30 cns Flashcards
Traumatic brain injury (TBI)
divided into
plus list
focal and diffuse brain injuries
focal
epidural hematoma
subdural hematoma
contusion
intacerebral hematoma
diffuse
mild concussion
diffuse axonal injury
Concussion
Mild TBI with a transient loss of brain function; loss of consciousness, loss of reflexes, temporary respiratory arrest, and amnesia for the event
Commonly due to impact against a rigid surface
Pathogenesis is uncertain
Complete recovery with no visible pathologic injuries
Amnesia for the event will persists
Diffuse axonal injury (DAI)
Shearing of axons at nodes of Ranvier with impairment of axoplasmic flow
Brain is injured as it shifts and rotates inside the bony skull
Most common in high energy trauma: high-speed motor vehicle accidents, falls, sporting accidents, assaults, child abuse, shaken baby syndrome etc.
It causes coma after trauma without evidence of direct parenchymal injuries on brain scanning
Lead to significant brain injury associated with long term disability
most susceptable in DAI
It is diffuse, but with a predilection for the corpus callosum, periventricular white matter, and hippocampus, as well as cerebral and cerebellar peduncles(Susceptable)
what is seen in DAI
Punctate hemorrhages in the corpus callosum or the dorsolateral brainstem
Axonal swellings appreciable in the white matter. Axonal spheroids (globular, eosinophilic structures), which stain with β-amyloid precursor protein
Contusions define and type
Bruising of the brain tissue
Coup contusions at site of injury and usually due to a blow to the head
Contrecoup contusion at site diametrically opposite injuries and usually due to a fall in which the head strikes the ground
Coup and contrecoup develop when the head is mobile at the time of impact.
Most commonly occur in alcoholics or the elderly
Complications: seizures and post-traumatic intracerebral hemorrhage (i.e., lobar hemorrhage)
acute and chronic contusion
Wedge-shaped hemorrhage
at crests of gyri and edema
Extravasated red blood cells; red neurons (after 12–24 hours).
chronis
Yellow-brown well-circumscribed depressions of variable depth
hemosiderin deposit
gliosis
Chronic traumatic encephalopathy (CTE)
define
symptoms
microscopic findings
syndrome called
Neurodegenerative disorder that occurs years or decades after a sports career with repetitive brain trauma
Symptoms; memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, anxiety, suicidality, parkinsonism, and, eventually, progressive dementia.
Microscopic: neurofibrillary tangles, cerebellar atrophy and gliosis, hypopigmentation of the substantia nigra, and cavum septum pellucidum.
punch drunk syndrome
epidural hematoma
aka
complication
define
what artery/vein
location
Collection of blood between the dura and the skull
Skull fracture with tearing of middle meningeal artery
LOC then lucid interval then LOC (“talk and die syndrome”)
Herniation is a lethal complication
Subdural hematoma
Predisposing conditions include brain atrophy and abnormal hemostasis.
Progressive neurologic signs: headache, drowsiness, focal neurological deficits, and sometimes dementia.
It recurs frequently
difference between epidural and subdural hematoma
location
artery or vein
symtpoms
shape of lesion
Monro-Kellie Doctrine
csf 150ml
blood 150ml
prain parenchyma 1400ml
brain herniation types
subfalcine herniation
transtentorial herniation
tonsillar herniation
trancalvarial
subfalcine herniation
what herniates
and effect
cingulate gyrus under falx
compression of anterior cerebral artery
transtentorial herniation
what and effect
uncus through tentorium cerebelli
compression of CN3
and
posterioir cerebellar artery
causes
colateral homonymous hemianopsia - occipital lobe infarction
durret hemorrhage in brainstem
tonsillar herniation
part and effect
tonsil of cerebellum
compress brain stem
trancalvarial
cortex through skull
effect depends on location
CN3 palsy causes
and innervation
down and out
mydriasis
ptosis
uncal herniation shown what kind of phenomenon
kernohans notch phenomenon
contralateral and ipsilateral limb weakness
because hernia crosses over the other side and compress
iicp triad
aka
cushings triad
bp high
respiration low
heart rate low
with shock
opposite
high icp causes
and moa
cushings ulcer
increased vagal stimulation
basilar skull fracture symtoms and clinical presentaion
racoon eye
hemotympanum
posttauricular echymosis
csf otorrhea
Cerebrovascular Disease
Variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation
Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders
Frequent cause of death and serious disability
Risk factors same as CAD
Types of cerebrovascular Disease
Global Cerebral Ischemia
Transient Ischemic Attack
Stroke
Global Cerebral Ischemia
where
because of
Involves widespread areas of the brain
Occurs when blood flow (specifically O₂ or glucose) to the brain is stopped or reduced
Hypotensive episodes (Shock, MI and Cardiac arrest), decreased oxygen (anemia, CO poisoning) and hypoglycemia (insulinoma)
Depends on duration and magnitude of the insult divided into
Depends on duration and magnitude of the insult
Mild global ischemia results in transient confusion with prompt recovery. e.g., syncope
Severe global ischemia results in diffuse necrosis; may lead to brain death and survival leads to a ‘vegetative state’
Moderate global ischemia leads to infarcts in watershed areas and damage to highly vulnerable regions such as pyramidal neurons of the cerebral cortex, Purkinje neurons of cerebellum and Hippocampus(CA1 gyrus)
pyramidal neurons of cortex layers?
