Exam 2 Flashcards
Peak ages for TBI?
24-35 is greatest with smaller peaks in infants and eldery
Who is at greatest risk for TBI?
Males (2x incidence, 4x mortality)
Disadvantaged populations in cities
What are the greatest causes of concussion?
Falls 35.2%, MVA 17.3%
What percentage of acute brain injury hospitalizations are concussion?
80%
Is LOC necessary for concussion?
NO
Large Vessel Stroke
Affects multiple systems (motor, sensory, etc.) and is still present at 24 hours
Small Vessel Stroke
Isolated defect still present at 24 hours
Atypical Causes of Stroke
Vasculopathies
Hematologic
Inflammatory
Vasculopathies causing stroke
FMD (Women, 30-40, medial hypertrophy)
Moya-Moya (Middle cerebral occlusion, EBV)
Dissection
Hematologic causes of stroke
Genetic Deficiencies Malignancy Hyperviscosity Oral Contraceptives Sickle Cell does NOT increase risk
Inflammatory causes of stroke
vasculitis, venous infarction, vasospasm, migraine
Causes of delirium (5)
Polypharmacy, toxins, metabolic disorders, infectious/inflammatory causes, structural lesions
Complete mental status exam in delirious patient?
No, too confused and inattentive
Treatment of delirium
Find and treat underlying cause
in the mean time, provide environmental manipulations, get good sleep, and give calming medications
Alzheimer’s Atrophy Location
Cerebral atrophy, autopsy needed for official Dx even though clinical sings are 90% sensitive
Genetics associated w/ late onset Alzheimer’s
Epsilon-4 gene of APOE
Do we test for AD genes?
No
Which transmitter is missing in AD?
Acetylcholine
What do we give for AD?
Cholinesterase inhibitors and Memantine (NMDA antagonist)
Cortical Dementias (2)
AD and FTD
FTD vs AD?
FTD is behavioral, memory is normal. Hippocampus is spared early.
Subcortical Dementias (2)
PD and Huntington’s
Where are Lewy bodies? What are they made of?
Sustantia Nigra, made of alpha-synuclein
Which NT is deficient in Parkinson’s?
Dopamine
What percentage of PD patients get dementia?
80%
Lewy Body Dementia vs. PD?
Psychotic symptoms (hallucinations, confusion)
Atrophy in Huntington’s
Caudate
White matter dementias (2)
Biswanger’s Disease and Normal Pressure Hydrocephalus
Which dementia is reversible?
Normal Pressure Hydrocephalus
Normal Pressure Hydrocephalus Symptoms
Incontinence, high ICP at night
Treatment for NPH?
Ventriculostomy
2 Fundamentals of Neurodegenerative Disorders
Progressive loss of select neuron populations
Protein conformation and metabolism are usually involved
Prion misfolding involves
Alpha helix to beta sheet (insoluble)
Incorrect ways to classify NDDs?
Physical symptoms: movement, dementia, neuromuscular disorders
Inherited vs. sporadic
Can determination of abnormal protein diagnose the NDD?
Not always, many proteins are shared among diseases.
Where in the brain are the changes associated w/ AD?
Cortex and Hippocampus
Where do pediatric tumors occur?
2/3 infratentorial
How do brain tumors kill patients?
No metastasis, but vital tissue destruction or mass effect are deadly
Do all tumors progress I to IV?
No. Some don’t progress (Pilocytic Astrocytoma) and others are de novo higher grade
Most common tumor in children?
Pilocytic Astrocytoma, infratentorial
Mutations common in astrocytic pilocytomas?
BRAF fusions, favorable
Gangliomas usually occur where?
Temporal lobe in young adults
Ganglioma Appearance
Cystic, likely calcified
Mutations in gangliomas
BRAF point mutations
Choroid plexus papilloma locations
Lateral ventricles in kids, 4th ventricle in adults
Astrocytoma Genetic Signature
IDH mutated, ATRX/P53 mutated, no LOH1p,19q
Oliogodendroglioma Genetic Signature
IDH mutated, no ATRX/P53 mutation, have LOH1p,19q
What good is genetic information?
