Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Neuro review 2

Head trauma, disoriented => lucid => coma Epidural Hematoma
Lens shaped hemorrhage Epidural Hematoma
Concave shped hemorrhage Subdural Hematoma
Unilateral facial weakness w/ inability to close eye Bell palsy (self-limiting)
Adolescent female w/ HA. +FHx. Severe HA, N/V, photphobia. +/- auras (usu contra to HA) Migraine HA
Male, recurrent relapsing HA. Worsened w/ EtOH, Lacrimation, salivation, rhinorrhea Cluster HA
Sudden onset thunderclap HA, "worse HA of my life" Subarachnoid hemorrhage
>50 yo female w/ HA. Temporal artery tenderness or blindness Temporal arteritis (Giant cell arteritis). Elevated ESR, get temporal artery biopsy
Recurrent episodes of vision change, diplopia, weakness & tingling in extremities that resolve MS
HA worse in AM w/ focal neuro deficits Brain Tumor (MC is glioma)
s/p Fall w/ bilateral LE weakness, urinary and rectal incontinence, decreased rectal tone Cauda equine syndrome = neurosurgical consult
Ascending paralysis GBS
Paralysis after Campylobacter enteritis GBS
Young kid with difficulty standing from seated position. Calf muscle wasting Muscular dystrophy (weakness begins at pelvic girdle)
Pediatric with fever or Hx URI with encephalopathy, emesis, hyperactive reflexes, hepatomegaly, elevated liver enzymes Reye's syndrome from URI/post-flu or aspirin use
"Ash leaf" hypopigmentation of trunk & Ext, shagreen patch, sebaceous adenomas, seizures, mental retardation; assoc w/ PCK, renal hemartomas Tuberous sclerosis (auto dominant)
Ortho BP defn drop of 20 (SBP) or 10 (DBP) within 3 min of standing
fluctuating weakness/fatigability of voluntary mx (diplopia, blurry vision, ptosis, difficulty swallowing); resp difficulty, limb weakness (worsened w/activity); bulbar sxs (dysarthria, dysphagia, fatigable chewing) Myasthenia gravis
Light touch: Side of Neck: C2-3
Light touch: Tip of Shoulder: C4
Light touch: Lateral Deltoid: C5
Light touch: Thumb: C6
Light touch: Middle Finger: C7
Light touch: Pinky Finger: C8
Light touch: Medial Forearm at elbow: T1
Light touch: 1st Dorsal web: Radial nerve
Light touch: Palmar middle pad: Median
Light touch: Palmar small pad: Ulna
Light touch: Groin: L1
Light touch: Upper thigh: L2
Light touch: Outer thigh at knee: L3
Light touch: Medial ankle: L4
Light touch: Dorsal 1st web space: L5
Light touch: Lateral ankle: S1
Light touch: Buttock: L2-3
Light touch: Perianal: L4
DTR: Biceps: C5
DTR: Brachioradialis: C6
DTR: Triceps: C7
DTR: Knee: L 3,4
DTR: Ankle: S1
DTR: 0: absent
DTR: 1: diminished
DTR: 2: average
DTR: 3: exaggerated
DTR: 4: clonus
Ischemic stroke pathophys atheroembolic (50%); cardioembolic (30%); OR 2/3 thrombotic & 1/3 embolic
Stroke pathophys 80% ischemic, 20% hemorrhagic
Hemorrhagic stroke pathophys parenchymal ICH (10-15%); subarachnoid (5-10%)
Most common parenchymal ICH: Hpertensive intracerebral hemorrhage
Primary ICH presentation HA, N/V; progressive hemiparesis & hemisensory def; HTN (on hx and on PE)
Primary hypertensive ICH: typical locations Thalamus; Basal Ganglia; Pons; Cerebellum
ICH presentation: Thalamus/ Basal Ganglia Contralateral Motor/ Sensory Deficit; Aphasia, Neglect; Depressed LOC with mass effect, IVC extension
ICH presentation: Cerebellum Ipsilateral Ataxia; Depressed LOC
ICH presentation: Pons Vertigo, Diplopia; Crossed signs; Depressed LOC
Anterior circulation consists of: Ant choroidal, ant cerebral, MCA
Anterior circulation supplies: Cortex, subcortical white matter, basal ganglia, internal capsule
Anterior circulation stroke Hemispheric s/s: aphasia, apraxia, hemiparesis, hemisensory loss, visual field defects
Posterior circulation consists of: Verterbral & basilar arteries
Posterior circulation supplies: Brain stem, cerebellum, thalamus, parts of temporal & occipital lobes
Posterior circulation stroke Sxs of brainstem dysfn: coma, drop attacks, vertigo, N/V, ataxia
Thrombotic vs embolic stroke sx progression Thrombotic: stepwise progression, often preceded by TIA; Embolic: abrupt & without warning
Amyloid angiopathy stroke: patho Blood vessel degeneration; Dementia; Lobar hemorrhage
Amyloid angiopathy: presentation Dementia; Episodic worsening; No h/ o HTN; poss acute limb weakness; BP less severe than in ICH; stroke d/t cerebral microhemorrhages
Venous infarction presentation h/o OCP/SMK; HA; aphasia, weakness
Most common cause of subarachnoid bleed aneurysm
Subarachnoid bleed: RF HTN; SMK; heavy EtOH; genetics (polycystic kidney dz; Ehlers-Danlos; 1st-degree relative)
SAH stroke presentation Abrupt severe HA; meningismus; depressed LOC; nonfocal neuro exam; BP rises precipitously; poss temp to 39C
Atheroembolic stroke characterized by: Single vascular territory; Warning signs; Stepwise progression
Atheroembolic stroke presentation Hx HTN, CAD; transient language disturbance; transient weakness
Ant cerebral art infarct: likely fx: contralateral leg (motor > sensory)
MCA infarct: likely fx: face/arm more than leg/vision; poss aphasia
Vertebrobasilar art infarct: fx: Midbrain: 3d nerve nuclei; ipsilateral ptosis; eye deviated outward (bc CN VI is fine, but III is affected); crossed signs: pt has CNIII probs on one side and sensory probs on opp side of body
Subcortical infarct effects by body area: face = arms = legs
