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NEUROLOGICAL DISEASES (Key Clinical Differentials (Stroke
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NEUROLOGICAL DISEASES
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Head Traumas
Missile Head Trauma
penetrating missile trauma
- object stays lodged in the brain
- most important thing is they are prone to infection
perforating missile trauma
- object exits out the other side of the head
- note the exit wound is larger than where the object entered
Blunt Head Trauma
- most are RTAs = road traffic accidents and falls
2 types of forces:
- rotational forces
- impact forces
--> impact forces cause more skull fractures, but rotational forces are more fatal
Non-missile TBI = Traumatic Brain Injury
- brain fracture
--> linear, depressed, compound, or hinge
--> hinge is where they come completely apart
- hemorrhage
--> Epidural = extradural
--> Subdural
--> intracerebral
- contusion = bruise
*Hemorrhages
- Epidural = extradural hemorrhage
--> usually by an artery on the outside of the dura
--> like the middle meningeal artery behind the pterion
- Subdural hemorrhage
--> under the periosteal dura layer or both dura
--> usually a cortical vein
Hematoma
- Hemorrhage leads to collection of blood in
one of these areas and is called a hematoma
Epidural = extradural hemorrhage
- usually by an artery on the outside of the dura
- like the middle meningeal artery behind the pterion
- usually in sports head injury or RTA
- if treated early at onset, epidural hemorrhage has a good prognosis
--> just need to drain the hematoma and repair artery
--> easy access to both
lucid interval
- clinically an epidural = extradural hemorrhage can initially have no symptoms
- if sports injury, even continue playing afterwards
- then hours later there is a gradual LOC
*Subdural hemorrhage / hematoma
- under the periosteal dura layer or both dura
--> usually a cortical vein or a bridging vein
--> bridging veins go laterally from the cortex to the sinuses
--> can also be a major sinus
- vein hemorrhage = slowly progressive and insidious mimic other things
Chronic Subdural Hemorrhage
- don't progress until weeks/months after the event
- Risk factors for chronic subdural hemorrhage
="Ants Shunt Eat Alcohol
- anticoagulants, shunt surgery, epilepsy, alcoholics
- these slowly grow due to osmotic effect
--> have high fibrin and RBCs --> draw in more blood continuously"
- from a MINOR fall in elderly
Clinical Cases
Clinical Case
- 3 more items...
Outcomes of Non-missile TBI = tramatic Brain Injury
- ONLY 30% will survive
- 20% make a good recovery
- 10% remain severely disabled
Contusions
- bruising of the brain
- usually on the opposite side to the trauma
= contra-coupe lesion
Healed contusions
- yelllow/brown due to HOMO SIDE HER IN hemosiderin accumulation
- wedge shaped areas of thinning cortex
- also with gliosis = neural scarring
- can have cavitation with healed contusions
DAI = Diffuse axonal Injury
- from rotational forces on the brain
- usually no fracture of the skull
- people with DAI usually unconscious and
do not even mutter sounds
- either fatal or vegetative state with continuous degeneration of the brain
- "axonal retraction balls"
- "white matter hemorrhages"
Secondary Brain Damage and other common traumas
- after either head or missile trauma there is secondary brain damage
- in missile the main secondary damage is infection
--> usually meningitis
Diffuse Brain Swelling
- due to adema and vasodilation
- raised ICP
- herniation and hypoperfusion follows
Fat Embolism
- usually occurs after getting a fracture of a long bone like the femur
- recall femur has yellow bone matter and fat stores
- fat stores get released into circulation
- first trapped in lungs, but can slip back into systemic circulation if lung alveoli become saturated
- also if there ia an AV = atrioventricular shunt
--> can go directly into systemic circulation
Post- Traumatic chronic conditions
- persistent vegetative state
- post-traumatic epilepsy
- post-traumatic dimentia
Boxer's Dimentia
- also called "punch-drunk syndrome"
or "CTBI-B = chronic traumatic brain injury from Boxing"
- memory loss and parkinsons symptoms