Prognostic information, eventually treatment
Diffuse Astrocytoma age and location
30s-50s, in cerebral hemispheres
Surgery for Diffuse Astros? Necrosis in Diffuse Astros?
Yes, only for debulking
No
Diffuse Astrocytoma or Oligodendroglioma better prognosis?
Oligodendroglioma
Ependyoma age and location
by 20 years, usually in 4th ventricle but lateral ventricles have better prognosis
Is anaplastic astro or oligo enhancing on MRI?
Anaplastic Oligo
Diffuse vs. Anaplastic distinctions
Mitotic Activity and MIB-1 labeling intensity
Are glioblastomas usually de novo or progressive?
De novo
Peak incidence of Medulloblastoma and location
3-8 years, cerebellum
Where do medulloblastomas come from?
External Granule Layer, SHH abnormality
3 types of MS
Relapsing Remitting (85%) Primary Progressive Secondary Progressive (50% of RRs around 45 years)
MS Epidemiology
2/3 Women
75% present 15-45
1/500 Coloradans, Wyoming Residents
Genetics of MS?
100 linked genes, HLADR2, IL2/7 have some connection
MS Lesion progression
Inflammatory then scar-like on scans
MS Pathogenesis
T cell activation, MMP activation to make BBB leaky, Immune cells enter CNS, Cytokines increase BBB damage, myelin damage occurs
Most important prognostic factor in MS?
Atrophy
Can you see axonal injury on scans?
No, look for small hemorrhagic lesions or stain for hemosiderin
Treatments for concussion
Recovery Time
Rest the brain!
Typically 7-10 days
Methanol Toxicity
Putamen Necrosis
Ethanol Acute and Chronic CNS effects
Acute: cerebral edema
Chronic: cerebellar atrophy (superior vermis) with gliosis, cerebral atrophy initially in white matter
Wernicke’s Encephalopathy/B1 Thiamine Deficinecy
Alcoholics and Hyperemesis
Ataxia, Ophthalmoplegia, Confusion
Mamillary body degeneration!
Also hypothalamus, thalamus (confusion), PAG (occulomotor), 4th ventricle (ataxia)
Central Pontine Myelinosis
Sustained hyponatremia w/ rapid replacement
Degeneration in Pons but also grey-white admixture areas
Afferent Sensory Fiber Types
A-alpha = muscle proprioception A-beta = skin enteroception A-delta = sharp pain, cold temp C = burning pain, warm temp
Pressure Effects on Sensory Afferents
Largest first (most metabolically active), leaving C fibers for last
Electrical Stimulation Effects on Sensory Afferents
Same as pressure, smallest fibers are last to activate as shock is increased.
Which fibers have polymodal receptors?
C fibers
4 Nociceptor Activators
Bradykinin, Acid, Serotonin, POtassium
5 Nociceptor Sensitizers
Prostaglandins, Substance P, Serotonin, ATP, Acetylcholine
Substance P
Released with persistent C fiber firing, binds neurokinin1 receptor which closes K channels which second order pain afferents
Tripartite Structure of Local Anesthetics
Lipophilic Ring: membrane crossing
Ester/Amide Intermediate Alkyl Chain: determines onset, duration, and potency.
Tertiary Amine: protonation status determines membrane crossing and action w/in cell
Amide v Ester
Ester: metabolized in plasma by esteraes, making them less potent, shorter acting, and longer time to onset
Amide: high protein binding to alpha1-acid glycoprotein increases duration, only metabolized in liver.
LA potency determined by
Lipid Solubility
LA Duration determined by
protein binding capacity
LA Speed of Onset determined by
inversely to pKa
Allergic Reaction to LAs caused by
metabolite PABA, very very rare
Paresthesia
Abnormal sensation (burning, pricking, tingling, numbness)
Dyesthesia
Impairment of sensation short of analgesia
Paresis
muscle weakness caused by nerve damage, short of paralysis
Dermatome
Cutaneous area innervated by an individual sensory root
Myotome
muscles innervated by an individual motor root
Radiculopathy
sensory and/or motor dysfunction due to nerve root injury
Myelopathy
spinal cord dysfunction disorder