Cortical infarct fx by body area: gradation btw face, arms, & legs
Lacunar syndromes Pure Motor Stroke; Pure Sensory Stroke; Ataxic Hemiparesis; Clumsy Hand Dysarthria
Cardioembolic stroke presentation h/o A fib; aphasia; hemiparesis/hemisensory deficit affecting face and arm
Cardioembolic: dx Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface)
Cardioembolic: possible etiology A fib; Cardiomyopathy; Acute MI; Valvular heart dz
TIA S/S Acute focal neuro def; S/S resolve within 24 hr; No rad evidence of infarction; Ischemic etiology, usu carotid or vertebral vascular distn
TIA: risk of subsequent stroke: 11% risk of stroke within 3 mo; 1/3 of TIAs have stroke within 5 yrs; 63% of strokes occur within the first wk, 85% within first month
Modifiable RF for first stroke *HTN*; A fib; carotid stenosis; DM; hyperlipidemia; prior stroke/TIA
Prevention of A fib RF: Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin
Stroke prevention DM pts glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins
TIA carotid: S/S contralat hand-arm weak & sensory def; ipsilateral visual sx & aphasia or amaurosis fugax; poss carotid bruit (absent in high grade stenosis)
TIA vertebrobasilar S/S diplopia, ataxia, vertigo, dysarthria, CN palsies, LE weak, blurred vision, perioral numbness, poss drop attacks
TIA DDx Sz, migraine, syncope, hypoglycemia, mass lesion
SAH etio: aneurysm nontraumatic: 75% saccular (berry) aneurysm, 50% mort; 5th-6th decade, M=F
aneurysm RFs SMK, HTN, high chol; PKD, coarct
complex partial sz may have aura, then impaired consciousness
simple partial sz has no: impairment of consciousness
Most common cause of tonic-clonic in pts (onset < 30 yo): idiopathic epilepsy
Clonic seizures: usu in childhood; impaired consciousness, followed by asymmetric bilateral jerking
Most common seizure type: complex partial
complex partial sz: 10-30 yo; common post-head trauma; 50% abnml CT/MRI; 50% mesial temporal sclerosis; 20% hamartoma
complex partial sz: etio by age 30-60 yo: poss brain tumor; >60 yo: more likely stroke
Status epilepticus dx does not apply to: continuous simple partial seizures
EtOH withdrawal seizure: onset 6-48 hr after last drink; often primary generalized, often have Todd paralysis
Sz remission: usu within 3 yrs of first seizure; prolonged remission in 60% of such pts
Factors against sz remission FH; psych comorbid; febrile seizure hx; more seizures; age
Todd paralysis = post-ictal focal weakness in part of body, confined to L or R, usu arms/legs
Most common agent of meningitis in adults S. pneumo
Meningitis general S/S HA, fever, neck / back stiffness, neuro impairment
Meningitis presentation acute (hrs - days), usu w/ fever, HA, stiff neck, lethargy; usu without focal sx
Typical purulent meningitis orgs N. meningitidis, S. pneumoniae, or H. influenzae
Chronic meningitis: orgs TB; fungal
Encephalitis presentation diffuse infxn; confusion, lethargy, often seizures; CSF may be normal
N. meningitidis petechial rash; GN diplococci; often assoc w/DIC
H flu meningitis: commonly found: less common in adults; in setting of otitis or sinusitis
Tuberculous meningitis S/S usu gradual onset; listlessness & irritability; CN palsies;
Abscess: common orgs streptococcus, staphylococcus or anaerobes
Rabies S/S (> 10 days) delirium, painful swallowing, rage alternating with calm
Rabies incubation period >10 days (usu 3-7 wks) (infected animal dies within 5-7 days)
Herpes encephalitis: commonly found: more common in elderly; often medial temporal lobes
CJD S/S usu later in life; rapidly progressive dementia, myoclonus, ataxia & somnolence; epileptiform pattern on EEG
MS S/S Optic neuritis; Transverse myelitis; Paresthesias; focal neuralgia; Ataxia; Weakness/ incoordination; Spasticity; Cognitive impairment
Lhermitte's sign = electrical sensation down body w/ neck flexion; seen in MS
MS pathophys immuno d/o assoc w/CNS Ig prodn & T-lymph alteration; poss viral etio
MS pattern of sxs affect multiple areas over time (if they don't, prob not MS)
Anti Epileptic Drugs: titration Start low & gradually increase; initiate with 1/3-1/4 of anticipated maintenance dose & increase over 3-4 weeks
when Anti Epileptic Drugs may be dc'd: If onset btw age 2-35 & normal EEG; seizure-free period 2-4 yrs; complete ctrl within 1 yr; very gradual taper over 6 mos; relapse usu within first few mos after withdrawal; f/u in 5 yrs if no probs
Majority of malignant gliomas are: grade IV tumors (GBM or gliosarcomas)
Gliomas include: Astro (Grade 1); oligo (2); ependymoma; glial cells
Grade 3 Glioma = Anaplastic Astrocytomas, Anaplastic Oligodendrogliomas
Grade 4 Glioma = GBM; Gliosarcoma
Diffuse astrocytomas include: Low-grade infiltrative Astro (WHO II); anaplastic astro (WHO III); Glioblastoma (WHO IV)
Circumscribed astrocytomas include: Pilocytic Astro (WHO grade I); Pleomorphic xanthoastrocytoma (PXA); Subependymal giant cell Astro (SEGA)
Well-differentiated Astro: 10-15% of Astros; 35 yo; 5-10 yr surviv; cerebral hemi / cortex; slow growing; often undergo malig progression to AA or GBM
characteristic of high-grade gliomas (III/IV): Invasion via white matter tracts, cross via corpus callosum
Primary characteristic of a grade IV glioma = necrosis with vascular proliferation