- pathology looks similar to Alzheimer's disease with amyloid plaques and neurofibrillary tau tangles
- occurs in 15-20% of professional boxers and usually 12 years after career
--> from continuous concussions and blows to head
CTE = chronic Truamatic Encephalopathy
- common in football and rugby players
- leading theory says that it is due to banging of the head releasing APP into the brain from cell membranes
- the APP then become beta amyloid plaques and cause similar disease as Alzheimer's
Spinal Trauma
- usually with horse riders or breech babies, gymnasts
--> anything where the spine or neck is hyper flexed
- cervical vertebrae most common and most fatal the higher up the neck
- usually atlas and axis are most fatal
*Demyelination
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*Demyelination Diseases
- 4 root causes of demyelination
--> infective
--> Autoimmune
--> Metabolic/Toxic
--> Neoplastic Tumor
*Autoimmune in CNS
- eg: Multiple Sclerosis
- NMO = neuromyelitis Optica
*MS = Multiple Sclerosis
- multiple lesions in SPACE and TIME
- auto immune IgG oligodendrocyte antibodies
--> antibodies against oligodendrocytes
--> COPS oligodendrocytes make CNS myelin
MS Subtypes
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- most are relapse and remitting = RRMS
- primary vs. secondary Progressive
--> secondary means after having RRMS
- then you can have a mix of primary and RRMS where all attacks are few and far between, but there is always a steady progression of the attacks
MS - Pathophys
- lesions are multiple in space and time
- 3 types of plaques form:
--> active plaques
--> inactive plaques
--> shadow plaques
Plaque formation
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3 types of plaques:
- active plaques
--> have inflammatory cells present
--> active inflammation
- inactive plaques
--> NO inflammatory cells present
--> the lymphocytes, microglia, etc. digest the myelin and release the proteins etc
--> gliosis occurs
- shadow plaques
--> NO inflammatory cells present
--> the oligodendrocytes try to reproduce the myelin that was lost
--> myelin thus present, but thinner
MS - Diagnosis
- History, MRI, CSF, Visual Evoked Responses
- IgG - Oligoclonal bands
--> in CSF screen
--> antibodies against oligodendrocytes
--> COPS oligodendrocytes make CNS myelin
- Periventricular white matter lesions = oligodendrocyte destruction
--> CT brain
CSF
- IgG antibodies present in CSF called
oligoclonal bands present in MS
- these IgG antibodies are used to attack myelin sheaths
- bad prognosis if found early in the disease
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MS and MRI
- periventricular lesions in white matter
- diffuse
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MS - Epidemiology
- "white women in their 20s and 30s"
--> Northern European countries have high incidence
- highest in Ireland and Northern Ireland
--> Irish immigrants carry the disease risk with them the 1st generation, then lose Risk
- onset usually in twenties
- most common is remittance and relapse over several decades and progression
- usually die from secondary things like
--> infections
--> secondary complications
""Young pretty women make a MULTIPLE SKULL ROSE garden of SIN
- SIN
--> scanning speech
--> intention tremour and incontinence
--> Nystagmus
- Rose Garden and pretty girls distract the HULA HOOPING TUTU Doctor driving by the garden
--> HLA DR2 human leukocyte antigen
--> spills his tennis balls all over the road
--> T cell mediated
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""The young pretty lady MULTIPLE SKULL ROSE garden of SIN
--> "Send her EMO exboyfriend a MULTIPLE ROSES birthday present that his PET ROBOT is suspicious of"
- EMO kid just plays BOOMERANG all day
--> relapse remitting of MS
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SIN symptoms of MS
- scanning speech
- intention tremour
- incontinence of urine
- nystagmus
Incontinence of MS
- part of SIN
- note the bladder distends since you lose the neuronal control for it to relax and distend
--> get bladder hypertonia
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Internuclear ophthalmoplegia (INO)
- disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus.
