Neurology Shelf

eesohbel's version from 2015-09-23 01:49


Question Answer
diagnosis of SAHCT followed by LP to demonstrate presence of blood. Can use angiography to note exact location of bleed
low pressure headaches usually complication of...lumbar puncture. headaches are worst in the upright position. alleviated by recumbency
what type of headaches increase in severity with recumbencyidiopathic intracranial hypertension aka pseudotumor cerebri
what is an important mimic of IIH and should be excludedvenous sinus thrombosis is an important mimic of this syndrome and should be excluded with venous sinus imaging
what is special about basilar migraineshave distinct neurologic deficits. such as visual changes that may evolve to complete blindness. irritability that may develop into psychosis
Prophylatic treatment for migraineamtriptyline, propanolol, verapamil and valproate
acute attack of migraine treatmentmetoclopramide, sumatriptan and ergotamine tartrate. Do not use daily. Can cause rebound syndrome
what type of headachetension headache associated with neck muscle spasm leading to reduced neck range of motion and paracervical tenderness
treatment for post-herpetic neuralgiaimipramine


Question Answer
right hemiparesis, right hemisensory loss, aphasia, when caused by ICA occlusive disease, transient left monocular visual lossleft cerebral stroke (anterior circulation)
left hemparesis (often arm hand and face), left hemisensory loss, poor drawing and copying, neglect of the left visual fieldright cerebral hemisphere stroke
right homonymous hemianopia, amnesia, alexia without agraphia (when splenium of corpus collosum involved)left PCA stroke
left homonyomous hemianopia, left-sided visual neglectright PCA stroke
gait ataxia, dysarthria, ipsilateral arm dysmetriacerebellar infarction (usually PICA or SCA or cerebellar hemorrhage)
ipsilateral facial pain or reduced temperature sensation, loss of pain and temp in contralateral limbs, ipsilateral Horner's, dysphagia and hoarsenesslateral medullary
lateral medullary blood supplyvertebral artery
locked-inbasilar artery occlusion
if signs localize to anterior circulation where should do vascular imagingICA
if signs localize to posterior circulation where should do vascular imagingVA
left internal capsule infarctioncontralateral hemiparesis
left parietal lobe infarctionsensory defects
left thalamic infarctioncontralateral hemisensory and hemiparesis
What must be checked before administering TPAcomplete blood count, glucose level and coagulation profile (could also check for syphillis, troponins and inflammatory markers)
most likely mechanism of injury for lateral medullaryVA dissection
treatment for acute VA dissectionIV heparin with conversion to warfarin
what is the most common site of injury in the brain in a pure motor strokeposterior limb of the internal capsule
in wallenberg syndrome what type of loss is ipsilateralataxia and Horner's syndrome
in wallenberg syndrome what type of loss is contralaterallateral spinothalamic injury (pain and temperature disturbances)
injury to what nucleus causes dysphagia and hoarsenessnucleus ambiguus
what is the most common cause of lobar hemorrhage in elderly adults without hypertensioncerebral amyloid angiopathy
focal seizures that generalize after a hemorrhage should be treated withan anti-epileptic drug ex. levetiracetam
classic symptoms of extracranial internal carotid artery diseaseepisodes of ipsilateral transiet monoocular blindness (amaurosis fugax) and contralateral transient motor weakness
what procedure can reduce the risk of stroke in patients with symptomatic disease of internal carotidcarotid endarterectomy
what causes the transient monocular blindness in carotid artery diseaseembolism to central retinal artery
lacunar infarct in the posterior limb of the internal capsuleunilateral motor deficit. No sensory
stroke in ventrroposterolateral nucleus of the thalamusunilateral numbness. hemisensory deficit
lacunar infarction in the anterior limb of the internal capsuleweakness that is more prominent in the lower extrimity
lacunar stroke at basis pontishand weakness, mild motor aphasia. no sensory abnormalitie


Question Answer
global aphasiaimpaired comprehension, repetition, and fluency
wernicke aphasiafluent aphasia. impaired comprehension and repetition.
conduction aphasiadamage to arcuate fasciulus which is how frontal lobe and temporal lobe communicate. problems with repetition
anomic aphasiaisolated word finding deficit
difference between broca and transcortical motor aphasiatranscortical is similar to broca but there is preserved repetition
difference between Wernicke and transcortical sensory aphasiasimilar except in transcortical there is preserved repetition
lesion in broca'sleft inferior frontal gyrus
fluency impaired, repetition impaired, comprehension preservedBrocas
fluency preserved, repetion impaired, comprehension impairedWernicke's
fluency preserved, repetition impaired, comprehension preservedconduction aphasia
fluency impaired, repetition preserved, comprehension preservedtranscortical motor aphasia
fluency preserved, repetion preserved, comprehension impairedtranscortical sensory
global aphasia where is the lesionlarge left hemisphere lesion
subcortical aphasia what is preservedrepetition
subcortical aphasia where is the lesionleft basal ganglia/thalamus
alexia without agraphiacharacterized by an inability to read despite a preserved ability to write. usually lesion in dominant occiptal lobe
apraxiainability to carry out a learned motor task despite presrvation of the primary functions needed to carry out the task
apraxia in frontal lobepatients are able to recognize the task done correctly by others, but cannot perform it.
apraxia in parietal lobepatients cannot recognize the task done correctly
def'n Gerstman'sagraphia, acalculia, right-left confusion and finger agonisa
where is lesion in Gerstman'sangular gyrus of dominant hemisphere

