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198 Cards in this Set

  • Front
  • Back
What is the basic function of the cerebrum?
Higher cortical function
What are the functions of the frontal lobe?
- Motor
- Pre-motor
- Broca's
Motor: discrete muscle activity

Pre-motor: muscle group coordination

Broca's area: motor aphasia
What is the function of the parietal lobes?
Tactile sense,

Proprioception
What is the function of the occipital lobe?
Visual sensation
What are the functions of the temporal lobe?
- Superior
- Inferior
- Posterior
Superior: auditory, hearing

Inferior: Short term memory

Posterior: Sensory integration (Wernicke)
What are the 4 functions of the cerebellum?
Maintain posture

Coordination

Balance/ gait

Speech
What are the functions of the deep brain structures (gray matter)? (3)
Basal ganglia: movement

Thalamus: processes sensory info and relays to cortex

Hypothalamus: maintains homeostasis and regulates temp, HR, BP, governs emotional behavior (hormone production)
Questions to ask regarding a headache that may be referable to the nervous system?
Age at onset,
Location,
Quality,
Preceding events,
Assoc sx,
Precipitating factors,
Family hx
What might nausea, referable to the nervous system, be a sign of?
Early sign of elevated icp.

Seizure
What might vomiting, referable to the nervous system be a sign of?
"projectile" w/ or w/out nausea might be elevated icp
What type of visual aberrations might be referable to the nervous system?
Loss of acuity

Double vision,

Visual field cut

Visual hallucinations
What type of hearing deficits might be referable to the nervous system?
Loss of acuity,

Tinnitus,

"Functional hearing"
What type of sensory aberrations might be referable to the nervous system?
Paresthesias,

Numbness

Pain,

Hyperesthesias,

Dysthesias
What type of weakness/ plegia might be referable tot he nervous system?
Clumsiness,

"heavy" limbs
What types of personality changes might be referable to the nervous system?
Disinhibition

Emotional lability

Irritability
What types of gait abnormalities might be referable tot he nervous system?
Dysequilibrium,

Falls
What is a manifestation of functional decline that may be referable to the nervous system?
Unable to care for oneself
What are manifestations of incoordination that may be referable to the nervous system?
Dropping objects,

Sloppy handwriting
How might patients refer to dizziness/ vertigo that may be referable to the nervous system?
Light headed

"spinning"
6 components to the neuro exam?
Cerebral function/ mental status
Cranial nerves,
Motor function,
Sensory function,
Coordination and gait,
Reflexes
How is language assessed? (many)
Fluency/ spontaneity: look for paraphasic errors,
Comprehension: understand simple q's, commands,
Naming: common objects and parts,
Repetition: no ifs ands or buts,
Reading,
Writing,
Mechanics of speech,
Aphasias
What are 3 types of aphasias?
Global: difficult w/ naming, repetition, comprehension (dominant hemisphere cva?)

Broca's: difficult producing language, naming, intact comprehension (dominant frontal lobe) Broca's broken boca.

Wernicke: fluent, impaired comprehension, word salad (left temp lobe)
How is visual field tested other than the finger confrontation test?
Goldmann perimetry
What are 5 deficits that could be discovered with confrontation?
Anopsia: blindness (damage to optic nerve).
Hemianopsia: loss of half VF of one eye/ compression at chiasm.
Homonymous hemianopsia: temporal field loss on one side, nasal field in the other (optic tract, visual cortex).
Bitemporal hemianopsia: loss of temporal halves (optic chiasm compression).
Causes of visual field deficits?
Pituitary tumor,
Aneurysm,
Suprasellar mass,
Cortical blindness: bilateral occipital
What is the sensory function of the facial nerve?
Taste anterior 2/3 of tongue
What are the tests for motor function of facial nerve (looking for asymmetry)?
Smile,
Puff cheeks,
Clench eyes,
Wrinkle brow,
Control of facial movement: frontalis, orbicularis
4 ways to determine if a facial nerve lesion is central or peripheral?
1. if forehead (frontalis) spared, then central lesion.
2. If frontalis dysfunctional: peripheral.
3. UMN lesion: frontalis intact because of bilateral representation, but weak orbicularis oris.
4. LMN lesion (facial nerve injury): whole face involved (bell's palsy: idiopathy facial paresis).
2 ways to test cortical sensation?
Graphesthesia

Stereognosis
What are 4 ways to assess coordination and gait?
1.Coordination of skilled movements.
2. Rapid alternating movements: dysdiadochokinesia (abn).
3. finger nose finger, heel- shin: dysmetria, past pointing.
4. gait/ balance: Romberg, ataxia (truncal and appendicular)
What is dysdiadochokinesia?
Impaired ability to perform rapid alternating movements
What is dysmetria?
inability to properly direct or limit motions.
2 of what 3 senses need to be working for normal in Romberg?