type of necrosis
pyramidal neurons of hippocampus so loss of?
which layer of cerebellum
i. Pyramidal neurons of the cerebral cortex (layers 3, 5, and 6)—leads to
laminar necrosis
ii. Pyramidal neurons of the hippocampus (temporal lobe)—important in longterm memory
iii. Purkinje layer of the cerebellum—integrates sensory perception with motor
control
TIA(Mini stroke)
define
cause
TIA(Mini stroke)
Reversible neurologic deficit that lasts from a few minutes to no more than 24 hours (but usually lasts less than 30 minutes).
Usually small platelet thrombi or artheroemboli from carotids and rarely severe carotid stenosis (>75% occlusion)
Increased risk of stroke ∼10% at 30 days and 30% to 5 years
Stroke (brain attack)
Rapidly developing clinical signs of focal (or global) disturbance of cerebral functions, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin (WHO)
Second leading cause of mortality after ischemic heart disease and disability worldwide
The extent of damage depends on the duration and severity of the ischemia. If ischemia persists for more than 5 minutes with perfusion below 5% of normal, some neurons will die. However, if ischemia is mild, the damage will occur slowly and may take up to 6 hours to completely destroy the brain tissue. In case of severe ischemia lasting more than 15 to 30 minutes, all of the affected tissue will die, leading to infarction.
Risk factors
for stroke
Age and hypertension (most important)
Smoking, DM, hyperlipidemia, atrial fibrillation, coronary artery disease (CAD), family history of stroke, previous stroke/TIA
In younger patients, risk factors include oral contraceptive use, hypercoagulable states (e.g., protein C and S deficiencies, antiphospholipid antibody syndrome), vasculitis, vasoconstrictive drug use (e.g., cocaine, amphetamines), polycythemia vera, PNH and sickle cell disease.
2 types of stroke
Evolving stroke is a stroke that is worsening
Completed stroke is one in which the maximal deficit has occurred
Depend on the affected arterial distribution
anter cereb arter
middle
poster
ante
trunk leg foot
middle
hand face tongue
2 types of stroke major
ischemic stroke
hemorrhagic stroke
types of ischemic stroke
thrombotic, embolic, and lacunar strokes.
thrombotic stroke
Thrombotic stroke is due to rupture of an atherosclerotic plaque.
i. Atherosclerosis usually develops at branch points (e.g., bifurcation of internal
carotid and middle cerebral artery in the circle of Willis).
ii. Results in a pale infarct at the periphery of the cortex
Embolic stroke
due to
where
artery incvolved
type of infarct
is due to thromboemboli.
i. Most commo n source of emboli is the left side of the heart (e.g., atrial
fibrillation).
ii. Usually involves the middle cerebral artery
iii. Results in a hemorrhagic infarct at the periphery of the cortex
lacunar stroke
due to
where
Lacunar stroke occurs secondary to hyaline arteriolosderosis, a complication of
hypertension.
i. Most commonly involves lenliculostriale vessels, resulting in small cystic
areas of infarction (Fig. 17.5)
ii. Involvement of the internal capsule leads to a pur e motor stroke.
iii. Involvement of ihe thalamus leads to a pure sensory stroke.
gitter cells
lipid laden microglia
Acute complications of Ischemic stroke
Progression of neurologic insult
Cerebral edema occurs within 1 to 2 days and can cause mass effects for up to 10 days increased ICP
Seizures (<5%)
Hemorrhage into the infarction (rare)
Intracerebral hemorrhage (ICH)
Intracerebral hemorrhage (ICH)
= Intraparenchymal hemorrhage
Causes severe headache, frequent nausea/vomiting, steady progression of symptoms over 15–20 minutes, and coma.
Due to hypertension(50%-60%)»_space; vascular malformations (especially arteriovenous malformations), cerebral amyloid angiopathy (CAA), neoplasms, vasculitis, abnormal hemostasis, hematological malignancies, infections, and diabetes mellitus.
High mortality rate (50% at 30 days)
parts of brain in order
putamen
lobar
thalamus
cerebellum
pons
ICH is due to rupture of
ICH Classically due to rupture of Charcot-Bouchard microaneurysms of the lenticulostriate vessels; Complication of hypertension and Basal ganglia is the most common site
Chronic HTN small arteries microaneurysms rupture
subarachinoid hemorrhage
Bleeding into the subarachnoid space
B. Presents as a sudden headache (“worst headache of my life”) with nuchal rigidity
C. Lumbar puncture shows xanthochromia (yellow hue due to bilirubin breakdown).
D. Most frequently (85%) due to rupture of a herry aneurysm; other causes include AV
malformations and an anticoagulated slate,
1. Berry aneurysms are thin-walled saccular outpouching» that lack a media layer , increasing the risk tor rupture.
2.
