3 signs of basilar skull fracture
Raccoon’s eye – frontal fossa
Hemotympanum (blood in ear) – middle fossa
Battle’s sign (behind ear) – posterior fossa
subdural hematoma location
- Between arachnoid and dura mater; torn bridging veins;
* Needs urgent intervention
epidural hematoma location
focal injury of meningeal artery, often seen with skull fracture
above what ICP do you start treatment for cerebral edema
20 mmhg
CPP =
MAP - ICP
cushing triad
increased BP, decrease HR, decreased RR
uncal cerebral herniation
What is it
What does it cause
side of brain down into cerebellar area = CN3 palsy, contralateral motor deficit
subfalcine cerebral herniation
What is it
What does it cause
to other hemisphere – problems with ACA causing contralateral leg paresis
transcalvarial cerebral herniation
What is it
What does it cause
outside, skull fracture
usually lethal
diffuse axonal injury
result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults, often with loss of consciousness
risk factors for atheroma
HTN
smoking
diabetes
pathophysiology of small vessel disease
lipohyalinosis or microatheroma due to HTN
2 types of stroke
cerebral infarction / ischemic
hemorrhagic
hypotensive watershed stroke
period of hypotension (i.e. due to cardiac arrest) can lead to ischemia in two areas: between the middle and posterior cerebral arteries
intracranial venous thrombosis
blood clot in vein, from surgery, infection, tumor; results headaches, seizures, confusion, raised ICP
MCA stroke symptoms
arm and face weakness and sensory loss
language disorder if on dominant side
contralateral hemianopia
ACA stroke symptoms
leg predominant weakness
PCA stroke symptoms
vision - contralateral homonymous hemianopia
thalamic syndrome
locked in syndrome if basilar artery
lacunar stroke (5 symptoms)
pure motor hemiparesis ataxic hemiparesis clumsy hand pure sensory sensorimotor
pure motor hemiparesis
internal capsule lesion
face, arm and leg weakness
ataxic hemiparesis
motor hemiparesis with cerebellar ataxia on that side, could be lesion in posterior internal capsule, midbrain or pons
dysarthria clumsy hand
dysarthria with tongue and face weakness with hand clumsiness on the same side, basilar pons lesion
pure sensory
hemisensory loss of superficial sensation, usually from thalamic lesions
contraindications for thrombolysis in stroke
onset > 4.5 hours no motor deficit PMH of epilepsy or ICH recent LP, surgery or pregnancy BP > 185/110
what is the most common COD following stroke
ischemic heart disease
anterior circulation TIA
o Amaurosis fugax (fleeting blindness) – in one eye ‘like a shutter coming down’
o Aphasia, or other language problems such as dyslexia or dysgraphia
posterior circulation TIA
o Homonymous visual field loss (same side of both eyes)
o Brainstem symptoms: vertigo, diplopia, dysphagia
o Bilateral weakness or sensory loss
Subarachnoid Hemorrhage symptoms
o Sudden severe headache - ‘as if hit by a bat’
o Transient loss of consciousness and vomiting
o Neck stiffness
Subarachnoid Hemorrhage pathophysiology
rupture of an intracranial aneurysm into subarachnoid space that is usually full of CSF
Epidural hematoma shape on imaging
convex bulge
Subdural Hematoma on imagine
crescent shape that follows bumpy contours
rule of pupil
if pupil is dilated –> means aneurysm rupture
most common etiology of hemorrhage is _____ and occurs in _______
HTN
deep cerebral nuclei
pale infarct usually occurs due to _____
arterial occlusion
hemorrhagic infarct usually occurs due to ____
venous occlusion
hemorrhagic transformation of pale infarct occurs due to ____
reperfusion injury
timing of neuronal ischemia
what occurs 12-48 hours?
eosinophilic swelling
red neurons
timing of neuronal ischemia
what occurs 24-72 hours?
neutrophilic infiltate
timing of neuronal ischemia
what occurs 3-5 days
macrophages infiltrate
timing of neuronal ischemia
what occurs 1-2 weeks?
gliosis
timing of neuronal ischemia
what occurs after 2 weeks?
