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95 Cards in this Set

  • Front
  • Back
What is the criteria for a Neurosurgical/Neurological Emergency?
loss possible of vital function resulting in death of tissue or death of patient
Can the brain regenerate itself?
What causes the death of a neuron?
Lack of oxygen & glucose
What are some neurological EMERGENCIES that we have learned?
status epilepticus, syncope, coma, temporal arteritis, acute retinal artery/vein occlusion, acute glaucoma, spinal cord lesions (central cord, acs, brown sequard), intracranial infections (empyemas), brain tumors, stroke (missing therapeutic window to administer TPA), venous thrombosis, carotid/vertebral artery dissection
Increased intracranial P causes what?
Cerebral herniation
Which herniation is the first one you see with increased intracranial P?
Subfalcine Herniation
Which herniation is terminal and beyond recovery b/c it compresses the medulla?
Tonsillar herniation
What are the 2 causes of loss of consciousness?
1. bihemispheric pressure
2. knocking out the RAS
An expanded mass lesion forces the brain tissue to herniate in which direction?
Towards the compartment of lower pressure
At which age do the cranial sutures close?
6-8 y/o
What three things does the cranial vault contain?
Brain tissue (neurons & glia)
CSF (150 cc)
Blood (150cc)
What types of things can cause the intracranial volume to increase?
edema, hematoma, tumor, CSF, abscess (pus)
Initial increases in volume are accommodated by compensatory mechanisms. What are the 3 methods of compensation?
1. Movement of CSF out of the vault.
2. Mvmt of venous blood out of vault.
3. Collapse of ventricular, cistern systems.
What is the normal intracranial pressure and @ what level do you have a 80-90% change of mortality.
10-12 ml normal, 40ml-80-90% mortality.
What is the Monroe-Kellie principle?
Cranium is closed container (so if you inc volume of one pt-->its compensated by dec volume of another pt (like CSF, blood) or P in system will rise.
What are cisterns & which one is especially important to look for on a CT?
Cisterns are openings in the subarachnoid space of brain thats filled w/ CSF. They can be compromised in cases of increased intracranial P. Be sure to look for Ambient cistern.
Acute Cauda Equina Syndroms is almost always a cause of what?
Acute disc herniation, most often @ L4/5 or L5/S1. (can also be from upper lumbar). Usually a combo of large herniation + small spinal canal.
What are the symptoms of a patient w/ Cauda Equina Syndrome?
saddle anesthsia, motor diffuse weakness in lower extremity, distended bladder, periumbilical tenderness, anal sphincter tone diminished, nl bowel sounds. Males often get sexual dysfxn. Unilateral sx's-->better overall prognosis.
Disc herniation is most likely to be in which direction?
What is the tx or a patient w/ Cauda Equina syndrome?
Urgency in tx-Surgical decompression. Microdiscectomy vs total laminectomy. (as soon as you find lesion, then do surgery for better prognosis & best recovery of bladder fxn)
Which other condition presents very similarly to Cauda Equina syndrome?
Conus Medullaris syndrome
What account for 80% of intracerebral hematomas?
Supratentorial hematomas
50% of intracerebral hematomas are related to what clinical condition? What age group has the highest incidence for intracerebral hematomas?
hypertension, 40s & 50s.
What are the 2 types of intracerebral hematomas?
Basal Ganglia & Lobar. Basal ganglia hematoms include those in basal ganglia & thalamus
What is a major cause of strokes in young people?
Drug abuse
What are some causes of nontraumatic intracerebral hematomas?
HTN, Aneurysm, AVM, Tumor, Blood dyscrasias, anticoagulants, vasculitis, drug abuse, conversion ischemic CVA, Amyloid Angiopathy.
When would a young patient get amyloid angiopathy? (Exception to rule!)
If they had Alzheimer's, Down's syndrome, degenerative conditions.
What is amyloid angiopathy and what age group does it affect?
Deposition of amyloid protein in small & mid sized arteries of the cerebral cortex. Affects elderly > 70 y/o. Prevalence >90 y/o is 50%.
Amyloid angiopathy causes what percent of all strokes & what type of intracerebral hemorrhage.
1% of all strokes, lobar hemorrhage.
How much of an increased of an intracerebral hemorrhage do thos e on anticoagulants have compared to those who are non anticoagulated?
8x greater risk. 1 out of every 100 on anticoagulants will suffer an ICH. (& 1% of all on thrombolytics)
What are the top three street drugs and top three prescription drugs causing intracerebral hematomas?
Street drugs: 1. Cocaine (most common overall, often present w/ chest pain), 2. Amphetamine (speed), 3. Phencyclidine (PCP).
Prescription drugs: 1. Talwin, 2. Phenylpropanolamine (Dexatrim), 3. Ritalin (Methylphenidate).