Anaplastic astro High-Grade; 1/3 of Astros; 45 yo; 3 yr surviv; usu in cerebral white matter; relatively fast-growing; Frequent progression to GBM
GBM usu in cerebral hemi white matter; spreads rapidly & diffusely; Ring of tissue around necrotic core; Highly vascular
Oligodendroglioma Usu presents at low-grade (II) stage; young / middle-aged; grade II >10 yr surviv; Fried-egg cells
Most common primary brain neoplasm = GBM
Untreated GBMs: growth double in size in 14 days
Brain tumor: genl clin presentation HA; seizures; Cognitive dysfn; Focal neuro deficits; N/V; Sx endocrine dysfn; Visual sx; Sx from plateau waves (ICP changes)
Headache in brain tumor 20% of pts present w/HA (more w/ post fossa tumor); usu d/t inc ICP; Progressive increase in HA freq & severity; Classic HA on waking or HA that wakens one from sleep
Seizure in brain tumor 35% of pts present with this; often the sx that precedes dx; focal or secondarily generalized
Probably most common problem in pts w/brain tumors = cognitive dysfn (Frontal personality; Memory problem; Depression)
Cognitive dysfn: Left hemispheric tumors: language dysfunction
Cognitive dysfn: Right hemispheric tumors: problems with visual perception & scanning
Brain tumor: Focal neurologic deficits Hemiplegia; Hemiparesis; Ataxia; Nystagmus; Can mimic stroke
Brain tumor: N/V more common in: posterior fossa tumors
Endocrine sxs in brain tumor: hypothyroid; dec libido
Visual symptoms in brain tumor include: Contralateral flashing lights; Visual field loss; Diplopia
Low grade glioma: Tx Bx (confirm dx & r/o high grade); seizures only: defer tx til progresses; if progressive sx: resect +/- CTx (+ RTx only if refractory)
Second leading COD in brain tumor pts: thromboembolic complications
Meningioma slow growing, benign; attached to dura mater; 13-26% of primary IC tumors; RF: prior radiation; often Asx; visual complications; DDx: neurofibromatosis; Firstline tx: Surgery
Ependymoma: worse prognosis: <3 yo
Ependymomas within brain: locations Infratentorial > supratentorial (2:1)
Ependymoma Usu slow growing; kids & YA; young adults; 4% all BT; from walls of ventricles or spinal canal (obstructive hydrocephalus); 90% are in brain, 10% in spinal cord (often adults)
Characteristics of Medulloblastoma Malig, invasive embryonal cerebellar tumor; kids & YA; 70-80% 5-yr survival; Most arise in vermis (4th ventricle involvement)
Medulloblastoma: metastases Metastasize via CSF pathways (Drop Mets); Rare mets to bone, lymph nodes, other extracranial sites
Characteristics of Primary CNS lymphomas Usu present deep in brain parenchyma; usu multifocal (diffuse lg cell B-cell lymphoma); Survival w/o tx <1 yr; Steroid tx & Methotrexate CTx
most common spinal tumor: ependymomas; 10% of spinal tumors are intramedullary
Brain tumor: frontal lobe: S/S: cog decline; contralat grasp reflex; expressive aphasia
Brain tumor: temporal lobe: S/S: sz, olfactory hallucination, depersonalization, vis field def, auditory illusions
Brain tumor: parietal lobe: S/S: contralat sensory def; cortical sens loss (stereognosis); inattention
Brain tumor: occipital lobe: S/S: crossed homonymous hemianopia / partial field defect; visual agnosia
Brain tumor: brain stem/cerebellar: S/S: CN palsies, ataxia, incoordination, nystagmus, pyramidal & sensory def
Lucid interval seen in what trauma? epidural hematoma
subdural hematoma: blood source usu venous (bridging veins in space)
subdural hematoma: etiology Acceleration/ Deceleration injury; Veins transversing subdural space
Orbital blowout fx comminuted floor fx: herniated orbital contents; inf rectus mx entrap or vert diplopia d/t edema; blood in max sinus when orbital trauma
2/3 of all cerebral infarcts are: MCA stroke
Lacunar stroke 15-20% of strokes; small vessel ischemia; HTN; usually pure sensory OR motor
Astrocytoma Glial tumors: 40-50% of CNS Neoplasms
Astrocytoma: Grade IV GBM (45-55 yo); necrosis/ hemorrhage, edema, ring enhancement
Meningioma 50-60 yo; may increase in PG; various grades (90% benign)
Brain neoplasm: mets 1/3 of all intracranial neoplasms; lung, breast, melanoma, colon, lymphoma, prostate
Brain neoplasm: most common site for kids (unlike adults) posterior fossa (medulloblastoma)
Argyll Robertson pupil = pupil reacts to light but does not accommodate (seen in tertiary syphilia/tabes dorsalis)
NPH (chronic hydrocephalus) S/S: Incontinence, gait abnormalities, dementia
Ulnar neuropathy stretch / compress ulnar n.; cubital tunnel or Guyon canal; d/t pressure, bone spurs, cysts; sensory precede motor sx
Ulnar neuropathy: provoking factors Elbow Flexion (Cubital), Wrist Extension (Guyon); Nighttime
Radial neuropathy: etiology axilla (crutches); Saturday night palsy; handcuffs; humerus fx
Radial neuropathy: S/S Motor>sensory; weakness in extension & arm ext rotation; forearm atrophy; xray shoulder/humerus
Meralgia paresthetica: S/S pain, paresthesia, numb; outer thigh; usu unilateral (relieved by sitting); no motor sx
Fem neuropathy: RF lithotomy posn (inguinal lig); DM; retroperitoneal neoplasm/hematoma; pelvic fx; fem art cath (n. trauma)
Fem neuropathy: S/S Quads atrophy/weakness; sensory impairment anteromedian thigh; decreased patellar DTR; EMG/NCS; CT/MRI