- SIN Nystagmus in MS
--> lateral gaze
--> comes from CN 3 not working and CN 6 ABDUCTING too much
--> OCNTRALATERAL eye to the INO has unnoposed CN6 so keeps abducting and nystagmus saccades
- note the CN6 projects to CN 3 since they have lateral and medial control of the eye
- CN 6 has 2 pathways
--> one directly to ABDUCTOR lateral rectus of eye
--> 2nd path is the CONTRALATERAL BALANCE path that stimulates the CN3 of the CONTRALAL side to ADDUCT
- Looking lateral to one side
--> actually requires BOTH CN6 to work
--> requires both ADDUCTION of the SAME side and ABDUCTION of the CONTRLATERAL side
--> one directly to ABDUCTOR lateral rectus of eye in the same direction
--> the other CN6 fires to stimulate the CN3 of the other eye to ADDUCT
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Metabolic/Toxic
- eg: central pontine myelinolysis
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Infective
- eg: progressive multifocal
leucoencephalopathy
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Neoplastic = tumor
- eg: multifocal pontine leucoencephalopathy
Dysmyelination Diseases
- note all dysmyelination disease are genetic
Leucodystrophy
Pathophys
- genetic defect in the metabolism of LCFA = Long Chain Fatty Acids
- LCFAs used to make myelin
- there are ALL forms of genetic inheritance
(both autosomal and x-linked also)
- when not forming properly, it gets degraded and all white matter areas look like jelly
Epi
- children's myelin usually doesn't form fully until about 3 years of age
- thus up until the age of 3, Leukodystrophy has no signs
ICP Diseases
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Hydrocephalous Ex vacuo
3 Causes of Odema in Hydrocephalous
- vasogenic = increased permability of blood vessels
- cytotoxic = injury to neurons and glia (eg: meningitis)
- interstitial = damage to ventricular lining
*Hydrocephalus
Facts and Epi
- pretty common = 1 in 1,000
- just as common as Down's Syndrome in the US
- Hydrocephalous has the exact same risk factors as NTDs
--> think "N Tube D = Hydro tubes"
--> Vit B12 and B9 = folate deficiency
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*Congenital Hydrocephalus (At birth)
- clinical features depend on whether younger or older than 2 years old
- age < 2
--> usually only the posterior fontanelle has fused by age 3-4 months
--> anterior fontanelle bulging and increase head circumference
--> still have room for the brain to handle the extra volume and size
--> will have macroencephaly
--> only symptom for < 2 usually is paralysis of upward gaze
- age > 2
--> will see more raised ICP and further neurological problems
- poor feeding
- hyperreflexes and hypertonicity
--> CNS always hyper for tone/reflexes?