Describe the management of an intracerebral hematoma.
ABC's, Early intubation to prevent aspiration, hypoxemia, hypercapnia; NS eval; Mannitol, hyperventilation, ventriculostomy, differentiate from ischemic CVA. Thrombolytics vs Surgery vs Medical Rx.
Should surgery be performed on a basal ganglia ICH? Cerebellar hemorrhage?
No, but evidence shows you should do it on cerebellar hemorrhages b/c can get to it w/o damaging higher cortical/primary motor path.
What is the best prognosticator for surgery to correct a cerebellar hemorrhage?
Best prognosis in pts whose GCS < 14, or large hematoma (vol >40 ml) =diameter > 3cm (if it doesn't meet these requirements, then no surgery, just observe)
In a patient who comes in complaining of back pain who also has a history of cancer, what factors should concern you that it could be more than a standard back problem?
Weight loss, back pain at rest, fever w/ back pain, neurological deficiency.
In a patient w/ back pain (esp w/ cancer hx), why should you make sure you pin prick up and down the entire thorax?
B/c the majority of metastatic disease will go to the thorax, so you don't want to miss it.
What are some causes of acute spinal cord dysfunction?
Acute disc herniation, metastatic cancer, epidural abscess/hematoma, intramedullary infection, hemorrhage, transverse myelitis (autoimmune condition).
What are some examples of subacute/chronic spinal cord dysfunctions?
MS (females, waxing & waning, Devic's-->only affects cord), tumors (ex. NF), Vitamin deficiency (B12-->Dorsal column degeneration), Congenital anomalies (ex Spina bifida, radiation myelopathy, arachnoitis (from surgery), infective HIV myelopathy (immunosuppressed), Degenerative disease.
The axial skeleton is the third most common site for what?
incidence of metastasis locations following liver, lung.
What percent of patients with spinal mets have that as their presenting symptom?
What are the most frequent primary tumors to spreads to spine?
1. Breast 2. Lung, 3. Prostate, 4. Hematopoietic System (Any neoplastic may involve spine!)
What is the MOST common metastatic tumor to CNS (brain & SC)?
Melanoma!! Greater incidence of lung & breast cancer just because there are more cases of those in general.
What is the clinical presentation of someone w/ Spinal Mets?
95% have pain as initial sx. Pain prevents for wks-yr (mean: 8 wks), pain referred/radicular; >50% @ time of initial presentation have neuro deficit (radicular wkness, paraplegia), loss of bowel & bladder fxn!
What is the pathogenesis of spinal mets?
Marrow replaced by tumor cells (myeloma), hematogenous dissemination tumor to VN, direct local extension from paraspinal focus, tumor growth thru intervertebral foramine or alone perineurium of spinal nerves, retrograde flow thru valveless vertebral plexus.
What are the four signs of metastasis on a plain X-ray?
1. Pedicle erosion
2. Collapse of Body/Wedging
3. Lytic Destruction
4. Focal Osteopenia.
What is the mainstay tx for spinal mets? Do something--Metastatic Cord Compression is a medical emergency!!
Radiation therapy (High energy X-rays generated by linear accelerator targets DNA replicating cells). 2 doses of radiation: 1. Palliative and 2. Curative dose.
Describe the patient response to radiation given for metastatic cord compression?
1/3-1/2-->improve & can walk pos t tx; Of responders, mediation duration response < 6mos. Pt w/ radiosensitive tumors & ambulatory prior to RT maintain ambulation; Local recurrence from Vertebral collapse or tumor regrowth is the norm;
What is the mandatory initial step to stabilize neuro deficits (dec edema) for mets CA compression?
Corticosteroids-->Dexamethasone is most common. Hi dose bolus-->taper. Big analgesic, no neuro benefit. (Decompressive laminectomy added in is no add'l benefit)
What is the differential diagnosis for ptosis?
1. Third nerve palsy
2. Horner's Syndrome
3. Myopathy (wkness of lid muscles-->myasthenia gravis, muscular dystrophy, ocular myopathy),
4. Congenital
5. Syphilis.
What is the pathway for CN III?
Exits midbrain near cerebral peduncle-->enters SAS travels medial to P. Comm Artery-->Enters Cavernous sinus in lateral wall superior to CN IV.
What muscles does CN III innervate?
S, I, M rectus, inferior oblique, pupillary sphincter, levator palpebrae.
What percent of aneurysms occur in the anterior circulation (A Comm, P Comm, MCA, Int Carotid) vs the posterior circulation of brain?
90-95% Anterior Circulation, 5-10% Posterior Circulation.
(also often occur @ vessel bifurcation--these are outpouchings from the Circle of Willis)
How would someone present to you if they had an aneurysm?