Interp of the test?
Senses: vision, vestibular sense, proprioception.

If sway w/ eyes closed = + rhomberg.
If sway w/ eyes open and closed = negative.
What is the advantage and functions of CT?

Caution?
RAPID assessment of intracranial and extracranial injury.

Patterns of hemorrhage.
Bone windows for fractures.
Assoc findings: sphenoid fluid levels.
Ventricular size.

May be normal w/ ischemic stroke.
What are 3 major things a CT can indicate?
Infection

Vascular etiology

Neoplasm
What is the weight limit and gantry in MRI?
Weight: 350

Gantry: 60 cm
6 advantages of MRI over CT?
Anatomic detail.
Posterior fossa,.
Ischemia.
Demyelination.
Brain stem.
Surgical planning.
3 adverse reactions to angiography?
Related to contrast:
Warmth, flushing, pelvic warmth, metallic taste: normal responses.

Hives: give benadryl.

Resp distress: anaphylaxis.
Complications of angiography?
Blood vessel damage (hematoma, pseudo aneurysm, closure devices).

Bleeding.

Stroke in 0.5-2.3%
3 types of patterns of a cranium fracture?
Linear: force applied over wide surface area.

Satellite: mltpl bone fragments.

Comminuted: implies more kinetic energy.
What are tables of the skull?
layers of compact tissue in the cranial bones.
What is the best protection in a cranium fracture?
Dura
What should you look for in a basilar skull fracture?

S&S?
To see if fracture is through cribiform plate or petrous bone.
Usually distant from site of impact.

Raccoon eyes, battle sign, Hemotypanum (blood in middle ear), otorrhea/ rhinnorhea.
What is the thinnest part of the calvarium?

What should you be suspicious of in a fracture of this area?
Temporal bone.

Suspect: Epidural w/ injury to middle meningeal artery.
What is the scoring method used for assessing severity of brain injury?

What are the interpretations of points?
Glasgow coma scale.

Severe: <8
Mod: 9-12
Mild: 13-15
What are 4 characteristics of a concussion?
Transient loss of consciousness.

Retrograde amnesia often (memory before event).

Anterograde amnesia brief (unable to retain memory after event).

Post-concuss syndrome: weeks to months.
What is included in post-concussive syndrome?
HA,
Difficulty concentrating,
Poor memory,
Neuropsych testing.
What is the classic triphasic presentation of concussion?

4 other presenting symptoms?
Mild closed head injury.
Transient loss of consciousness.
Lucid interval.
Rapid neuro deterioration (uncal herniation).

HA, speech abnorm, visual complaint, focal weakness
What is a subdural hematoma?
Collection of blood between dura and skull.

Often due to traumatic injury to bridging veins and assoc w/ progressive neuro deficit.

Often seen in elderly.
2 major predispositions to subdural hematoma?
ETOH

Anticoags
S&S of a subdural hematoma? (6)
HA,
Focal deficit,
Contralateral hemiparesis,
Pronator drift,
Mental status may wax/ wane,
Seizures sometimes.
Definitions of acute subdural? subacute? chronic?
Acute: w/in 48 hrs post injury, rapid progressing sx, bright density on CT.

Subacute: 48 hrs-2 weeks. isodense.

Chronic: > 2 weeks. Burr holes to drain.
3 causes of a subarachnoid hemorrhage?
Trauma, aneurysm, arteriovenous malformation
Calculation for cerebral perfusion pressure (ccp)?
CCP = MAP - ICP
What is "compliance" in regards to ICP?

What is normal ICP?
Relationship between volume and change in ICP

Normal: 2-12 mm Hg
5 treatments for elevated ICP?
elevate HOB,
Hyperventilation,
Diuresis,
Barbituate coma,
Surgery.
Steroids?
Why would hyperventilation help decrease ICP?
Promotes vasoconstriction.
Aim for PCO2 25-30.

Refractory.
Avoid in first 24 hrs.

Controversial.
Indications for diuresis to relieve ICP?

What is used?
Indications: evidence of herniation,
progressive deterioration,
dependent on renal function.

Mannitol (.25-1gm/ kg)
What is an uncal herniation?
Medial temporal lobe gets compressed between brain stem and tentorial notch.

Exerts pressure on CN3 = dilated pupil

Contralateral hemiparesis
What is a cingulate herniation?
Supratentorial mass exerts pressure on ipsilateral hemisphere.

Edge of falx cerebri herniates.

Subfalcine.
What is a tonsillar hernia?
Acute expansion of posterior fossa lesion.

Medulla compressed by cerebellar tonsil.
What is a central hernia?
Mass lesion.

