neuro Flashcards
C1
Anterior ring OR Posterior ring fracture
Aspen collar for stable fracture
burst fracture treatment
also known as a type II
Burst fracture ( Jefferson fracture)- 4 point fracture
anterior and posterior column
if cruciate ligament is intact you can treat with an aspen collar
if it is ruptured you get surgery or a hallo
type 1 C1 fx
Anterior ring OR Posterior ring fracture
type II C1 atlas fx
Burst fracture ( Jefferson fracture)- 4 point fracture
Need to check for ligamentous injury in order to determine treatment
If ligament is torn you need to wear the hallow or have surgery
Type III C1
lateral mass fracture
Associated Condylar fracture
C1 fx tx
Immobilization, Halo, Surgical Intervention
Stability determined by Integrity of the Transverse ligament
need MRI
really just in C1 type II that you need assess cruciate transverse ligament
how to differentiate odontoid fracture
Type I- tip of odontoid (rare)
Type II- base of odontoid
Type III- throughout the body
any injury above ___ can affect breathing
C3
bilateral fracture through pars, often associated sublux C2-3. Severe extension
Hangman’s fracture:
jumped facet/Perched facet-
jumped facet/Perched facet- severe flexion injury, unilateral vs
bilateral ,
quadriplegia due to ligamentous injury and SCI
Special consideration with jumped facet
CVA secondary to vertebral injury occlusion or dissection- evaluated on CTA,angiogram- Tx ASA/Heparin, endovascular repair
Tear drop fracture
posterior fracture with ligament injury
how to meausre level of spinal cord injury
either the last level of complete normal function or function level most caudal with 3/5 motor with temperature and pain present on exam
Can experience severe muscle spasm because reflexes still work but muscle tone does not
how do we manage
Upper motor neuron deficit
These spasms can result in fxs of bone in children
BACLOFIN (muscle relaxer)
Imaging: CT/MRI
Immobilization until surgical stability, Methylprednisone controversial
Complete spina; injury
no preservation of motor/sensory more than 3 segments below injury. If injury above C3 vent dependent
Incomplete quadriplegia
any residual motor or semsorpy for than 3 segments below the level of injury
Central cord syndrome-
greater motor deficit in UE>LE
Brown Sequard syndrome-
spinal cord hemisection with ipsilateral motor paralysis and contralateral seonsory loss of pain, temp and light touch
Posterior cord and Anterior cord injury-
rare, pain and parasthesia, in fact of anterior spinal artery respectively
GCS
what do we need to know
need to know neuro function and GCS GCS<8 NO BUENO Eyes-4 Verbal response-5 Motor response -6
what is the picture of SDH
n/v/HA→ start to look like a stroke
Signs usually develop later with slow progression
usually the result of direct impact
if you can not recall a word suspect this head injury
if you can not recall a word suspect SDH on the left side
SDH picture on CT
CRESCENT and crosses suture lines
PE of SDH
weakness, facial droop, speech issues, + Prontor drift, AMS, LOC, low GSC
treatment of SDH
surgical vs observation
Considerations: Stop Anticoags
PE EDH
Can see blown pupil on the same side of the bleed → get that kid to the hospital
Resp distress due to uncal herniation vs observation if small with stable GCS and neuro exam-serial imaging
story of EDH
young
direct head trauma with a + LOC, followed by a “lucid interval”, then become obtunded with contralateral hemiparesis and ipsilateral pupil dilation
IPH looks like what
Most common in temporal,
frontal and occipital poles
Usually sudden deceleration injury causes brain to hit bony prominences, coup/contrecoup injury
when do we worry about swelling the most brain edema
4-14 days really worry about swelling with maximum around 5-10 really have to worry about seizures
PE with IPH
Exam: LOC, AMS, irritability, HA, N/V, sz activity
Concern for blossoming, increased ICP, seizures- sz prophylaxis and close GCS monitoring
IPH treatment
Observation vs surgical treatment- craniotomy, evacuation hematoma
craniotomy/craniectomy: Leave the bone off and let the brain swell for two or three weeks
Can see with encephalomalacia
SAH You really need to rule out
You really need to rule out an anyuerism with these and know what happened first
Trauma is most common cause of SAH
SAH workup
If Trauma uncertain R/o other causes with CTA/Angiogram
Basal skull fxs might look like this with presentation
-Difficult to see on imaging without thin cut CT
Pneumocepahlus, CSF otorrhea or rhinorrhea, hemotympanum, CN VII or VIII injury ( usually temporal fracture), Olfactory nerve injury (anterior fossa BSF)
Depressed skull fracture why do you give prophylactic anbx
When it collapses in you can get a dural tear and increase the risk of meningitis
Prophylactic anbx treatment for this is completely reasonable