SAH (60-85%-->HA, Meningismus, LOC, NV)
Cranial Neuropathy 15-30%;
Pupil involving CN3 most common;
Post Communicating Artery Aneurysm.
Other: migraine, seizure
What are the risk factors for formation of an aneurysm.
Family Hx of aneurysm, various inherited d/o's (polycystic kidney dz, Ehlers Danlos), Age >50 y/o, female, currently smoke cigs, cocaine use.
If you have one aneurysm, what is the percent chance that you have multiple aneurysms?
If your patient has a family history of aneurysms, what do you recommend that they do for a better prognosis for themselves?
Do a CT or MRA Angiogram
How would someone present to you with a posterior communicating artery aneurysm & what is their prognosis?
Present w/ CN III palsy w/ ptosis, dilated unreactive pupil, ophthalmoplegia; Other signs: HA, meningismus, hypothalamic dysfxn.
Prognosis: good recovery w/ early surgery < day3, Levator palpebrae & PS fibers recover earliest.
What percent of adults have intracranial aneurysms?
2% of adults (4 million in US)
What is the mortality rate for those who have aneurym rupture and then SAH?
-If they arrive alive, mortality over 1st month: 45%
-Of those who do survive, >50% have major neuro deficits result of initial hemorrhage, vasospasm w/ infarction, hydrocephalus.
Why is it important that you don't miss an aneurysm rupture even when they do survive?
B/c those not obliterate have a rebleed rate of 20% in frst 2 weeks & 3%/yr thereafter.
Should an asymptomatic unruptured aneurysm be surgically removed?
No, the surgery risk is greater than the rupture risk.
Which asymptomatic unruptured aneurysm SHOULD be removed?
Giant aneurysm >2.5 cm which are 5% of all-->risk of rupture is 6% in 1st year & always stays high.
What causes a significant number of litigation claims b/c the doc fails to interpret CT/CSF properly, & thus fail to obtain CT or follow thru w/ LP on initial contact?
Subarachnoid Hemorrhage.
What are the causes of cavernous sinus syndrome?
Metastatic tumors, Direct extension nasopharyngeal tumors, pituitary tumors (carinomas>adenomas), apoplexy (sudden abrupt bleeding of pituitary), bacterial infections causing cavernous sinus thrombosis, fungal infections (mucoormycosis)-->common in DM pts, cavenous carotid aneurysms, fistulas.
Describe the Cavernous Sinus and its fxn.
Cavernous sinus is a pair venous structures located on either side of sella turcica. It receives venous tributaries from superior & inferior petrosal sinuses. Contains carotid A, sympathethic plexus, CN 3, 4, 6 & V1, & V2.
Describe Cavernous Sinus Thrombosis.
-Primarily infectious process involving paranasal sinuses A/O orbital cellulitis.
-Local & systemic signs infection.
-Staph aureus, cutaneous source on face, mucormycosis in diabetic patient.
Describe the pathophysiology of Cavernous Sinus Syndrome & what symptoms the patient would have when they came to your office.
Pt may come in w/ pain in eye thats become red as well as w/ orbital welling. Commonly present w/ pain, numbness in forehead. Lesions of CS or apex-->affect isolated or all nerves going thru CS. Complete lesion disrupts CN 3, 4, 6 causing total opthalmoplegia, accompanied by fixed, dilated pupil. Involvement CN 5 V1, V2 divisions-->sensory loss on face. Impaired venous drainage can cause vascular engorgement of orbital structures.
What are the three main characteristic sx's of lesions to CS?
1. Opthalmoplegia.
2. Orbital Congestion
3. Proptosis
(often fever, pain if infection present)
How would you classify a patient in terms of their difficulty to intubate them?
Mallmpati Class. (Class 3=difficult)
On a lateral spine X-ray, what should be the gap b/w C1 & C2 for adults & for kids?
Adults <3mm, Kids <5mm.
If patient comes in with upper extremity weakness > LE weakness, what condition would you think of? What is the major cause of this?
Central Cord Syndrome; Usually results from hyperextension.
What percent of moderate/severe RA patients get radiographic evidence & spine involvement?
>85% of those w/ moderate/severe RA have spinal involvement. 44-88% have involvement of upper cervical spine.
Why do RA patient have misalignment & instability?
From destruction of bone & supporting ligaments by synovial proliferation
What are the 2 most common types of Cervical Spine involvement?
1. Anterior atlantoaxial subluxation (25%).
2. Basilar Impression (upward translocation of odontoid process)-8%
What occurs in Atlantoaxial subluxation (in RA pts)?
Inflammatory involvement of AA synovial jts-->erosive changes in odontoid process & decalcification w/ loosening of insertion of transverse ligament on atlas--->instability allowing anterior subluxation of atlas on axis.