Downward displacement of diencephalons through incisura.

Generalized edema.
What is Todd's paralysis?
Transient neuro deficit.

AKA Post ictal paresis

Focal weakness in a part of the body after a seizure. Usually a hand, arm or leg. Usually unilateral and contralateral to sz focus. Mean duration 174 seconds.
3 types of seizures? (broad)
Focal,

Primary generalized (bilateral clinical and electrographic events w/out detectable focal onset),

Unclassified (neonatal seizures, infantile spasms)
5 types of primary generalized seizures?
Absence (petit mal),
Tonic-clonic (grand mal),
Tonic,
Atonic,
Myoclonic
2 types of focal seizures?
Without dyscognitive features,

With dyscognitive features (formerly CPS)
What is a focal seizure w/out dyscognitive features?
Consciousness not impaired.
Duration 5-30 seconds.
Types of focal seizures w/out dyscognitive features?
Motor: localized tonic or dystonic posturing or clonic jerking.

Somatosensory: localized tingling, flashing lights, unpleasant odor.

Autonomic: rising epigastric sensation, flushing, sweating, piloerection.

Psychic: cognitive - deja vu, unprecipitated fear.
What are focal seizures with dyscognitive features?
Consciousness is imparied or lost.
May include repetitive, automatic appearing movements or "automatisms"
Druation: 30-180 sec. begin as simple partial sz w/ impairment of consciousness at onset.
Characteristics of focal seizures wtih dyscognitive features?
Unable to respond to visual or verbal commands.
Impaired recollection or awareness of ictus (attack).
Often begins w/ aura.
Behaviors: lip smacking, chewing.
In motor: recruited area may enlarge resulting in a Jacksonian march.
Localized paresis may occur (todd's paralysis)
What is an absence (petit mal) sz?
Sudden, brief lapse in consciousness.
Arrest of activity w/ staring and minor motor activity (blinking).
No loss of postural control.
Begin in childhood.
Possible hundreds of x's a day.
Daydreaming.
60% spontaneously remit.
What is an atypical absence sz?
Lapse lasts longer.

More gradual onset.

Slower recovery.
What is a tonic-clonic grand mal sz?
10% of all sz.
Bilat stiffening followed by clonic contractions.
Duration 50-120 sec.
MC from metabolic abn.
Inital: tonic contraction.
Cries out & becomes cyanotic.
Tongue biting, secretions pool.
Cloic phase begins w/in 20 sec.
Post-ictal: unresponsiveness, flaccid, salivation, ha, fatigue.
What is an atonic sz?
Sudden loss of postural tone.

Usually w/ altered awareness.

Duration 5-30 sec.
What is a myoclonic sz?
Sudden, brief muscle contraction of body, typically both sides of body.

Duration < 1 sec.

Rash, gingival hyperplasia, hirsute.

Follows saturation kinetics.
What is status epilepticus?
Cont szs or repetitive, discrete szs w/ impaired consciousness in interictal period.

15-30 min.

MC neuro emergency.
Stages of brain abscess formation?
Day 1-3: entry, cerebritis, cerebral edema, loss of normal architecture/ structure of white matter (poorer blood supply vs gray). Focal vasculitis & thrombosis.

Day 10-13: Brain tissue liquifies, fibroblasts deposited and capsule formation occurs (takes ~ 2 wks).

Day 14: mature brain abscess: central region of pmns and necrotic material surrounded by inflam cells and fibroblasts, a collagen capsule, neurovascular layer and reactive astrocytes and edema.
4 possible causes of direct extension/ contiguous: paramengeal spread leading to brain abscess?
Paranasal sinuses (frontal)

Mastoid (air cells)

Middle ear (otitis media)

Dental manipulation
Causes of hematogenous spread of infection leading to brain abscess?
CHD w/ right to left or pulmonary a-v shunt.
Tetrology of fallot (congen defect).
Blood borne bacteria bypasses pulmonary capillary bed.
Focal areas of ischemia may occur due to shunting.
Clinical features of a brain abscess?
Expanding mass lesion, not infection presentation.

Cardinal sign: relentless/ progressive HA (constant, dull, aching, progressive).
Often followed by neuro deficit.
Fever in most (low grade).
N/V.
Lethargy, altered mental status,
sz.
meningismus.
What is vertebral osteomyelitis: spondylitis associated w/?
Infections of GU, soft tissue, upper resp tract (40%).
Predisposing factors of vertebral osteomyelitis: spondylitis?
IVDA,
DM,
Endocarditis,
Dialysis,
Trauma,
TB

Males>female
Most common site of vertebral osteomyelitis: spondylitis?

Then?
Lumbar (50%).

Thoracic (35%).