glial scarring
cerebral amyloid angiopathy
amyloid positive multiple lobar parenchymal hemorrhages in elderly patient
object relations theory
we tend to re-enact these internalized relationships later in life, especially those relationship patterns that are conflicted or have repressed, unresolved painful feelings
which brain structure controls inappropriate and impulse aggression from subcortical brain
frontal cortex
what brain structure ides inhibitory control over the amygdala
prefrontal cortex
which neurotransmitter facilitates aggression
dopamine
which neurotransmitters inhibit aggression
serotonin and epinephrine
negative cognitive triad
- Negative self-concept
- Negative view of the world
- Negative view of the future
syntonic
something is felt to be acceptable, harmonious, and consistent with one’s self-concept
alloplastic
coping with conflict by trying to change environment and others instead of one’s self
what diseases are in cluster A and what is the typical descriptor
paranoid
schizoid
schizotypal
odd or eccentric
what diseases are in cluster B and what is the typical descriptor
antisocial
borderline
histrionic
narcissistic
dramatic, emotional, erratic
what diseases are in cluster C and what is the typical descriptor
avoidant
dependent
OCPD
anxious or fearful
examples of mature defense mechanisms (5)
Altruism, Humor, Sublimation, Suppression, Anticipation
examples of immature defense mechanisms (4)
Acting Out, Somatization, Passive-Aggressive Behavior, Regression
disruptive mood dysregulation criteria
- 3 or more symptoms per week of temper/mood disorders
- occur in at least 2 of 3 settings (i.e., home, school, with peers), and are present for at least 12 months (cannot go 3 or more consecutive months without the symptoms)
- Age of onset <10 yrs, but dx should not be made for the first time <6 or >18
major depressive disorder criteria
5 or more symptoms in 2 weeks
depressed mood, loss of interest, change in weight, sleep disturbance, loss of energy, worthless, guilt, suicide thoughts
dysthymia criteria
persistent depressive disorder
depressed mood most of the time for 2 years
adjustment disorder criteria
emotional/behavioral symptoms in response to stressor, within 3 months butnot more than 6 months after stressor
bipolar 1 criteria
at least 1 manic episode of abnormally elevated or irritable mood, increase in goal-directed activity, last at least 1 week and includes 3 or more DIGFAST
bipolar 2 criteria
at least 1 hypomanic episode and 1 MDD episode
hypomanic - shorter (4 days), not cause decrease in function
cyclothymic disorder
chronic fluctuating mood disturbance that has occurred for at least 2 years
biochemical etiologies of bipolar
increased dopamine
amygdala changes
family history
predictors that mood swings may be bipolar
early age of onset
depression before age 25
parental bipolar before age 21
hypomania on antidepressants
what should you think of elderly person with first time onset of bipolar
personality disorder
lower motor neuron injury
flaccid paralysis, decreased reflexes, absent Babinski, atrophic with fasciculations
upper motor neuron injury
spastic paralysis, increased reflexes, present Babinski, non-atrophic without fasciculations
kennedy’s disease
X linked spinobulbar muscular atrophy
CAG repeat expansion in exon 1 of androgen receptor
Mid-life progressive weakness of limb and bulbar muscles with no UMN signs
werdnig-hoffman disease
spinal muscular atrophy
Mutation in SMN1 gene on chromosome 5
LMN signs only (Type 0 – fatal in utero, Type 1 – severe, Type 2-4 mild)
acute polyneuropathy
- Stocking and glove distribution of sensory loss
- Balance difficulties
- Atrophy of intrinsic hand and foot muscles
guillian barre
(acute inflammatory demyelinating polyneuropathy)
Motor ascending weakness, autonomic disturbance, decreased reflexes
Demyelinating with perivascular lymphocyte infiltrate
Preceding infection with campylobacter, CMV, EBV, mycoplasma
Chronic inflammatory demyelinating polyneuropathy
Chronic, multiphasic illness, often with at least partial recovery between bouts
Steroids do work
porphyria
- Related to hemoglobin synthesis, HMBS enzyme
- Motor (arm), autonomic and minimal sensory loss
- Axonal degeneration
diphtheria
- Cranial nerve onset that is mixed motor and sensory
- Demyelinating disorder without inflammation; from c. diphtheria exotoxin
myasthenia gravis antibodies
anti-Ach, anti-MuSK
myasthenia gravis symptoms
- Fatigue, bulbar weakness (dysarthria, dysphagia, ptosis), respiratory depression
- Decrease in nerve response to stimulation over time
lambert-eaton syndrome
- Antibodies to the calcium channels, sometimes seen as a remote effect of cancer
- Strength increased with effort; usually hip girdle weakness
Duchenne’s muscular dystrophy
Severe, childhood onset
X linked recessive mutation in dystrophin = absent dystrophin protein
- Proximal muscle weakness before distal
- Toe walking, falls, lumbar hyperlordosis, Gowers sign (uses arms to stand)
- Atrophy, contractures, respiratory disorders
Becker’s muscular dystrophy
- Like Duchenne’s but more mild, longer life span
- Still partially functioning dystrophin (10-40%)
- Progressive muscle weakness starting in hips, pelvis and shoulders
Myotonic muscular dystrophy symptoms
adult onset
- Hatchett face, ptosis, thin, frontal blading
- Distal weakness worse than proximal
- Dysphagia, respiratory problems, myotonia
Myotonic muscular dystrophy genetics
AD, type 1 CTG expansion I myotonin PK on Chr 19; type 2 CCTG repeat
“anticipation” due to CTG repeat in CNBP
______ neuropathy shows a reduction in conduction velocity in electrophysiology
Demyelinating
______ neuropathy shows a reduction in amplitude in electrophysiology
Axonal
Parkinson’s disease symptoms
hypokinetic, resting tremor, bradykinesia, muscular rigidity (increased muscle tone), and postural instability (imbalance)
Parkinson’s disease deposits
Lewy bodies
deposits of α-synuclein in substantia nigra of basal ganglia
Huntington’s disease symptoms
hyperkinetic, rapid jerks and twitches, chorea, athetosis, dementia that can become very severe
Huntington’s disease genetics
AD Huntington gene (Htt) with CAG expansion repeat
Fronto-temporal dementia
Atrophy of frontal and temporal lobes, loss of insight, judgment and social skills
Behavioral changes, language disturbance, movement disorders
Tau inclusions, TDP-43 inclusions, FUS depositions, progranulin
Lewy body disease
dementia and parkinsonian symptoms, hallucinations, delusions, depression, apathy, syncope, falls, Lewy bodies (a-synuclein) low dopamine transporter uptake in basal ganglia on PET scan
Creutzfeldt-Jacob Disease
Caused by prion, is a transmissible spongiform (lots of vacuoles) encephalopathy -> can cause dementia
Dementia, myoclonus, involuntary movements, psychosis, memory problems, speech loss