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Sequalae with Hydroencephalous
- think if the CSF increases the system will try to push out in certain areas to relieve the pressure and volume
- chiara malformation
--> type 1 CM = tonsilar ONLY herniation (cele)
--> type 2 CM = tonsilar and flocculonodular lobe herniation
- myeloencephalocele (Spina Bifida = where the spinal cord herniates through the vertebrae)
- septum pellucidum rupture
--> squeezing of the SP from the lateral ventricles
*HEV = Hydrocephalous Ex Vacuo
- EX = out of
- Vacuo = vacuum
- thus HEV can be secondary to any type of atrophy of the brain
- when the brain atrophies there is a vacuum of space that the ventricles fill
--> they enlarge and produce more CSF
--> HEV
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*RLS = restless leg syndrome
- common in middle aged people
--> think of Cramer
- basically is Parkinson Disease, but in your legs
--> treat with dopamine agonist though, not
- Tx = Dopamine agonists = Pramipexole
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*Meningitis
Meningitis Management and Treatment:
- Early antibiotics (IV 2G ceftriaxone/cefotaxime)
- throat swab
--> since nasopharynx colonization first
- Lumbar Puncture
--> contraindicated in raised ICP, resp problems,shock
--> NEED to always rule out raised ICP first before Lumbar puncture
--> can cause tonsilar herniation = respiratory centre depression
- people living near/with someone infected given prophylaxis = preventative treatment
--> ciprofloxacin, or rifampicin
- if culture negative for bacteria
--> TB or viral
--> if viral most likely HSV
--> Aciclovir
Streptococcal Meningitis - Special Treatment
- Strep pneumo = most common casue of meningitis in adults
--> important to identify bacteria in CSF blood cultures quick for meningitis treatment
- note that Strep Pneumo meningitis is pretreated with dexamethasone before given Abx
--> this is different from Hib and Niesseria meningitidis
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Causes of Meningitis = Virus vs. Bacteria
- viral more common
- bacteria more serious
Pyogenic = Bacterial vs Viral Blood tests
Bacterial
- +/- Lymphocytes
- ↑ Neutrophils
- ↓↓ Glucose
- ↑↑ protein
Viral
- ↑ Lymphocytes
- ↓ Neutrophils
- +/- Glucose
- ↑ protein
- note that TB meningitis would be the same bloods as viral, except protein would be highest and glucose would be somewhat down also
Bacterial Meningitis
- Cild bacterial meningitis = GBS and HIb (+ other G- bacteria)
- Adult bacterial meningitis = strep pneumo, Niessieria men.
3 NHS Meningitis Bacteria
- N = N. meningitidis
- H = Hemophylis Influenza Subgroup B Serum
- S = Strep. pneumoniae
Strep. pneumoniae = Pneumococcal
- 2nd most common bacteria
- Gram (+) coccus --> remember P = +
- remember the S in Strep. pneumo
--> means SOMETIMES resistant to penicillin
S. Pneumo Key Features
- Strep. Pneumo is similar to meningococcal
--> WITHOUT the petechiae rash
Neisseria Meningitidis = Meningococcal
- most common bacteria
- Gram (-) coccus
- N in Neisseria is for NOT resistant to penicillin
--> note counterintuitive since the gram - is sensitive to penicillin in meningitis bacteria, and gram + is ONLY sometimes
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- meningococci are kidney shaped and usually in pairs on histology
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Hemophylis Influenza Type B
- not as common anymore due to vaccine
--> was dangerous before though since it was resistant to penicillin (beta lactamase +)
- Gram (-) coccobacilli
- beta-lacatmase positive
- I in H. Influenza is for IS resistant to penicillin
Ways 3 NHS bacteria gain entry to body
- colonize the nasal cavity
- polysaccharide capsule --> slippery and hard for the complement system (host complement = mannose binding lectin) to attack it
- genetic variation
--> good at picking up new DNA
--> also use slip-strand mispairing
- type 4 pili --> used to first colonize the nasopharynx
- IgA protease --> cleaves antibodies that attampe to attach to it
- Host CFH = Complement Factor H
--> if mutated in the host, this part of the complement system is a RF for meningitis
Bacterial meningitis paradox
- NHS bacteria that cause meningitis actually don't want to invade the meninges of the CNS
- most stay and colonize within the nasopharynx
--> actually colonize about 5-30% of general population
- ONLY when they gain a new mutation
(or colonize a host with a compromised immune system)
--> invade CNS and cause meningitis
- some bacteria that cause meningitis require immune cells from say sepsis to break down the BB so they can enter the CNS
VACCINES
MenAfriVac
- used in the Meningitis Belt
Virulence factors used for vaccines:
- type 4 pili --> used to first colonize the nasopharynx
- IgA protease --> cleaves antibodies that attampe to attach to it
- capsular polysaccharide
--> A,B,C,Y,W135
--> essential for bloodstream spread