Cervical (6%).
Definition of meningitis?
Inflammatory dz of leptomeninges (pia, arachnoid, dura).
Classic triad of meningitis?
Fever

HA

Nuchal rigidity.

And altered mental status
How prevalent are sz in meningitis?
40%
Focal: d/t arterial ischemia or infarction, cortical venous thrombosis w/ hemorrhage, focal edema.
General or status: fever, hypona+, anoxia.
What is the rash of meningococcemia?
Diffuse erythematous maculopapular rash --> petichial.

Trunk, lower extremities, mucous membranes, conjunctiva, +/- soles and palms.
Signs of ICP in advanced meningitis?
Papilledema,
Dilated poorly reactive pupils,
CN 6 palsies,
Decerebrate posturing,
Cushing reflex: bradycardia, htn, irreg resp.
MCC meningitis in adults >20?
Strep pneumo
7 predisposing conditions to strep pneumo meningitis?
Pneumococcal pneumonia,
Acute/ chronic otitis media,
Alcoholism,
DM,
Splenectomy,
Basilar skull fx, rhinorrhea,
Complement deficiency
What is the MCC meningitis in kids 2-20?
N. Meningitidis.

Nasopharynx colonized (infection or carrier) - degree of invasive dz dependent on: host ability to produce ab and complement virulence factors of strain.
3 other causes of meningitis? Associations?
Enteric GNR: DM, cirrhosis, alcoholics.

Listeria: elderly, immunocompromised (transplant, preg, malig).

Staph aureus/ coag neg staph: post op.
A CT scan should be done prior to LP if ANY of the following are present: (6)
Immunocompromised state.
Hx of CNS dz.
New onset sz.
Papilledema.
Abnormal LOC.
Focal neurologic deficit.
Opening pressure, WBC, RBC, gluc, protein, culture findings in bacterial meningitis?
Opening pressure: >180 mmh20
WBC: >10.
RBC: absent.
Gluc: <40.
Protein: >45.
Culture pos: 80%
Focal or generalized S&S of compression, invasion or ICP?
HA (dull, constant, classic early AM ha is uncommon, worsens w/ change in position).
Nausea.
Sz.
Cognitive dysfunction.
Weakness.
Sensory loss.
Aphasia.
Visual spatial dysfunction.
Characteristics of benign primary brain tumors?
30-40% of all adult brain tumors.

Slow growth, lack of invasion of surrounding tissue.
Most common types of benign primary brain tumors? (3)
Meningioma

Pituitary adenoma

Vestibular schwannoma
How is a pituitary adenoma usually found?

What is classification based on?
Incidental finding. 10-20% of intracranial tumors.
Pathophys largely unknown.

Classification: hormones produced by tumor.
Distribution (classifications) of pituitary adenomas?
Prolactinoma 40%.
GH 12%.
ACTH 10%.
Lh FSH 6%.
TSH 2%.
Non-secretors: 30%.
Presentation of hyperprolactinemia from pituitary adenoma?
Males: loss of libido, impotence.

Females: amenorrhea, galactorrhea.

Elevated prolactin levels
Presentation of GH from pituitary adenoma?
Acromegaly: large brow, increasing size of nose, thick jaw, hands, feet.

HNT, cardiomyopathy, DM.
Presentation of cushings?
Excess cortisol or ACTH.

Moon faces, truncal obesity, striae, buffalo hump, hirsituism.
- DM, HTN, osteoporosis, cataracts, decerased life expectancy.
Presentation of hyperthyroidism?
Tachycardia, diaphoresis, weight loss.

HTN.
Presentation of hypopituitarism?
Non-secretors, can be fatal.
Clinical presentation of a pituitary adenoma in general?
Visual sx: bitemp hemianopsia (optic chiasm compression), homonymous hemianps (optic tract compression), loss of acuity, unilat atrophy: optic nerve compression.

HA: apoplexy: infarct, hemorrhage into gland, rapid deterioration, emerg!.

Incidental: asymptomatic during work up for unrelated process.
How is dx of a pituitary adenoma made?
Endocrine studies: TFT, prolactin, GH, LH, FSH, testosterone, Ig-F, cortisol.

Opthalmology eval: vf, acuity, fundoscopy.

MRI study of choice. Allows eval of vasculature.
What is the presenation of a vestibular schwannoma "acoustic neuroma"?
Unilat sensorineural hearing loss,
Progressive deficit,
Tinnitus,
Dizziness,
Dysequilibrium/ gait disturbance,
As expands, intern auditory meatus filled - compression of cochlear & facial nerves, brainstem and cerebellum.
sx: HA, ataxia, facial palsy, diplopia, dysphagia, facial numbness.
Clinical presenation of a glioma?
HA (55%).

