Chapter 22 Flashcards
what happens to the soma when there is reversible neuronal damage? irreversible?
reversible: somal swelling
irreversible: somal shrinkage
what happens to the Nissl body when there is reversible neuronal damage? irreversible?
reversible: Nissl body displacement
irreversible: loss of Nissl body
red neuron
dead neuron
shrunken soma, cerebral edema, loss of nucleolus & Nissl body
occurs bc of acute-hypoxic/ischemic injury
what happens when Astrocytes are injured
hypertrophy & hyperplasia
enlarged nucleus, eosinophilic
what happens when oligodendrocytes are injured
white matter damage = nuclear swelling
happens in acquired demyelinating disorders & leukodystrophies
enlarged nucleus
what happens when microglia are injured
proliferate & enlarge
what happens when ependymal cells are injured
ependymal granulations–> infections (CMV)
may involve chorioid plexus bc ependymal cells line ventricles & spinal cord
when do intracellular inclusions occur?
viral infections (rabies = Negri body, CMV = owl's eyes) parkinson disease = Lewy body Alzheimers disease = neurofibrillary tangles & beta-amyloid plaques; tau proteins
cerebral edema (general types)
vasogenic- BBB disruption, extracellular edema
cytotoxic- glial membrane injury, intracellular edema
hydrocephalus
• MC because of disturbed flow/resorption
• 2 years = ↑ ICP, ventricular enlargement
• Hydrocephalus ex vacuo : compensatory: infarct, neurodegeneration
• congenital
• 50% idiopathic
ventriculoatrial shunt
Untreated: lethal tonsillar herniation, respiratory arrest
Brain herniation (general)
• ↑ ICP
• Initially: vessel compression & CSF displacement
• Later: cerebrum shifts (herniation)
o ↓ blood supply = infarction; injury = swelling Dangerous positive feedback loop!
Brain herniation types
- subfalcine/cingulate (MC)– abnormal posturing, coma
- transtentorial/uncinated-CN III (blown pupil); hemiparesis & brainstem compression Duret hemorrhage (flame-shaped hemorrhage)
- Tonsillar–cardiorespiratory arrest
Arnold-Chiari malformations
herniation of cerebellar tonsils
Type I (MC)–adults
Type II–infants, more severe, misshapen midline cerebellum
cerebrovascular disease
3rd leading cause of mortality in US
MC cause of neurologic morbidity
Stroke = infarction
TIA = No infarction, temporary
ischemia cell response
neutrophils (12-48 hrs) –>nuclear fragmentation (48 hrs-2 weeks) –>Macrophages & gliosis (months to years, cavitation)
respirator brain
autolysis of neurons caused by mechanical ventilation
Focal cerebral ischemia
arterial occlusion = localized ischemia
sustained = infarction
collateral flow limit injury = circle of willis (deep tissues have limited collateral flow)
Emboli (MC): cardiac mural thrombi
MC cause of vessel wall injury
HTN
primary brain parenchymal hemorrhage
spontaneous
HTN (MC)
“worst HA i’ve ever had”
subarachnoid hemorrhage
ruptured saccular/berry aneurysm
MC in anterior circulation & branch points
Arteriovenous malformation
- Tangle of arteries & veins
- MC cerebrovascular malformations
- Males
- Age 10-30
Hypertensive cerebrovascular disease
- Massive parenchymal hemorrhage
- Lacunar infarct: single artery occlusion; silent devastating
- Slit hemorrhage: ruptured small cerebral vessel, ‘slit-like cavity’ remains
- Acute hypertensive encephalopathy: global cerebral dysfxn; HA, confusion, vomiting, convulsions, coma
polyarteritis nodosa
- Systemic autoimmune vasculitis
- Fibrinoid necrosis
- Small cerebral arteries & heart
1⁰ angiitis of the CNS
- Chronic inflammation
- Multiple parenchymal & subarachnoid vessels
- Only Brain & Spinal cord
- Idiopathic, Males
general CNS trauma
MALES
• Silent=frontal
• disabling=cord
• fatal=brainstem
• Damage to parenchyma &/or cerebral vessels
• Assess: ABCD (airway, breathing, circulation, disability)
Contusion
- Rapid displacement
- Impact site = coup injury
- Opposite impact site = contrecoup injury
- Gyri susceptible, frontal & temporal lobes
Laceration
• Tearing of cerebral parenchyma
Diffuse axonal injury (DAI)
SERIOUS
angular acceleration, shaking
• may NOT involve physical impact
• causes diffuse WHITE matter/axonal damage
• MC near lateral ventricles & brain stem
severe edema
• Cause of 50% post-traumatic comas
concussion
reversible
absence of contusion
secondary to trauma
• Standard neuroimaging studies are NORMAL!! =CT CANNOT confirm presence of concussion!
what does a concussion look like on a CT?