Sciatic n. palsy: S/S weakness w/ leg flexion, dorsiflexion & foot eversion (drop foot); hamstring & ankle DTR dec/absent; sensory loss posterior thigh/leg/foot; tingling/burning/lanceting pain (worse w/standing, cough)
Peroneal n. palsy: S/S weak dorsiflexion (foot drop) & eversion; sensory loss/ paresthesia: anterolateral calf & foot dorsum
CN VII palsy (Bell): etiology idio; HIV, sarcoid, Lyme, tumor; HSV infxn? RF = PG, DM
CN VII palsy: S/S abrupt; facial paralysis (some upper sparing); drooping corner of mouth; ptosis/ forehead smooths out; ear pain; dysgeusia; hyperacusis
CN VII palsy: to distinguish btw peripheral & central lesion: peripheral: complete paralysis forehead mx; central: partial sparing forehead mx
CN VII palsy: prognosis 60% spont resolve; 10% perm disfigurement/dysfn; best indicator of severity = progress first 2-3 days; worst: complete palsy at onset, advanced age, hyperacusis, severe initial pain
Charcot-Marie-Tooth: genetics usually auto dom
Charcot-Marie-Tooth: patho Type I: demyelinating; II: axonal; Motor>Sensory; Lower > Upper; childhood/young; slow progression
Charcot-Marie-Tooth: CMT I vs CMT II: S/S CMT II: less mx wasting/ secondary weakness; less common postural tremor/arm involvement; NO peripheral n. hypertrophy
Dejerine-Sottas Dz (CMT III): pathophys phytanic acid disturbance; prog demyelinating neuropathy; infancy/kids
Dejerine-Sottas Dz: S/S weakness, ataxia; sensory loss; DTR: global hyporeflexia
Refsum dz: patho Progressive demyelinating neuropathy; early childhood
Refsum dz: S/S weakness, ataxia; sensory loss; DTR: global hyporeflexia; retinitis pigmentosa; Tx supportive
Systemic-metabolic neuropathies include: DM; uremia; alcoholic & nutrition def; paraproteinemias; CTD, amyloidosis
DM neuropathy sensory precedes motor; lower ext precedes upper; Hx: autonomic sx?; NCS nml / mildly slow
Charcot arthropathy 2/2 Joint Subluxation, Periarticular fx; rocker bottom foot; pain, swelling, ulceration
Uremia: S/S Symmetric sensory-motor; lower ext > upper; distal > proximal; severity correlates with degree of renal insufficiency
Neuropathy: EtOH/ Nutritional deficiency cobalamin (B12) def; axonal > myelin; slow progression
EtOH/Nutritional deficiency: S/S Distal symmetric Polyneuropathy; sensory precedes motor; Lower ext precedes upper; cramps, painful paresthesias, tenderness; CNS Sx often precede PNS; mental status change; myelopathy; optic neuropathy
AIDP (GBS): patho Progressive Demyelinating; prob immune-mediated; Axonal Subtypes (AMAN; AMSAN)
AIDP (GBS): Motor S/S Ascending weakness; Symmetric; Proximal > Distal mx; Lower ext before Upper; Advanced: Resp mx Compromise, CN Involvement
AIDP (GBS): Sensory S/S Pain/paresthesias; Loss of Sensation; Distal before Proximal; DTR: Global hyporeflexia or areflexia; autonomic dysfn: tachycardia, cardiac irreg; BP changes, pulmonary dysfn, loss of rectal tone
Leprosy: 2 Types: tuberculoid (multifocal) & lepromatous (symmetrical)
MG pathophys Abs vs acetylcholine receptors
LEMS pathophys: defective release of Ach in response to nerve impulse; may be assoc with small cell ca
MG vs LEMS: S/S LEMS: power increases w/sustained contraction; MG: fatigability
Ataxic (intention) tremor Absent at rest/start of movement; dysmetria; Dz of cerebellum / connections (MS; tumors; infarct; ethanol-induced cerebellar degeneration)
Athetosis = slow writhing purposeless movements usu involving hands, tongue & face; usu in kids w/ cerebral palsy or result of kernicterus or hypoxia
Chorea: Sx Involuntary, irregular jerky movements; can cause continuous movements.
Chorea: may be due to: untreated strep infxn (Sydenham chorea), PG (chorea gravidarum) or Huntington dz
Tics onset 2-13 yo; tx Haldol/pimozide
Hemiballismus Violent flinging movements; Unilateral hemiballismus usu d/t infarct in contralateral subthalamic nucleus of Luys
Dystonia: Maintenance of a persistent extreme posture in one or more joints.
Focal dystonias: torticollis, writer's cramp, blepharospasm; tx Botox / surg
Parkinson dz: Sx Rest tremor/3-6 hz; pill rolling; cogwheeling; rigidity; bradykinesia; difficulty initiating movement; masked facies; stooped posture, shuffling; disturbance of postural reflexes; diminished eye blinking rate
Parkinson dz: Patho Degen nigrostriatal pathway, raphe nuclei, locus ceruleus & motor nucleus of vagus; dramatic loss of DA-containing neurons
Huntington Dz presentation AD, varying age of onset; Sx often begin w/ psych disorder (immaturity, impulsivity, depression); later apathy & dementia; Chorea, Athetosis; butterfly ventricles (caudate atrophy)
Huntington chorea due to: DA excess state
Wilson dz Auto rec; onset 2nd-3rd decades; first sx: hepatic dysfn/cirrhosis; tremor/ bradykinesia, dysarthria, dysphagia; limbs rigid, facial mx fixed empty smile; arms: wing-beating tremor; Kayser-Fleischer (deep cornea)
Wilson: patho CNS changes: brownish discoloration of some basal ganglia; proliferation of protoplasmic astrocytes (Alzheimer Type II cells)
Tardive dyskinesia: Sx Abnormal BLM (tongue thrusting & chewing); head movements (turning & bobbing); poss also abnormal limb movements; Sx can fluctuate & may take mos-yrs to resolve (sometimes permanent)
Tardive dyskinesia: most successful tx: achieved with DA-depleting agents (tetrabenazine); also Vitamin E?