Sz (23-56%)

Focal deficit

Duration of sx short (weeks)
3 grading levels of gliomas?
Astrocytoma,

Anaplastic astrocytoma,

Glioblastoma multiforme
What is the most common type of intracranial tumor (50% in adults)?
Metastatic brain tumor from somewhere else.

20-40% of pts w/ cancer develop brain mets.
Most common types of primary cancers that end up as brain mets in order of decreasing incidence?
Lung (squamous, adenocarcinoma, small cell, large cell).
Breast.
Unknown.
Melanoma.
colorectal.
Other.
When would you not treat metastatic brain tumors (natural hx)?
Poor prognosis regardless of tx.

Median survival of untreated = 1 month.

Usually fatal.
2 types of medical therapies for metastatic brain tumors?
Corticosteroids,

Chemo (generally not effective) :-(
How do corticosteroids treat metastatic brain tumors?
Reduce surrounding edema.
70% improve sx.
Max effect w/in 3-7 days.
Effect clinically noticable 6-24 hrs.
Median survival w/ steroid alone = 2 months.
Modes of radiation therapy for brain mets?

Complications?
WBRT (increases median survival to 3-6 mos).
Fractionate.
Stereotactic radiosurgery.

Comps: dementia, ataxia, incontinence.
What is the treatment of choice for brain mets?
Surgery w/ adjuvant XRT

Median survival: 40 wks w/ single brain met.

Craniotomy for bx, debulking, resection.
Interstitial brachytherapy: placement of radioactive implants. Allows delivery of high dose focal radiation w/ minimal risk to surrounding structures.
10 factors suggestive of a serious underlying disorder with headache?
Worst ever,
First severe,
Subacute worsening over days/ weeks,
Abn neuro exam,
Fever,
Vomiting preceding ha,
induced w/ bending, lifting, cough.
Present immed upon awakening, disturbs sleep,
Known systemic illness,
Onset > age 55
Characteristics of a tension-type headache?
Chronic,
Bilat tight/ band-like discomfort,
Head "in a vice"
Pain builds/ fluctuates in severity/ may last days,
Not exacerbated by exertion,
Episodic or chronic,
Common all ages,
Predom females
Characteristics of cluster ha?
1-3 short attacks of periorbital pain/ day > 4-8 weeks.
Followed by pain free ~ 1 yr.
+/- chronic pattern (no pain free interval),
Men >>women.
Onset age 20-50.
Lithium may help.
Clinical features of cluster ha?
Periorbital or temporal pain,
Begins w/out warning,
Crescendo w/in 5 min,
Excruciating and explosive,
Unilat usually on same side,
30 min-2 hrs,
Assoc sx: red eye, lacrimation, ptosis, nausea.
Provoked by etoh.
onset nocturnal 50% time.
Treatment of cluster ha?
Prophylaxis: prednisone 10 day course. Lithium.

Acute attack: O2 (9 L/min for 15 min)., sumatriptan (6 mg sc) shorten attack to 10-15 min.
Clinical features of a migraine without aura (common)?
No focal neuro disturbance precedes,
More freq type,
Mod/severe head pain,
Pulsating, unilateral,
Aggravated w/ walking upstairs,
N/V, photophobia, phonophobia
Clinical features of migraine w/ aura (classic)?
Premonitory sensory, motor, visual sx.
Focal neuro disturbance more common.
Without headache = migraine equivalents.
Complicated migraine = lasting deficit.

Most common aura is visual: scotoma or hallucinations.
Fortification specturm "C"
Triggers of migraines?
Red wine,
Menses,
hunger,
Sleep deprivation,
Glare,
Estrogen,
Anxiety,
Perfumes,
High altitude,
Exertion
Difference between dementia and delirium?
Dementia: loss of intellectual ability - interferes w/ ability to function at work or socially.

Delirium: acute onset, motor signs, slurred speech, altered LOC, metabolic abnormality
Treatable or somewhat treatable causes of dementia?
Neoplasm,
Normal pressure hydrocephalus,
Subdural hematoma,
Infection,
Metabolic derangement.
Features of Alzheimers?
Progresses over years.

Hallmark: loss of memory for facts and events (recent).

Personality changes (disengagement).

Cognitive dysfunction (word finding, anomia)
- functional impairment (motor apraxia - can't perform task asked to do)
- visual agnosia (can't recognize input)
Characteristics of Huntingtons?
Insidious intellectual deterioration.
Personality changes, emotional lability.
Dancing quality movements: deteriorates over 10-15 yrs to veg state.
High suicide rate.
Manifestations of personality changes in huntingtons?
Complaining constantly.
Nagging.
Suspicious, irritable.
Poor self control.
Begins subtle fidgeting hands and face: look fidgety, increased blinking, poor control of tongue.
Characteristics of Parkinsons?
Relentless, progressive - affects elderly. Unk etiology.