3. Associated with Marfan syndrome and autosomal dominant polycystic kidney
disease
Most frequently located of subarachinoid hemorrhage is
anterior most affected
common complications of subarach hemor
Vasospasm is a common complication that may occur 5 to 10 days after SAH. Irritating blood byproducts cause the walls of an artery to contract and spasm. Vasospasm narrows the inside diameter (lumen) of the artery and thereby reduces blood flow to that region of the brain, causing a secondary stroke.
Retinal hemorrhages—in up to 30% of patients.
Mortality rate ≤ 50% at 30 days
Vasospasm 3–10 days after hemorrhage ischemic infarct
Rebleed (1/3)
Communicating and/or obstructive hydrocephalus
SIADH
associated with
marfan
ehlers danlos
adpkd
Meningitis
specific names
Inflammation of the leptomeninges (Pia and arachnoid)
May extend to brain, spinal cord, optic nerves and ventricles
Inflammation of dura (pachymeningitis): This is usually due to extension of infection from chronic suppurative otitis media (CSOM) or fracture skull
Types and infectious causes of meningitis
Acute purulent (pyogenic) meningitis: Usually bacterial in origin and is a medical emergency
Acute lymphocytic (aseptic) meningitis: Viral in origin; commonly echovirus, coxsackie, mumps, or HIV
Chronic meningitis (bacterial or fungal): Causes include tuberculosis, Cryptococcus, or dimorphic fungi
Clinical presentation
of meningitis
triad
Presents with classic triad of nuchal rigidity, fever and headache/altered mental status
May also present with neurological deficits and seizures
In infants and young children, the presentation is often nonspecific
and tetanus like sigh called
opisthotonos
Sign of meningitis
pain when extending the kneekernig o
brudzinsku sigh
neck flexion leg flexion
csf findings
Pus accumulating in the subarachnoid space. Pus may interfere with normal flow of CSF leading to obstructive hydrocephalus
Complications: usually seen with bacterial meningitis includes
Diffuse cerebral edema carries ↑ICP fatal herniations and Cushing ulcer
Mental retardation or focal cranial nerve deficits.
Cerebral abscess formation
Hydrocephalus(obstructive and/communicating)
Subdural empyema
Cerebral infarction
Epilepsy (seizures)
Waterhouse-Friderichsen Syndrome
Acute lymphocytic (aseptic) meningitis
age
type and mainly
gross
prognosis
Affects children and young adults.
Enteroviruses, mumps, ECHO virus, coxsackie virus, EBV and HSV 2 (more common than with HSV-1)
Gross pathology: No distinctive change; sometimes swelling of brain
Benign and self-limiting, usually ends in complete recovery, unless accompanied by encephalitis
Better prognosis than bacterial meningitis
Tuberculous meningitis
M. tuberculosis or atypical mycobacteria (MAI)
Affects children and adults
Usually due to haematogenous spread (miliary tuberculosis) and less commonly, spreads directly from tuberculosis of the vertebral body
Late sequelae: Exudate and fibrous adhesions leading to obstructive hydrocephalus and Tuberculous encephalitis and Myelitis
Fungal meningitis
More indolent
Patients may have only headache and a decreased level of consciousness.
Candida, Aspergillus, Cryptococcus, and Mucor species are the most frequent agents
………….and ……….have a marked tropism for blood vessels, which leads to vasculitis, rupture of blood vessels, infarction and hemorrhage
Aspergillus and Mucor
Cryptococcal meningitis
Classic “meningeal” symptoms and signs are often absent
Seen in debilitated or immunocompromised persons (e.g, AIDS)
Usually due to haematogenous dissemination from a pulmonary lesion
Exudate in cryptococcal meningitis is scanty, translucent and
gelatinous
Cryptococcus causes diffuse meningoencephalitis, which leads to invasion of the brain through
the Virchow-Robin space
cryptococcal capsule forms ………….abcesses
soap bubble
Clinical presentation
Signs and symptoms due to local destructive effects:
Hemiparesis, aphasia, personality changes, seizures, ataxia, and visual disturbances.
Signs and symptoms due to mass effect causing increased intracranial pressure:
Headache, nausea and vomiting, papilledema, and cranial nerve palsies.
Encephalitis
Encephalitis is inflammation of the brain
Clinical manifestations are variable, and can include mental status change, fever, and headache, often progressing to coma.
Thought to be due to a latent infection spreading to the brain via the olfactory or trigeminal nerve.
HSV 1 infection neurons and glial cells
Hemorrhagic necrosis of temporal lobes