CN VII or VIII injury suspect baslar fx here
usually temporal fracture
Olfactory nerve injury think about basalar skull fx here
anterior fossa BSF
what is a DAI
Diffuse axonal injury
A primary lesion of rotational acceleration/deceleration head injury
Rips all axons in the brain
Shearing injury
GCS is always 3
imaging of DAI
Diffuse edema
, hemorrhagic foci of corpus callosum and brain stem, changes in white matter fiber tracts
prognoses of DAI
Mild if less than 6 hours coma, moderate over 24 hour coma with amnesia, severe- coma lasting months with posturing and severe Neurologic deficit
Intra cranial hypertension normal and no bueno
Normal pressure 10-15 mmHg
> 20 NOT GOOD
management of intra cranial hypertension
This is when a GCS of 8 is super important
If the pt is not responding they get EVD automatically
Tube that drains CSF and works by gradient pressure (lowering and raising the bag)
Can also give mannitol or change respiratory status to change MAP
sxs of increased intracranial pressure
papilledema
abducens nerve palsy
decreased LOC
Cerebral perfusion pressure (CPP)
Mean Arterial pressure (MAP)- Intracranial Pressure (ICP)
concussion
Confusion, amnesia or LOC, or sxs after head trauma = concussio
sxs of concussion
vacant stare, delayed verbal or motor responses, difficulty focusing, disoriented, speech alterations, incoordination( tandem gait difficult), exaggerated emotion, memory deficit(repetitive)
Second Impact syndrome puts you at increase risk for
More likely to have increase in symptoms and sequelae
More likely to have alzheimer’s dz
Multiple concussion when do you stop playing
If 2 within 1 season- recommend imaging and if WNL 1 month no play
If 3 concussions or 2 severe( LOC) then season ending injury and consider ending all contact sports
Post concussive syndrome
HA, dizziness, visual changes, anosomia, hearing changes, balance issues, congivive changes- difficult concentrations, mild dementia, memory problems, impaired judgement, easy fatigue, depression
Post traumatic Alzheimer’s disease
CTE-what is it
Chronic Traumatic Encephalopathy
mild to severe dementia pugilistica
CTE presentation
Motor, cognitive an psychiatric impairments- mental slowing, emotional lability, violent outburst, paranoia, slowness sin though and speech, parkinson’s, dysarthria, tremor, ataxia
Second most common reason people seek medical attention
Low back pain
Most common cause of disability for persons >45 yo
Most common disc issues at
when would you do surgery
L4-5, L5-S1 followed by L3-4
L4/5 would see with foot drop with maybe some numbness in the big toe
With motor weakness= surgery
Microdiscectomy
Take out piece to alleviate the nerve
Degeneration is
desiccation, narrowing of disc space, changes in endplates and osteophyte formation
Herniation
localized displacement of disc material, can extrude leading to specific nerve compression
Degeneration causes
Causes chronic pain
Epidural injections or spinal cord stimulator
Annular tear
donut to the pulposa jelly
- annulus fibrosus with nucleus pulposus
disc
bulging vs herniation
generalized displacement of disc material, can lead to lateral recess or focal stenosis
bulging not as serious as herniation
History and PE of back pain
OPQRST- new vs old pain, acute exacerbation, describe pain location and quality.
Radiating pain- radiculopathy- muscle weakness, sensation changes. Bowel/bladder dysfunction. Ability to walk far ( claudication)
previous tx Medrol, PT, Chripracter, NSAIDs, Oral pain meds, conservative treatments, etc
PE for back pain
Inspection- spine for deformity, Muscle tone and bulk- specific atrophy noted, Motor and sensory exam.
Hyporeflexia vs hyperreflexia, gait, +SLR
L4- knee reflex, quads weak, L5- foot drop S1- diminished achillis reflex, weak plantar flexion
Imaging: Xray, CT, MRI
weakness in myotomes
suspect herniated disc
really any narrowing
tx for herniated disc
oral steroids, time, PT, EPI, surgery
degenerative disc disease -what is it
Slow progression of disc changes associated with facet disease, ligamentous changes
Broad based disc displacement
Can lead to lateral/foraminal recess stenosis over time or central stenosis with symptoms of radiculopathy or neurogenic claudication
tx fo degenerative disc
Tx: Conservative treatments unless severe stenosis
neurogenic claudication
leg pain with walking around that is not vascular
Get a doppler of the legs and check vascular supply
Not associated with edema but often leg cramping in calves
No skin/hair changes, not in stocking distribution, normal pusles
lumbar stenosis sxs
Alleviated by sitting to rest or bending forward for a period of time
Increased heaviness and weakness in legs with walking
Lumbar stenosis tx
oral meds, Pain management PT, EPI, Surgical intervention – laminectomy
causes of cauda equina
Compression of cauda equina leading to neuro deficits.