Disruption of norm dopaminergic- cholinergic balance d/t destruction of dopaminergic pathway and reduction in dopamine.
Pathology in parkinsons?
Loss of pigmented cells in substantia nigra.

Eosinophilic cystoplasmic inclusions = Lewy bodies
Presentation of Parkinsons?
Bradykinesia (slow initiation of movement).
Shuffling gait (festinating).
Postural instability.
Resting tremor (pill rolling) - +/- unilat, MC sx.
Rigidity of limbs,
Decreased facial expression,
Change in voice quality,
Often depressed,
Micrographia,
Decreased blink rate (5-10).
4 common comorbid probs w/ parkinsons?
Psychosis,

Hallucinations - visual,

Daytime sleepiness,

Fatigue
4 cardinal signs for dx of parkinsons?
Rest tremor.

Rigidity.

Akinesia (bradykinesia)

Gait disturbance.
What is multiple sclerosis?
Chronic condition - episodes of focal disorders of optic nerve, spinal cord and brain, which remit to a varying extent and recur over period of many yrs.
Pathophys of MS?
Lesions multiple in time and space.
Pathology is multifocal areas of demyelination w/ relative preservation of axons, loss of oligodendrocytes and astroglial scarring.
Demyelination process that affects CNS, not periph myelin.
MC autoimmune inflammatory demyelinating dz of CNS.
Demyelination impedes salutatory electrical conduction of impusles from one node of ranvier where Na channels are concentrated to next node.
Plaque formation (periventricular, subpial).
Characteristics of relapsing and remitting of MS?
In early stages, complete recovery after attack.

Onset usually subacute or acute (days).

85% of pts.

If progressive (secondary): may accumulate disability w/ each attack.
What is chronic primary progressive MS?
Steady decline in function w/out acute attacks.
5 main presentations of MS?
Unilateral loss of vision/ blurry vision.

Optic neuritis.

Acute myelitis.

Bladder incontinence.

Brainstem sx: diplopia, vertigo, dysarthria.
Characteristics of optic neuritis in MS?
25% initial sx.

Partial to total loss of vision over days.

Most recovery completely.
Characteristics of acute myelitis in MS?
Rapidly evolving paraparesis, ascending paresthesia, bilat Babinski signs.
Weakness or numbness of lumbs is inital sx in 50% of pts.
Gait disturbance.
Sx in one leg, but signs in both.
L'hermitte sign: flexion of neck produces tingling down shoulders and back. Increase sens of demyelinated axons to stretch or pressure on spinal cord.
What is ALS: amyotrophic lateral sclerosis (Lou Gehrig's dz)?
Dz of unk cause and pathogenesis.
Relentlessly progressive, presently incurable, neurodegen disorder that causes muscle weakness, disability and eventually death.

Most devastating of all neurdegen disorders.
What occurs with degeneration of the UMN in ALS (lou gehrigs)?
Weakness, hyperactive DTRs, clonus, Babinski, Hoffman's signs.

Degeneration of lateral corticospinal tracts (gliosis) = lateral sclerosis.
What occurs w/ degeneration of the LMN in ALS (lou gehrigs)?
Weakness, wasting, fasciculation.

Direct consequence of muscle denervation = amyotrophic
Clinical manifestations of ALS (lou gehrigs)? LOTS!!
Asymmetric limb weakness (MC presentation!)
Muscle weakness, atrophy, fasciculations.
Weakness legs hands prox arms oropharynx.
Slurred speech dysarthria dysphagia.
Bulbar sx: tongue pharyngeal laryngeal muscles.
Impaired gait - foot drop.
Weakness --> muscle cramps & wt loss.
Resp compromise.
LMN & UMN dysfct.
Fasciculations of tongue.
Destruction of anterior horn cells --> muscle wasting, fascic, denervation --> atrophy.
Cognitive fx affected.
Relentless & progressive course - no remis.
Death from resp failure.
What sx are almost pathognomonic for ALS (lou gehrigs)?
Hyperactive reflexes w/ Hoffman's sign in arms w/ weak, wasted fasciculating muscles.
What is usually NOT affected in ALS (lou gehrigs)?
Sensation
What is Guillain Barre?
Acute idiopathic inflammatory demyelinating polyneuropathy.

Sensory disturbance.

Progressive muscle weakness and areflexia.
Heterogeneous syndrome w/ several variant forms.
What is the MCC of acute flaccid paralysis in healthy people?
Guillain Barre
Associated conditions w/ Guillain Barre?
Antecedent resp tract or GI infection.

EBV, CMV, HSV, Lyme, H influenzae.
What is a syndrome that has be seen after receiving a vaccine?