Action of acetylcholine & DA: Act in opposite directions; adding DA is equivalent to blocking acetylcholine
Huntington dz genetics Huntingtin gene is on short arm of chromosome 4; >35 CAG trinucleotide repeats = penetrance/affected/dz
RLS can be primary, or secondary to: periph neuropathy, uremia, PG, Fe def
Migraine dx criteria ≥2 of: (Unilateral; Pulsating; Mod/ severe intensity; fx: avoidance of routine physical activity); 1 of: (N/V; Photophobia & phonophobia)
Severe episodic HA with cerebellar sx = basilar migraine
Chronic migraine: dx chronic daily HA ≥3 months; >8 d/mo x 3 mos
Sinus HA vs migraine sinus usu continuous (not intermittent); TTP over sinuses; tx w/ Abx
chronic daily HA ≥ 15 d/mo; primary or secondary (usu considered primary); ≥1 migraine/wk = RF for dev chronic daily HA
SUNCT = Short-lasting; Unilateral; Neuralgiform HA, with Conjunctival injection & Tearing; rare; M>F (>50 yo)
SUNCT sx burning, stabbing, throbbing; seconds to 4 min; 5-6 per hr; SBP may rise
Cluster HA = M>F (older than migraine); severe, unilateral, nasal congestion, injected conjunctiva, ipsilateral sweating; at night (wakes pt)
HA red flags (SNOOP) Systemic sx; secondary RF; neuro sx; onset sudden; older pt; Progression/prior HA hx; Pattern changes
Sumatriptan: indications migraine (abortive tx); acute tx cluster HA; Fast onset, short duration; repeat dose in 1 hr if nec; Never give IV or IM
Ergotamine MOA direct sm mx vasoconstrictor
Beta blockers: MOA: central/serotonergic, beta-1 mediated
Migraine: prophylaxis Beta (50-60% efficacy); TCA; SSRIs; bupropion; Valpro; verapamil; NSAIDs (ST for predictable)
Prophylactic tx: adequate trial of tx: 6-8 weeks
Menstrual migraine: Tx NSAIDs: begin 2-7 days prior to menses, continue through last day of flow; Hormonal therapy (OCP)
TCA MOA antagonism of vascular or brainstem 5-HT2
concomitant dysphasia, hemianopia, or focal epilepsy is a __ lesion supratentorial
brain tumors seldom__ metastasize outside the CNS
__ spread the soonest with metastatic brain tumors lung and renal cancer cells
mets to the brain in men generally come from __ lung, colon, and renal cancers
mets to the brain in women generally come from __ breast, lung, and melanoma
epilepsy that has failed two medications is medically intractable epilepsy
to reduce risk of damaging language and memory, patients can undergo a __ test before neurosurgery WADA
Subarachnoid hemorrhage may block __ causing hydrocephalus arachnoid villi
T or F: diplopia, syncope, dizziness, vertigo, and paresthesia are symptoms of carotid disease false
Cause of Amurosis Fugax embolization of retinal arteries
a tumor in the supratentorial region may result in which pathologic disorder epilepsy
which cancers metastasize to the brain the fastest? lung and renal
in which area of the brain do most mets tumors arise? cerebrum 80%
tethered cord abnormally low conus medullaris
Acute subdural hematoma: timeframe Acute: 0-1 week
Chronic subdural hematoma: timeframe >2 weeks
Most common cause of SAH Trauma
Loss of consciousness requires: Both cerebral hemispheres damaged OR brainstem lesion
Coma: causes Cerebral infarction 10%; Cerebral hemorrhage 20%; Metabolic causes 50% (Drug ingestion >50%; Hypoglycemia 5-10%); Psych 2%
Hollenhorst plaque cholesterol emboli from carotid
Decorticate posturing: hemispheric or diencephalic dysfn d/t destructive lesions or metabolic abnormality; hands come up (response to stimuli) but do not localize
Decerebrate posturing: midbrain or upper pons dysfunction on a structural or metabolic basis; wrists flex (response to stimuli), not localizing
Cheynes-Stokes: Bilateral hemispheric lesions; most commonly seen in non-neurologic disorders (CHF); crescendo-decrescendo
Central neurogenic hyperventilation is 2/2: Commonly metabolic cause (Sepsis; DKA)
Apneustic = Rare, but usually associated with pontine infarction; pt breathes in, holds breath 15-20 sec, breathes out
Ataxic breathing (Biot's respiration) Damage to the medullary respiratory centers; breathing slows; long breathless pause; then inhales; this is often premorbid
Most common reason for noting unreactive pupils: an inadequate light source
Reactive pupils = midbrain is intact
Intact pupillary responses in unresponsive pt w/ absent EOM & corneal responses: metabolic (e.g., hypoglycemia) or drug ingestion (e.g., barbiturate)
Midposition (3-5mm) nonreactive pupils = midbrain damage
Blown pupil = unilaterally dilated, nonreactive pupil: sx of CN III (oculomotor nerve) compression (Aneurysm, Mass Lesion); dilated nonreactive pupil may also be 2/2 DM or drugs (atropine, scopolamine)
Small, reactive pupils: seen in: pontine damage (infarct or hemorrhage) or with some drug use (opiates, pilocarpine).