-AA subluxation in 25% pts w/ RA
-Mean time onset RA & AAS-14 yrs.
What is the mechanism for spinal cord compression in pts w/ AA subluxation (for RA pts)?
-Scissoring effect of C1 on C2
-by pannus of granulation tissue that forms around dens.
What are the radiological findings of RA?
-Lateral C spine X-ray--nl atlanto--dental distance in adults 4mm.
-Widening of ADI suggests incompetence of transverse ligament.
-Natural hx AAS is progressive (5mm will progress to 8 mm etc.)
-Once myelopathy occurs majority irreversible.
-Myelopathy high once ADI >9mm.
What ligament gets eaten up by RA?
Transverse ligament.
How does RA affect your lifespan?
Life expectancy w/ RA is 10 yrs less than general population
When would you tx a patient w/ Atlantoaxial subluxation?
-Symptomatic pts w/ AAS almost ALL require surgerical tx (arthrodesis).
-Surgery usually withheld until ADI distance > 6mm & symptomatic.
-Myelopathy severe-hi risk sudden death.
-Asymptomatic pts w/ >8mm subluxation often fused prophylactically.
-Post surgery only if subluxation is reducible & pannus isn't causing significant compression:transoral odontoidectomy.
What is the most common tpye of incomplete spinal cord injury syndrome?
Central Cord Syndrome
What are the results of a complete cord transection?
-Loss of sensory & motor fxn below lesion level.
-May result in neurogenic shock.
-Loss of bowel & bladder control
What are the results of and what is the major cause of anterior cord syndrome?
Typically result of HYPERFLEXION injuries;
Sx's: loss of voluntary & reflex motor activity.
Loss of pain & temp sensation.
-Preservation of proprioception, vibratory sense, & ability to sense light pressure.
What is the major cause of and what are the sx's of Brown sequard Syndrome?
Major cause: Penetrating Trauma.
Cord damage limited to 1 hemisphere.
-Ipsilateral motor loss.
-Ipsilateral loss of proprioception
-Contralateral loss of pain & temp sensation.
What is in the differential diagnosis for a patient who comes in w/ diaphoresis, w/ neurodysfxn of acute onset.
Meningitis, acute transverse myelitis, disc herniation--Cauda Equina Syndrome, Spinal Cord tumor, Spinal Hemorrhage, Spinal Epidural Abscess.
What are the 3 types of spinal infections?
1. Vertebral Osteomyelitis (Pyogenic, Nonpyogenic (TB-Pott's dz)
2. Epidural Abscess
3. Discitis (spontaneous, post-operative, post-procedure)
What are the risk factors for getting a spinal epidural abscess?
DM, Drug Abuse, Chronic Renal Failure, Post-Op, Alcoholism, Immunocompromised
When would you consider a spinal epidural abscess in a patient?
Consider in all pts w/ back pain, fever, spine tenderness.
-Progressive myelopathy.
-Fever, sweats, rigors common.
-Often seen w/ V. osteomyelitis(infection in bone), esp anterior SEA.
Describe the epidemiology of Spinal Epidural Abscesses?
Incidence on rise, avg age: 50s, Thoracic (50%) > Lumbar (35%) > Cervical (15%).
-82% posterior to cord, 18% anterior.
What are the clinical features of Spinal Epidural Abscesses?
-Excruciating back pain, localized over spine.
-Tender to palpation, percussion.
-Radicular S &S follow w/ distal cord findings.
-Common bladder & bowel disturbance early.
-Abdominal distention.
-Wkness progressing to paraparesis & plegia.
-Avg time: 3 days from back pain--root sx's, 4.5 days to wkness
-Patients may be encaphlopathic
-Post op pts may have few S & Sx's.
What is the most common source on infection for spinal epidural abscesses?
hematogenous (extradural space, verebrae)
(other sources: direct extension, post spinal procedures)
What are the top 2 organisms leading to spinal epidural abscesses?
1. Staph aureus (>50%)
2. Aerobic & anaerobic strept
(no organism in 29-50% cases)
What is the tx for spinal epidural abscesses w/ no deficits?
immobilization, IV Abx-->empiric Abx: 3rd gen cephalosporin +vancomycin (until MRSA rule out) 204 wks IV abx & 4 wks PO., 6-8 wks abx if osteomyelitis present
What is the prognosis of an SEA?
fatal 18-23% (higher in older pts & those paralyzed before surgery), severe neuro deficits rarely improve even w/ surgery <6-10 hrs onset paralysis, immunocompromised do poorly.
If a patient presents with CN3 palsy with ptosis, dilated unreactive pupil, ophthalmoplegia, what should be your number one thought?
posterior communicating artery aneurysm (very common) - esp in with fam. hx, female, current smoking, cocaine use