Which vaccine? When?
Guillain Barre has been seen following swine influenza in 1976.
13 days post vaccine.
Clinical features of Guillain Barre?
Sx develop 2-4 weeks post infection.
Fine paresthesias of toes and fingertips.
Symmetrical lower extremity weakness.
Weakness ascends to arms, CNs (7).
Resp muscles +/- involved.
Sciatic pain +/-,
25% req mechanical vent.
Mild form: upper ext weakness, areflexive, gait difficulty.
Mod form: unable to walk alone.
What would you expect to see in severe Guillain Barre?
Ascending paralysis, may require vent.
What are the red flags of low back pain?
Change in bowel &/or bladder.
Unexplained wt loss.
Fever.
Night pain.
Loss of sensory &/or motor fx.
Hx of malignancy.
Acute trauma.
Characteristics of neurogenic claudication in lumbar spinal stenosis?
Pain worse w/ walking/ standing.
Pain relieved w/ sitting/ lying.
No trophic changes in ext.
Pulses intact.
Relief w/ waist flexion.
Pain (93%), Sensory (63%), weakness (43%)
What percentage of strokes = ischemic?

3 causes of ischemic stroke?
80%

Thrombosis

Embolism

Systemic hypo perfusion
What percentage of strokes = hemorrhage?

2 causes of hemorrhagic stroke?
20%

ICH

SAH
Characteristics of a TIA?
Caused by focal brain, spinal cord or retinal ischemia w/out acute infarction..
5-15 min. thought to be "warning" of imminent stroke.
Greatest risk for stroke w/in 3 weeks of TIA.
33% w/ TIA will have CVA w/in 3 yrs.
50-65% pts w/ thrombo CVA have hx of TIA.
Crescendo TIAs (2 or more w/in 24 hrs) = medical emergency!!
Mechanism of ischemic stroke?
Embolus from aortic arch, carotid bifruc, IC vessels.
Characteristics of intracerebral hemorrhage?
Mass effect results in neuro S&S.
Blood = toxic --> neuro dysfunction.
Localized hematoma spreads along white matter pathways.
30% - SAH (5% of all strokes) - 30,000/yr. 80% from aneurism rupture. Age 40-60. Women > men.
Etiologies of Intraparenchymal hemorrhage (other 70% of intracerebral hemorrhage)?
Long standing HTN.
Amyloid angiopathy.
Vascular malformations.
Coagulopathies.
Tumors.
Vasculitis.
Drugs abuse (cocaine).
Typical locations of intraprenchymal hemorrhage?
Basal ganglia,

Thalamus,

Pons,

Cerebellum
What occurs in amyloid angiopathy --> intraparenchymal hemorrhage?
Lobar hemorrhages.

Degen disorder affecting media of small arteries.
What types of vascular malformations can cause intraparenchymal hemorrhage?
ACMs (arterio venous malformation).

Dural AV fistulas.

Cavernous malformations.
10 hypercoaguable disorders?
Venous sinus thrombosis of small cortical veins/ sagittal sinus.
Polycythemia.
Factor V leiden mutation.
Protein S def.
Homocysteinemia.
Protein C def.
AT III def.
Antiphospholipid syndrome.
Sickle cell anemia.
OCPs.
What is factor V leiden mutation?
Resistance to activated protein C
Causes of venous sinus thrombosis of small cortical veins/ sagittal sinus?
Comp of pregnancy, post partum.

Sepsis.

Brain abscess/ meningitis.
Risk factors of stroke?
DM.
HTN.
Smoking.
Dyslipidemia.
Afib.
Obestiy.
OCPs.
Hormone therapy.
Phys inactivity.
Dietary factors.
ETOH abuse.
Drug abuse.
Clinical presentation of storke?
ABRUPT onset - focal neuro deficit.
Often don't seek med attn: no pain and may not realize deficit.
Most present via EMS.
Syndromes of ischemia.
Pts at risk should be counseled to seek aid if they have sudden onset of what 3 things?
Loss of sensory/ motor function of 1/2 the body.

Change in vision, gait, ability to speak or understand.

Sudden, severe HA.
2 major areas of ischemia?
Carotid territory

Middle cerebral artery
What occurs if ischemia is in carotid territory?
Amaurosis fugax: transient monocular blindness d/t central retinal artery ischemia (branch of opthalmic and ultimately internal carotid.).
May visualize Hollenhorst plaques (embolic particles) in retinal artery branches.

Transient aphasia.
Motor/ sensory deficit in single extremity. (bear paw clumsy)
What occurs if ischemia is in middle cerebral artery?
Contralateral weakness, sensory loss, homonymous hemianopsia.

If dominant hemisphere: language affected.