- Capsular vaccines can be conjugated with proteins also
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PCV7 = Prevnar
- S. Pneumo
- used in Ireland
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Recombinant Meningococcal B Vaccine
- multicomponent protein vaccine
- Note MenB vaccine is a polyprotein and not a polysaccharide vaccine (same polysacharides as host)
BBB and 3 points of meningococcal entry into the CNS
- tight junctions of capillaries
- post capillary venules and veins
- tight junctions in the endothelial layer of the choroid plexuses
*Viral Meningitis
- VIRAL meningitis "ENTERS your MENINGES" = Enteroviruses
- Enteroviruses = most common cause of viral = aseptic meningitis
- HSV 2 is 2nd most common cause of viral meningitis behind enteroviruses
--> recall HSV1 = most common cause of sporadic encephalitis in young people (Temporary Labialis = Temporal lobe encephalitis)
--> HSV2 causes meningitis of the brain on the other hand
- Treatment of viral = aseptic meningitis = supportive ONLY
--> self limiting and doesn't require treatment after ruled out fungal and bacterial meningitis
--> viral = aseptic meningitis = Diagnosis of exclusion
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*CSF lab differentials in Meningitis
- Bacteria = low glucose, high protein, PMNs = neutrophils
- Fungi = low glucose, high protein,
WCC = lymphocytes
- Viral = NORMAL glucose +
--> protein MAY or MAY NOT be raised
--> WCC = lymphocytes
1 = CSF Glucose in meningitis
- for meningitis cause, First you look at Glucose CSF
--> HIGH glucose = bacteria or fungi
--> LOW glucose = viral (since they satay inside the cells and multiply)
2 = CSF WCC type in meningitis
- for finding meningitis bacteria, you look at WCC type in CSF
--> PMNs = neutrophils = bacteria ONLY
--> **lymphocytes = BOTH fungi and viral have lymphocytes since they are both intracellular usually
3 = CSF Proteins in meningitis
- note that proteins in meningitis are non-specific since they can be raised in all 3 causes
- the only differentiator is if you have NORMAL protein
--> then it is viral
- HIGH protein = thus tells you nothing
--> sincce viruses can have either NORMAL or raised protein
Meningitis - Pathophysiology
- meningitis affects the leptomeninges
(= pia mater and arachnoid mater)
--> think it affects the boundaries of the subarachnoid space that contains the CSF = leptomeninges
Meningitis Epidemiology
- most common meningococal in Western countries is serotype B,C
- Meningitis Belt
--> many different serotypes, A most common
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3 Age Groups of meningitis
- infants (<1 year old)
--> highest incidence
--> note you can't receive vaccine until about
3 months I believe?
--> E. coli and other coliforms main ones
- toddlers (< 4)
--> N. meningitidis and s. pneumo
- children and adults (>4)
--> N. meningitidis and s. pneumo
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*Ulnar Nerve Compression
- common for the ulnar nerve to be compressed at the ulnar bone of elbow
- this causes inflammation and degeneration of Shwann cells
--> you get pains, paresthesia, weakness in the 4th and 5th digits of hand
PNS Neuropathies
- either axonal degeneration or myelin degeneration
- axonal degeneration
--> will see a decreased amplitude of APs
- myelin degeneration
--> will see a slower AP due to less insulation
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*Ataxic Tangelectasia
- classic triad of
--> ataxias
--> tangelectasia
--> recurrant RTIs (upper and lower from IgA deficiency)
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*Horner's Syndrome
- "PAM is HORNY"
--> ptosis, anhydrosis, Mydriasis = Horners
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*Osmotic Demyelination Syndrome = ODS
- you see characteristic demyelination of the nerve in the PONS
--> from treating chronic hyponatremia with saline infusion
--> osmotic gradient causes astrocytes to lose water and die
- common in alcoholics and other people who have chronic hyponatremia
--> their astrocytes are adapted to the low sodium levels and secrete their stores of NTs (glutamate, etc) to make up for the low sodium
- correcting the hyponatremia with normal saline
--> increases the Na+ in the brain and the astrocytes of the PONS in particular can't react fast enough
--> the high osmotic gradient outside the cells causes them to lose water and they shrink and die
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*GREEN BERET syndrome = Guillan Barre Syndrome
- "Guillain - Campylo- BARE bacteria syndrome"
--> most cases are proceeded by a diarrhea
GI infection with campylo - BARRE bacteria
--> campylobacter infection
--> secondary causes can be other viruses or vaccinations (very small #)
"FECES to FEET --> FEET to FACE"
- F stages of Guillan Campylo BARRE bacteria
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GREEN BERET GUILLON up that WALL at BOOT CAMP!