IT LOOKS LIKE NOTHING
**bonus: What does osteoporosis look like on x-ray?
IT LOOKS LIKE NOTHING; unless 30-40% already gone
Epidural hematoma
ARTERY
lucid during bleed
emergency
MC middle meningeal artery
subdural hematoma
VEINS
shaken baby
infants & geriatrics
MC self limited
MC CNS malformation
Neural tube defects
spina bifida occulta
Neural tube defect
bony defect
asymptomatic
myelomeningocele
Neural tube defect
extension of CNS thru lumbosacral vertebral defect
urinary incontinence
anencephaly
Neural tube defect
absence of brain
encephalocele
Neural tube defect
CNS diverticulum thru cranium
hydromyelia
spinal cord abnormality
cavity
connected to 4th ventricle
syringomyelia
spinal cord abnormality
syrinx
cyst w/in cord
adults
- Intraparenchymal hemorrhage
prematurity,
near ventricles,
may cause hydrocephalus
Infarct (perinatal brain injury)
supratentorial white matter,
chalky plaques,
possible cyst
cerebral palsy
perinatal brain injury
NON-progressive
motor neuron defect
how are infections of NS acquired MC?
hematogenous
epidural abscess
‘makes the cavity’
cord compression = emergency
subdural empyema
‘fills an already made cavity with pus’
infxn of skull/sinus = subdural space = emergency
meningitis types (list)
acute pyogenic
aseptic
chronic: insidious onset
acute meningitis
HA, nuchal rigidity, photophobia
CSF: ↑pressure, ↑neutrophils, ↑proteins (exudate), ↓ glucose, bacterial culture
fatal if untreated
aseptic meningitis
• nuchal rigidity, pyrexia, ↓ consciousness, cerebral edema –> self-limiting,
CSF: ↑ lymphocytes
Chronic: insidious onset meningitis
tuberculous: CSF = moderate ↑ WBC’s & ↑ proteins
Spirochetal: 3⁰ syphilis or Lyme disease
Parenchymal infections
- bacterial abscess: localized, liquefactive necrosis
- viral encephalitis: diffuse, assoc w meningitis, poliovirus, varicella-zoster virus
- fungal: mixed granulomas, meningitis, MC among immunosuppressed
Multiple Sclerosis
- MC disorder of myelin
- Episodic, ‘relapsing-remitting’, incomplete recovery
- White matter lesions (plaques)
- Risks: young adults, females, family history
Thiamine disorders
- Wernicke-Korsakoff syndrome
* Beriberi: LE paralysis, paresthesia, nystagmus, pain
Cobalamin disorder
demyelination
hypoglycemia
mimics global hypoxia; hippocampus
hyperglycemia
uncrontrolled DM
patterns of neuronal loss (dementia)
o Cortex = memory, language, insight/planning
o Cerebellum = ataxia
o Motor neurons = weakness
alzheimer disease
• MC cause of dementia in elderly • Brain: β-amyloid plaques o Neurotoxic, Tau proteins insidious/progressive lethal infection: pneumonia • 10% genetic down syndrome, early onset
Parkinson Disease
- Parkinsonism tremor,
- Damage to dopaminergic neurons altered CNS synaptic transmission, Substantia nigra,
- Lewy bodies–> neuronal inclusions: α-synuclein
- Avg onset: 45-65 years
- Progressive
- Tx: L-DOPA; does not slow progression just treats symptoms, becomes less effective
Huntington Disease
- Autosomal dominant
- Severe cerebral atrophy caudate & putamen nuclei, severity depends on degree of neuronal loss; intranuclear inclusions = Huntingtin protein
- 1⁰ feature: chorea, entire body ↓ cognition: memory loss = severe dementia
- Delayed age of onset: 30-40 years
- MC lethal w/in 15 years
Amyotrophic Lateral Sclerosis (ALS)
BOTH UMN & LMN death!!
• Preserves sensation & **extraocular motor fxn
• MC males
• Insidious: asymmetric distal extremity weakness
• RAPID progression
fasciculations: involuntary muscle contraction
• Eventual respiratory paralysis: Death respiratory infxn (pneumonia)
• 10% familial;
CNS tumors general info
- Spinal more common than cranial
- Most are 1⁰ no premalignant stages, non-resectable = bad
- Rarely mets outside CNS
types of gliomas
astrocytoma (diffuse & pilocytic), oligodendroglioma, ependymoma
diffuse astrocytoma
Malignant • 80% of adult gliomas • Cerebral • Poorly circumscribed o Glioblastoma = worst BAD prognosis
pilocytic astrocytoma
benign
• Cerebellar, spinal cord
• Well circumscribed
kids/young adults
Oligodendroglioma
benign or malignant
cerebral: frontal & temporal
adults
Ependymoma
• Periventricular region: kids
• Spinal canal: adults
o NF2
medulloblastoma
malignant, KIDS MC embryonal malignancy 20% pediatric brain tumors • Only CEREBELLAR • Tx: excision • Similar to PNETS, just in CNS
primary CNS lymphoma
• Aggressive, extranodal lymphoma
• MC CNS tumor in immunosuppressed pts
• Spread via ventricles
Any age But risk ↑ with age (>60)
meningioma
• MC benign tumor of adults (FEMALES) • Invasive • Transformed arachnoid cells • Risks: history of irradiation, NF2 • Easily excised Female Adults
CNS metastasis
- 25% of intracranial tumors
- Mets from: lung, breast, melanoma,
- Syncytial (whorled) cell clusters