If non-dominant: spatial orientation affected.
Describe how ASA functions as an anti-platelet agent.
It interferes w/ plt function by inhibiting enzyme COX-1 which catalyzes the synth of thromboxane A2.

Inhibits platelet aggregation.
Interferes w/ formation of thrombi and atherosclerotic plaque.
Prostacyclin is inhibited (transient effect) - a vasodilator and anti aggregating agent.
For patients w/ acute ischmic stroke who are not taking thrombolytics, how much ASA is recommended?
80-1300 mg/ day.

Most recommend 325 mg q day.
Adverse effects of ASA?
Dyspepsia,
Nausea,
Abd pain,
Rash,
PUD
Gastritis,
GI bleed.
How does Clopidogrel (Plavix) inhibit platelet aggregation?

Recommended dose?
Binds ADP receptors on plt surface and inhibits aggregation.

75 mg daily
Adverse effects of Clopidogrel?
TTP,
Diarrhea,
Rash,
Thrombocytopenia
Recommended prophylaxis for pts w/ chronic AFib, age >65 w/ risk factors of HTN, poor LVEF, DM?
Coumadin w/ INR 2-3
Would you give treatment tto pts w/ chronic AFib age < 60, no prior stroke, normal ekg, no htn, no DM?
No. No coagulation required.
Contraindications for thrombolytic therapy?
Sustained BP >185/110.
Platelets <100, hct <25.
Gluc: <50, >400.
Coagulopathy.
Rapidly improving sx.
Major surgury w/in 2 wks.
GI bleed in last 3 wks.
Recent MI.
Coma.
Actions to take for prevention of stroke?
Eval risks.
Control HTN.
Tx hypercholesterolemia.
Statins.
Smoking cessation.
Wt loss.
Proper nutrition.
Antiplatelet therapy.
Angiocoagulation.
Best ways to control HTN in prevention of stroke?
Hope Trial Heart Outcomes Prevention Evaluation.

Suggest ACE may prevent stroke to some degree.

SBP <130-140.
Cholesterol level goals for prevention of stroke?
LDL < 100.

HDL > 35

TG < 200
Antiplatelet therapy to prevent stroke?
Aspirin (50-325 mg daily): recommended for pts w/ noncardioembolic stroke or TIA of atherothrombotic, lacunar or cryptogenic type. Risk reduction 22%.

Plavix: inhibits cascade of glycoprotein IIb/IIIa which ultimately prevents fibrinogen binding and plt aggregation.
Who would you give coumadin to to prevent stroke?
Chronic AFib

Pts w/ previous stroke.

Recent MI, LVEF dysfunction, valvular dz/ prosthetics.
Sites of intracranial aneurisms and SAH?
Arise at branching site of vessels
Point of maximal stress.

Anterior circ = 85% (anterior communicating, posterior communicating and internal carotid, middle cerebral).

Posterior circ = 15% (apex of basilar, vertebral/ PICA).
Clinical presentation of intracranial aneurisms and SAH?
Sentinel bleed, warning leak.
SUDDEN ONSET OF SEVERE HA - WORSE HA OF LIFE!
(blood released into CSF under arterial pressure - rapid increase in ICP).
N/V, photophobia, nuchal rigidity.
Neck pain, sz, altered mental status.
Sentinel HA at initial minor leaking from aneurism.
HTN.
What does the clinical presentation of intracranial aneurisms and SAH depend upon?
Location and extent of hemorrhage.
Sx of "sentinel headache" from initial minor leaking of blood from aneurism?
HA,
Stiff neck,
N/V,
Syncope,
Visual

Occurs in 10-43% pts.
How common is SAH misdiagnosed?
25%!!!!!!!!!!!!!!
What can be an acute trigger for SAH?
Physical exertion.
Clinical presentation of AVMs?
Hemorrhage,
Sz,
HA,
Neuro deficit.
What would you see in hemorrhage in AVM?
Occurs in 39-53%.
Intraparenchymal or SAH.
Usually venous rupture.
Smaller AVMs more likely to hemorrhage.
Mortality rate for initial bleed 10-18%.
23% rebleed.
Steal phenomenon may occur.
Hemorrhage can cause mass effect, direct compression, decreased perfusion and ischemia-infarct.
What would you see in sz in AVM?
Occurs in 36-53%

Focal or generalized.

EEG often norm.
What would you see in HA w/ AVM?
Occurs in 52%.

Severe and sudden onset.

Secondary to increased ICP or large draining veins which stretch dura, vascular dialtion.
What would you see in neuro deficits w/ AVM?
Often transient.

Depends on location of lesion.
Treatment options of AVM?
Expectant.
Embolize.
Surgical resection.
Radiosurgery.
Combo therapy.
Goal - total obliteration of lesion.