- loses reflexes and gets muscle weakness
- Once GREEN BERET ascends it affects your RESP and FACE
--> Respiratory dyspnea
--> DIPLOPIA and BORKEN SPEECH
- GREEN BERET is told he has to do the BOOT CAMP course AGAIN
- GREEN BERET then literally LOSES HIS SHIT and PEE and his BP goes out of WACK
--> BOTH urinary and fecal incontincence
--> BP changes
- GREEN BERET goes AWALL and leaves the CAMP
--> the head BOOT CAMP SARGENT then gives him aggressive airway management
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GREEN BERET camp Counciller at CAMP CAMPYLOACTER 42 DEGREES
- note that GREEN BERET syndrome has muscle paralysis that ascends from the FEET UP
CAMP CAMPYLOACTER 42 DEGREES
- the WRITER KING ARTHUR who sits on his THRONE writes home to his mother about how terrible CAMP CAMPYLOACTER 42 DEGREES is
--> Rieters Syndrome comes after a CAMP CAMPYLOACTER infection
- the flag at CAMP CAMPYLOACTER 42 DEGREES is made of a
--> CORKSCREW shape
--> the flag is a flagella at CAMP CAMPYLOACTER 42 DEGREES
- GREEN BERET camp Counciller
--> GB syndrome happens after a CAMP CAMPYLOACTER infection
- the CHCKEN is served RAW at CAMP CAMPYLOACTER 42 DEGREES
--> 42 degrees is not hot enough to cook the chicken
- the weirdest thing that the WRITER KING ARTHUR has seen at CAMP CAMPYLOBACTER 42 degrees is a dog sucking MILK right from the TIT of a COW and then SHITTING with DIARRHEA everywhere at the camp
--> campylobacter can be in raw milk
--> campylobacter can be in dogs diarrhea
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*Global Ischemia
- Global Ischemia affects illegally parked cars FIRST
- "CAN'T PARK NEAR here"
--> Caudate
--> Perkinje of Cerebellum
--> neocortex
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*Cauda Equina Syndrome
- compression of the cadua equina nerves
*Spinal Cord Compression Differentials
- you must always rule out the 3 major cancers that metastasize to the vertebrae
--> prostate, breast, lung
- they can casue mets in the spine
--> these invade the epidura and compress the nerves of the spinal cord
--> causing cauda equina like symptoms
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Brain *Herniations
Intracranial Shift/Herniation
- obvious on MRI or CT
- common areas of herniation
--> lateral shift at subfalcine area common in SOL where the cingulate gyrus of the swelling SOL side push past the falx cerebri into the other hemisphere cranial space
- contraindicated for lumbar puncture since LP reduces the ICP and CSF volume --> pulls the brainstem further down by negative pressure
3 common herniation areas:
- transfalcine = cingulate herniation
--> (cerebral falx - SOL)
- transtentorial = uncal herniation
- Tonsilar (forman magnum)
Transtentorial = *Uncal herniation
- Uncus (part of hippocampus of temporal lobe) goes through tentorium cerebelli and pushes on brain stem
- Uncus can push on basilar artery
--> Duret Hemorrhages
- Uncus can also push on the CN 3
--> give CN 3 palsey
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