Bilateral midposition unreactive pupils: hypothermia
Eye deviation occurs in what direction? toward a unilateral hemispheric lesion and away from a unilateral brainstem lesion
Functional testing of eye movements is done by: oculo-cephalic reflex (Doll's head) or oculo-vestibular reflex (ice water calorics)
Oculo-cephalic reflex (Doll's head): CI if: if there is a question of cervical spine injury
Oculo-cephalic reflex: Abnormal response = absent or asymmetric eye movement: destructive lesion at midbrain or pontine level; poss also deep barbiturate poisoning
Oculo-vestibular reflex: Normal response (conscious pt): Tonic (sustained) deviation of eyes toward stimulated side, w/ quick phase of nystagmus toward the opposite side
Oculo-vestibular reflex: Response in comatose pt w/ intact brainstem: Tonic deviation of eyes, but no nystagmus
Oculo-vestibular reflex: Response in comatose pt w/ brainstem dysfn: Loss of tonic deviation w/ stimulation of one, or both ears; if there is no tonic deviation there can be no fast response
Oculo-vestibular response does not distinguish between: metabolic and structural causes of coma
Corneal sensation: carried by CN V (Trigeminal); test with cotton swab pressed gently onto cornea; abnormal reponse suggests a pontine lesion
GCS: 3 tests Eye, verbal, motor; range: 3-15; <8 means coma
ALS: Dx criteria UMN & LMN sx in 3 regions; UMN: clinical; LMN: EMG; CK nml or high
Primary lateral sclerosis: path degeneration of lateral corticospinal tract
Primary lateral sclerosis clin findings usu legs before arms; leg weak/stiff; spasticity; ave duration >8 yrs; many pts develop LMN sx & transition to ALS
progressive muscular atrophy pure LMN dz; slower progress than ALS; often spares bulbar mx; CK very high
Kennedy dz genetics X-linked rec, TNR; mutation in androgen receptor
Kennedy dz S/S facial fasciculations, weakness mouth/tongue; dysphagia, limb weakness; gynecomastia, DM, oligospermia
Disorders of neuromx transmission (NMJ): MG, LEMS, botulism
MG: pathophys Acquired autoimmune: Ach receptor insufficiency
MG S/S fluctuating mx weakness (worse w/reps); asymmetric ptosis; tired face, difficulty chewing/swallowing; SOB
LEMS S/S usu paraneoplastic (autoimm rare); proximal weakness / autonomic sx (dry mouth); hypo/absent reflexes; voltage gated Ca channel Abs; facilitation w/ RNS
Botulism MOA irreversible blockade of Ach release
Duchenne MD onset at 3-5 yrs; calf pseudohypertrophy; loss of ambulation by teens; cardiomyopathy; death in 20s
Emery Dreifuss Humeroperoneal / scapuloperoneal weakness w/ early contractures (ankle neck elbow); teen onset (very thin); scap winging/deltoid sparing; x linked or auto dom; cardiac conduction block/arrhythmia (need pacemaker)
Most common MD's Duchenne/Becker; myotonic; Facioscapulohumeral dystrophy
Myotonic dystrophy auto dom; any age; TNR
Myotonic dystrophy S/S tenting upper lip; distal weakness; frontal bald; cataracts; conduction block; DM, infertile; cognitive impairment; percussion myotonia
Autosomal dominant disorders Huntington, NF1/NF2, spinocerebellar ataxias, familial Alz, CMT
NF1: manifestations: hydrocephalus, seizures, learning disabilities, short, lack of GH, precocious puberty, renal artery stenosis
Auto recessive disorders PKU, Tay-Sachs, MSUD, Friedreich's, Wilson, homocystinuria, sickle cell
Wilson manifestations: hepatolenticular degen (impaired ceruloplasmin synth); presents in teen years (hepatitis); tremor, dysarthria, slow, hoarse, chorea
X-linked recessive pattern F-toM trans; M=affected, F=carrier
X-linked rec dz Duchenne/Becker MD; Kennedy; adrenoleukodystrophy; Menkes (kinky hair); Lesch-Nyhan; Fragile X
X-linked dom dz F-to-F transmission (lethal to males); Rett; Aicardi; Lissencephaly 2
Rett dz Onset 6-18 mos; live to 40s; autism; cardiac & scoliosis
Mitochondrial dz multi generations; trans by F only; 1:1 M:F affected; MERRF, MELAS, LHAN, Kearns-Sayre
MELAS manifestations 2/2 pt mutation of transfer DNA from leucine; <40 yo; lactic acidosis; HA, stroke, seizure, short; progressive dementia; no tx
TNR: mode of inheritance can be multiple modes of inheritance
TNR dz Huntington, Fragile X, myotonic dys; Kennedy; spinocerebellar ataxia; Friedreich
Alz: APOE gene E2: protective vs Alz; E4: inc risk of dev Alz
Parkinson dz S/S usu unilateral onset; resting tremor, slow, cogwheel rigidity, festinating gait, masked facies, postural instability
Parkinson: TRAP = Tremor, Rigidity, Akinesia, Postural instability
Most common genetic form of Parkinson: PARK8
Central cord syndrome S/S motor deficit in UE > LE; Varying degrees of sensory loss (pain/temp); most common of the incomplete spinal cord lesions (better prognosis)
Ligamentum flavum buckles into spinal cord => contusion to central regions of spinal cord = Central cord syndrome
Anterior cord syndrome S/S Paraplegia and dissociated sensory loss with loss of pain and temperature sensation; 2/2 infarction of the cord in the region supplied by the anterior spinal artery
Anterior cord syndrome: what fn is preserved: Posterior column (position, vibration, deep pressure) preserved
Brown-Sequard syndrome: cause Hemisection of the cord; From penetrating injuries; Rare
Brown-Sequard syndrome S/S Ipsilateral motor loss w/loss of vibration, pressure, proprioception; contralateral loss of pinprick, pain, temperature sensations
Progressive demyelinating; brain, sp cord, optic n.; viral; F>M, peak 20-40yo MS
Bell palsy sx Abrupt onset upper & lower (ipsilateral) facial paresis/ paralysis, mastoid pain, hyperacusis, dry eyes, altered taste; ipsilat ear pain may precede