Can be due to Herniated disc, lesions, infections, trauma/fracture.
sxs of cauda equina
weakness or loss of function LE, Decreased or loss of sensation to LE, Bowel/bladder dysfunction, impotence/sexual dysfunction(late finding)
PE cauda equina
Weakness to LE, diminished/loss of sensation, absent sphincter tone, saddle anesthesia
work op and plan for cuada equina
MRI
Plan: Surgical decompression- emergent in most cases
Decompressive laminectomy
Lumbar spondylosis
Degenerative vs
congenital condition with misalignment of vertebral bodies with anterior subluxation of one vertebral body on another
most common lumbar spondylosis
Most common L5-S1 followed by L4-5
tx for spondylotlithiss
PLIF/TLIF/ALIF vs conservative treatments
which grades of spondylotlihtasis is are risk for cauda equina
III and IV usually surgical due to nerve root impingement and possible cauda equina syndrome
surgical tx
treatment of I and II spondylolithiasis
III and IV usually surgical due to nerve root impingement and possible cauda equina syndrome
Post op concerns for lumbar spine
rare complication of epidural hematoma- watch for increase pain or decline in exam, dural tears with CSF leaks, injury to nerve, hardware failure
neck pain tx
worry post op
Anterior ACDF , posterior decompression
hematoma
or laryngeal nerve
neck injuries sxs
related to nerve root impingement radiating pain or radiculopathy, neck pain, radiating pain to posterior head, shoulders and arms, weakness in grips, balancing issues, b/b issues if severe, dexterity issues.
greatest concern with cervical spine
concern cervical stenosis leading to cervical myelopathy
Ankylosis Spondylitis (bamboo spine)
Seronegative arthropathy (ANA, RF negative)
primary site of AS
Spine primary site involved starting at SI joints and moving rostrally
sxs of AS
non-radiating back pain , morning back stiffness hip pain, worse with inactivity and improved with exercise
imaging for AS
CT, XRAy and MRI- evaluate for stenosis, high risk with trauma
tx for AS
Surgery if cauda equina syndrome, SCI following fracture/trauma, spinal stenosis (rare)
two types of scoliosis
Degernatie vs idiopathic
get the COBB
<20 leave it lalone
MC most malignant brain tumor
GBM- most common, most malignant
RIM INHACING lesion
Schwannomas
Schwannomas (acoustic neuroma)
Vestibular-
benign lesion
sxs of schwannomas
hearing loss- insidious and progressive, tinnitus, disequilibrium. Can also develop V and
VII CN palsy if large enough due to location-otalgia, facial numbness, facial weakness, taste changes.
If large enough can cause brain stem compression leading to ataxia, HA, N/V, diplopia, cerebellar signs- threatens brain stem functions- resp. distress, coma, death
PE Schwannomas (acoustic neuroma)
Weber lateralizes to uninvolved side, = Rhine test, CN III deficit(hearing test prior to OR), nystagmus, facial weakness or paresthesias
MC benign tumor
Meningioma (most common?)
What is the meningioma where does it come from
Extra-axial lesion
Slow growing
Arise from arachnoid with attachment to the dura
peak age 45, F>M
can cause mass affect
most pituitary tumors are
Most are benign adenomas arising from anterior pituitary
labs for pit tumors
Go Look For The Adenoma- GH, LH, FSH, TSH, ACTH. Prolactin, cortisol
what type of visual changes might you see with a pit tumor
if causing symptoms, if increasing in size rapidly, visual changes on formal visual field testing.
Prolactinoma tx
Bromocriptine tx and will go away
post op concerns with pituitary surg
SIADH- watch Na+, Panhypopit- check endocrine labs and consutl endocrine
Most common mets in order:
#1 Lung CA, Breast CA, renal cell CA, GI, melanoma in adults Prostate cancer=spine mets
multiple myeloma
Bone pain: especially spine* & ribs due to osteolytic, destructive lesions & osteopenic fractures, spinal cord compression (plasma cells can form a tumor), radiculopathy.
Recurrent infections: (Strep pneumo, gram negative) from leukopenia. Hyperviscosity.
Elevated Calcium (hypercalcemia): only heme malignancy associated with bone destruction.