LP w/ decreased glucose, increased protein Bacterial meningitis
LP w/ decreased protein, very few neutrophils syphilitic meningitis
3 mHz spike-and-wave on EEG Absence (petit-mal) seizures
Emergent eval of stroke CBC/plt; PT/ PTT; Lytes, glu, renal; ECG/ markers of cardiac ischemia; Brain CT or MRI
Atheroembolic stroke dx studies Normal head CT; Doppler US: high grade stenosis (e.g., L ICA)
Atheroembolic stroke: dx studies Neuroimaging; Carotid US; MRA; CTA; Catheter angiography
Cardioembolic stroke imaging Carotid US normal (no brain lg vessel prob)
Cardioembolic stroke: dx studies pulse; EKG; 24-48 hr EKG; TTE (microcavitation); TEE
Asymptomatic carotid stenosis: dx studies Carotid bruit; Doppler US; MRA, CTA
best modality to distinguish ischemic from hemorrhagic stroke: CT
TIA definitive study: arteriography; MRA more common (less invasive)
TIA dx studies CT or MRI to r/o cerebral hemo; cardiac w/u; cbc, esr, coags, antiphospholipids; Poss echo, ecg, carotid doppler
SAH dx studies CT (90%); CSF: hi opening P & bloody fluid; cerebral angiography, EEG
EEG: focal rhythmic discharge at onset, poss no ictal activity seen: simple partial seizure
EEG: interictal spikes assoc w/slow waves in temporal/frontotemp complex partial seizure
Seizure: labs Glucose; lytes; AED levels; LP if poss meningitis; EtOH/tox if susp; ABG if susp hypoxia; poss CXR, CT, MRI
MS: MRI findings multiple characteristic white matter lesions or plaques: periventricular or subcortical U-fibers, corpus callosum lesions
MS: CSF findings oligoclonal bands, increased IgG index, myelin prodn/fragments
MS: types of dx criteria Schumacher; Poser: Macdonald
When do LP? suspect meningitis; not if suspect abscess
Glucose depressed: usually: bac mening, or TB or fungal
Increased WBC in CSF indicates: inflammation (not necessarily infection)
Tuberculous meningitis dx studies active TB elsewhere in body; CSF inc WBC (100-150), mostly lymphs; abnormal CXR; acid-fast normal
Ring enhancing lesion is usually: abscess or tumor
Symptoms from plateau waves Transitory episodes of altered consciousness & visual disturbances
Brain tumor: eval & dx H&P; CT +/- MRI; EEG; LP; PET
Brain tumor: VEGF higher the VEGF, worse the prognosis; anti-VEGF Ab's effective in xenografts
MRI: T1/T2 T1: fat bright (water dark); T2: water bright
quadrigeminal cistern: should smile
suprasellar cistern: (if healthy): resembles a star
Trauma/Bleeds: imaging of choice noncontrast CT
epidural hematoma: appearance on CT lenticular (biconvex)
subdural hematoma: appearance on CT Cross suture lines and extends over larger area; Crescent shaped
SAH: appearance on CT Linear, within cisterns and sulci; bleed follows outlines of the gyri
Normal vertebral disk on MRI: low T1 signal, High T2 (nuc pulposus is mostly water); normal disks do not extend past margin of vert
Degenerative disk on MRI: dehydrates: decreased T2; loses height
Spinal cord lesion types: Demyelination; Cysts; Infarction; Tumor
Demyelination on MRI patchy T2 signal; may be d/t: MS; Post infectious Myelitis; Compressive Myelopathy; Post Radiation
Spinal cord infarction on MRI Gray Matter Affected Preferentially: H-pattern high T2 signal
Edema on MRI T1: dark; T2: bright
Purpose of CT in CVA Not dx; only to r/o other conditions that would CI some tx (tumor, bleed)
CVA on CT Hyperdense artery sign; loss of grey; CT normal up to 12 hours post; insula ribbon sign: blurring of gray-white junction
Brain neoplasm: imaging of choice MRI
Brain neoplasm: imaging Gray-white matter junction; marked edema; can be multiple, bilateral
AIDS-related CNS infxn: imaging of choice MRI; 2/3 develop CNS infxn
MS imaging MR sensitive, but not diagnostic; Periventricular T2 bright signal: inflammation
NPH on CT Ventriculomegaly out of proportion to sulcal prominence
Imaging findings assoc w/ 4 stages of brain abscess evolution early cerebritis (swollen/edema; high T2); late cerebritis (inc central necrosis; vasogenic edema at edges); early capsule; late capsule (well define ring)
Meningioma: imaging Often along brain surface; hyperdense, homogeneous enhancement
Ulnar neuropathy: Dx Hx; EMG/NCS can help find site of lesion
Sciatic n. palsy: Dx tests EMG/NCS (distinguish from peroneal neuropathy); xray
Charcot-Marie-Tooth Dx: H&P; DNA testing; Nerve/mx bx (confirmatory); EMG/NCS
CMT: EMG/NCS CMT I: segmental demyelination; reduced motor & sensory conduction velocity; CMT II: axonal loss; normal/sl dec motor conduction, dec SNAPs; chronic partial denervation in affected mx
Dejerine-Sottas Dz: Dx high CSF pro; EMG/NCS: dec motor velocity, sensory conduction
Refsum dz: Dx findings CSF protein normal; nerve bx; EMG/NCS: dec motor velocity, sensory conduction
Guillain-Barre dx studies NCS: slow S/M nerve conduction velocities; poss denervation/axonal loss; CSF high pro
CNS neoplasm CSF xanthochromic; inc pro, normal cell count & glucose
MG dx studies NCS: decrementing mx response; CXR to r/o thymoma; serum acetylcholine Ab
Wilson: labs Serum ceruloplasmin (Cu carrying pro) very low; urine Cu high
Huntington dz on CT atrophy of cerebrum & caudate nucleus
Huntington dz on MRI/PET decreased glucose metab
Neuroimaging not needed when: No focal neuro findings; Pt has stable pattern of recurrent HA; No h/o seizures
HA: Consider neuroimaging when: Neuro exam abnormal; progressively worsening HA; new persistent HA; new, rapid onset HA (thunderclap headache); HA does not respond to standard tx
Use LP only after: normal CT obtained & platelet count is normal