Anemia: fatigue, pallor, weakness, weight loss, hepatosplenomegaly, soft tissue masses.
Kidnev Failure* - antibody light-chain protein deposition in the kidney. Neurologic involvement.
hemorrhagic RF
HTN, Cocaine use, Cigarette smoking, high consumption ETOH, anti platlet therpy
Ischemic CVA
Carotid Stenosis, Vertebral stenosis, Cerebral stenosis, hyperlipidemia
progressive bilateral occlusion of ICAs with collateral compensatory capillaries, on angio look like ”puff of smoke”
Moya moya
Amyliod disease
deposits of amyloid proteins, recurrent lobar hemorrhages, often elderly
sxs to search for in CVA
Facial palsy, Motor weakness, ataxia( difficulty with finger to nose if cerebellar), paresthesia, aphasia/fluency/word finding, dysarthria, neglect, AMS, Coma
imaginign for CVA
Imaging: CT, MRI-best for acute stroke, CT angiogram/MR angiogram, Cerebral angiogram
three types of vascular malformations
Arteriovenous anomoly
Cavernous Malformation
Cerebral Aneurysms
what is AVM
Hereditary and present in 20’s or 30’s with a bleed
Engorge and grow and get big over time
Abnormal collection of blood vessels with arterial blood flow directomy into draining veins ( no capillary bed)
imaging for AVM
CT- r/o acute hemorrhage,
MRI- evaluate draining veins and feeding arteries, evaluate for edema, Angiography
tx of AVM
Surgery- eliminates bleeding risk and sz control. high risk, invasive
Decrease risk for bleeding again
Usually just use radiation for treatment
Endovascular embolization-
Cavernous malformation
Benign vascular lesions with thick irregular vascular channels, large feeding arteries and large draining vein
benign and multiple
if you do have sxs with cavernous malformations
Sz, neuro deficit related to hemorrhage of hydrocephalus, incidental finding often
Usually don’t present till after it has bled
imagining and tx cavernous malformations
CT- acute hemorrhage, MRI
Will show up as black spots on a MRI
Usually just observe
Treatment: Observation, Surgery if hemorrhage
cerebral aneurysm what is it and what does it look like
SAH
Cerebral aneurysm→ dead chicken
“worst headache of my life”- thunderclap HA, AMS, obtunded, 3rd nerve palsy( P-comm aneurysm), sentinel HA
down and out
imaging for cerebral aneurysm
CT/MRI -SAH on imaging, CT Angio, Cerebral angiogram
CTA or MRA
LP done for RBC
tx for cerebral aneurysm
Aneurysm >5mm, symptoms related I.e 3rd nerve palsy, enlargement on observation
Watch if <5 mm unless they have a 1st degree relative with rupture or if they have had a previous bleed
Surgery options- clipping, endovascular coiling/stent coil assist
Hydrocephalus sxs and when would we see it
Wet wacky wobbly
looking for
We are watching for this after SAH
Forgot how to get rid of fluid
can get it secondary to mass affect
treatment from hydrocephalus
Can set EVD to 20 or 10 to get off extra fluid
Once pressure is relieved pt is back to normal
Can also do a VP shunt into the abdomen
Diverts fluid into the intestines
NPH
Wet wacky and wobbly again
Condition of ventriculomegaly without increased pressure
Can do a LP and will see completely normal pressures
But when you pull off fluid they wake up
hydrocephalus from infection
Valley fever- Disseminated coccidioidomycosis
In the valley seen with severe hydrocephalus, spinal abscess, and osteomyelitis
Need debulking and shunts
If it has weakened the bone maybe spinal fusion
Can see the failing of shunts with obtunded
Osteomyelitis
Osteomyelitis is very common in IVDU
Can also see in field workers
and field workers
can also see in Potts (TB)
Cranisynostosis
bossing when cranial plates close too early
CALL THE DOCTOR
Hypertension Changes in RR, irregularity Bradycardia Sever HA Decline in neuro exam -speech, motor, etc Decline in GCS>2 pts Anisocoria characterized by an unequal size of the eyes' pupils. Elevated ICP >20 FOR 5 MINUTES No output from EVD >2HR PERIOD
Post op Concerns
Pain not well controlled- see the patient
Drains not working- check them yourself
Any decline in GCS should be notified and repeat imaging immediately
AVOID NSAIDS
Avoid anticoags as long as possible for ICH
why avoid NSAIDS
Research has shown that the fusion will fail if NSAIDS are given
Leads to chronic back pain
Chiari Malofrmaiton
hoffmans test- sign showing
(problems with corticospinal tract)
brain grows into formane magnum