LP should be performed if: Neuroimaging is normal or suggests dz that must be dx by measuring cerebrospinal fluid (CSF) pressure, cell count, and chem
lemon sign on US Myelomeningocele: 2 frontal bones appear convex inward
banana sign on US Myelomeningocele: elongated and curved posterior fossa 2/2 Chiari malformation
5 steps to dx & tx pt w/suspected brain tumor MRI is TOC to confirm; Pan CT of chest/abd/pelvis to detect other tumors; Bx of distant tumor or Br tumor resection to confirm patho; xrt/CTx for malig; F/U MRI, PET
Fisher grade is used to: classify appearance of SAH on scan
Hunt Hess scale is used to: classify severity of symptoms in SAH
Coma: labs GLUCOSE, lytes, renal, Ca, PO4, ABG, CBC, tox screen; CXR, imaging (after stabilization)
Diagnostic LP: indications CNS infxn (meningitis, encephalitis); HA (SAH); Pseudotumor cerebri (idiopathic ICH); MS; Support dx of NPH & predict response to surgical shunting
LP: CI Suspected brain / epidural abscess; elevated ICP, esp if papilledema; suspect mass lesion; Ventricular obstn;
LP: insert needle into: L3-L4 space (elderly: may need to do cisternal procedure)
LP in kids: spinal cord extends more caudally, do low LP
CSF collection: amount: 1-2 mL CSF per tube
Routine CSF analysis includes: Opening pressure; Appearance/color; Consistency; Tendency to clot; Diff cell count; Protein; Glucose
CSF cloudy = Inc WBC or protein
CSF: Xanthochromia (yellow tinge) = hyperbilirubinemia, hypercarotenemia, melanoma
CSF: Red tinge = Blood from bleeding into SA space or traumatic tap
CSF: Cells Normal 0-5 small lymphs/ml; PMNs, lg monos & RBCs are never normal
CSF: RBCs & WBCs: only present via ruptured blood vessels or by meningeal response to inflammation or irritation
WBC in CSF Inc WBCs = inflam (>100, prob infxn); PMNs: bac infxn; Lymphs = viral or other (TB, fungal, ca); Eosinophils: shunt, parasitic infection & allergic rxn
CSF pressure Normal 60-200 mm H2O (mean = 120); usu drops 5-10 mm for each ml CSF removed
CSF pressure: Marked elevation: poss purulent meningitis or intracranial tumors
CSF pressure: Moderate elevation: mild inflammation, encephalitis, neurosyphilis
CSF pressure: Elevated pressure with normal CSF: confirms pseudotumor cerebri (benign ICH): one instance where LP is done despite presence of papilledema
CSF protein: increased in: inc permeability of blood-CSF barrier (tumor, trauma, inflam), or increased intrathecal synthesis of Igs
CSF protein: decreased in: CSF protein leak, hyperthyroidism, water intoxication
CSF glucose Normal CSF glu 60-70% of plasma glu; Low levels assoc w/ bacterial or TB infection
CSF lactate: usu parallels blood levels; if markedly different from blood level = biochem abnormality in CSF
Increased CSF lactate associated with: CVA, IC bleed, bacterial meningitis; Not altered in viral meningitis; lactate may differentiate btw viral & bacterial
Organism conc required for detection on CSF smear: 10,000/ /ml (Gram & AFB stains may be neg despite org presence in CSF; cx on several media; consider empiric tx)
CSF antigen serology: More rapid, but less specific, than cx; cryptococcal Ag test very specific/accurate
Primary lateral sclerosis: dx studies EMG, MRI (br & spcord), LP, evoked potls; B12, Lyme, RPR, long chain fatty acids
Myasthenia gravis Dx studies Tensilon test; Ach receptor & MuSK Abs; Repetitive nerve stim; Single fiber EMG; CT Chest to exclude thymoma
MD: labs/studies ultrastructural protein abnormalities; mx bx: mx fiber necrosis
Duchenne/Becker: Dx studies Mx bx; genetic testing (need complete sequencing); CK sometimes >10,000; FH
Wilson: dx high ceruloplasmin & copper; low copper on liver bx; Kayser Fleischer rings
Duchenne/Becker Dx genetic testing, elevated CK, EMG
Alz dx dx of exclusion (neuropsych eval); MRI/CT: hippocampal atrophy; amyloid on PET (Pittsburgh B); LP: inc tau, dec amyloid-beta 42
Pathological hallmark of Parkinson: Lewy body (alpha-synuclein is main component)
MELAS dx studies Mitochondrial inheritance, labs: high pyruvate / lactate; stroke lesions (don't conform to normal vasc distn)
Pseudoseizure Clinically resembles seizure; does not have EEG evidence of seizure, or respond to epilepsy meds
NCS uses electrodes; record response to shock (amp & timing)
EMG uses needle; electrical activity observed during rest & activitation
NCS / EMG utility: suspicion of peripheral nerve or mx injury; detect CTS; investigate polyneuropathy /poss etiology or radiculopathy
Evoked potential studies to study conduction of CNS pathways; electrodes on scalp; brain potentials recorded in response to stim
Evoked potential studies: 3 kinds: Visual; Brainstem (auditory); Somatosensory
Evoked potential studies: useful to dx: MS (VEP, SSEP), spinal cord diseases
Visual evoked potential: optic neuritis: After optic neuritis, the VEP will often remain abnormal indefinitely even after recovery of vision
SSEP record potentials from stimulus at wrist or ankle
Blood EtOH usu measured on: whole blood (serum levels 12% higher than whole blood)
Chronic alcohol use: labs macrocytosis; anemia (later); high AST, ALT, GGT, CDT
Urine drug test methods Immunoassay; GC-MS (HPLC)
Drug test: Immunoassay fast; large-scale screening; false pos & req confirm by HPLC
Drug test: HPLC accurate; time consuming; expensive
Opiates Natl: heroin & hydrocodone; synthetic: meperidine & methadone (less detectable)
Drug with longest detection time: Benzo or THC
Drugs with lowest/highest detection thresholds: Lowest: THC; highest: amphetamine
oligoclonal bands in CSF = MS
Acoustic neuroma (vestibular schwannoma): dx with: CT or MRI; surgical tx
Created by: duanea00