Aphasia Anatomy

Question Answer
Broca'sposterior inferior frontal gyrus
Wernicke'sposterior superior temporal gyrus
conductionarcuate fasciculus
transcortical motor aphasiaanterior superior frontal lobe
transcortical sensory aphasiainferior temporal lobe


Question Answer
simple partial seizuresfocal area of the brain and do not impair awareness
sensory phenomenaparietal lobe
visual phenomenaoccipital lobe
gustatory, olfactory and psychic phenomenatemporal lobe
complex partial seizuresfocal onset and impair awareness
EEG findings for absence seizuresclassic three per second generalized spike and wave form
Jacksonian marchpatient develops focal seizure activity that is primarily motor and spreads. This type of seizure often generalizes at which point the patient loses consciousness and may have a generalized tonic clonic seizure.
what type of seizures may be mistaken for a psychiatric problemcomplex partial seizures
epilepsia partialis continuacondition of persistent focal motor seizure activity. these seizures may persist for hours or for months

Selected Epilepsy Syndromes

Question Answer
age of onset lennox-gastaut syndromechildhood
seizure types lennox-gastauttonic, atonic, myoclonic, generalized tonic-clonic, absence
associated findings w/lennox-gastautintellectual disability
EEG findings w/lennox-gastautslow (1 to 2 per second) spike and wave discharges
treatment for lennox-gastautvalproate, lamotrigine, felamate, rufinamide
age of onset for benign rolandic epilepsychildhood
type of seizure benign rolandic epilepsysimple partial involving mouth and face and generalized tonic-clonic
associated findings for benign rolandic epilepsynocturnal preponderance of seizures
EEG findings for benign rolandic epilepsycentrotemporal spikes
treatment for benign rolandic epilepsycarbamazepine
age of onset for absence epilepsychildhood and adolescence
associated findings with absencehyperventilation as a trigger
treatment for abscenceethosuximide, valproate and divalproex soduim in children who cannot tolerate ethosuximide
age of onset for juvenile myoclonic epilepsyadolescence and young adulthood
seizure type for juvenile myoclonic epilepsymyoclonic, absence, generalized tonic clonic
associated findings for juvenile myoclonic epilepsyearly morning preponderance of seizures
EEG findings for juvenile myoclonic epilepsy4 to 6 per second polyspike and wave
what is West syndromegeneralized seizure disorder of infants characterized by recurrent spasms, EEG patern of hypsarrhythmia and retardation

Evaluation of head trauma in children

Question Answer
focal neurologic findings, skull fracture, seizure, persistent altered mental status, prolonged consciousnesshead ct without contrast
GCS=15 and either vomiting, headache or loss of cosncioussnessobservation for 4-6 hours or head ct without contrast
minor head traumahead CT


Question Answer
recurrent episodes of vertigo, ear fullness/pain, unilateral hearing loss and tinnitusmenieres
recurrnet episodes brought on by position change and Dix-Halpike causes nystagmusBPPV
vestibular neuritispatients fall down toward side of lesion
brainstem/cerebellar strokesudden-onset persistent vertigo


Question Answer
optic nerve damageright eye blindness
chiasmbitemporal visual field defect
optic tractleft homonymous hemianopia
parietal lobeleft inferior homonymous quadrantonopia
temporal lobeleft superior homonymous quadrantonopia
occipital cortexleft homonymous hemianopia with macular sparing
comitant strabismusmisalignment is constant in all directions of gaze and each eye has full range of movement (usually opthalmologic)
incomitant strabismusdegree of misalignment varies with direction of gaze (usually neurologic)
phoriamisalignment of the eyes when binocular vision is absent
tropiamisalignment of the eyes when both eyes are opened and binocular vision is possible
clinical characteristics of a left INO (affecting left MLF)inability to adduct the left eye in right lateral gaze plus nystagmus of the abducting right eye
one and a half syndromedamage to left PPRF and both MLF (knock out entire left eye) and right medial rectus (so at baseline right eye is abducted). so when you look left, left eye doesnt move and right eye cannot adduct. if you look right, left eye cannot do anything but right eye can abduct
if you damage left MLFknock out left medial rectus (inability to adduct the left eye in right lateral gaze)
if you damage left PPRFknock out left lateral rectus (CNVI) and right medial rectus (CNIII)
inability to produce saccadesocculomotor apraxia


Question Answer
direction of peripheral nystagmusunidirectional; fast away from the lesion
inhibited by fixation C or Pperipheral
horizontal saccades initiated wheresuperior colliculus
direction of central nystagmusbidirectional or unidirectional
pure vertical nystagmus C or Pcentral
tinnitus C or Pperipheral
vertigo severe C or Pperipheral
duration of central nystagmuschrnoic
causes of peripheral nystagmusvascular disorders, trauma, toxicity, Meniere disease, vestibular neuronitis
causes of ventral nystagmusvascular, demyelination and neoplastic/paraneoplastic


Question Answer
axillary nerveshoulder abduction
musculocutaneous nerveelbow flexion
elbow extensionradial nerve
wrist extensionradial nerve
finger flexionmedian and ulnar nerve
finger extensionradial nerve
finger abductionulnar nerve
hip abductionsuperior gluteal nerve
hip extensionsciatic nerve
knee flexionsciatic nerve
plantar flexiontibial nerve
foot eversionperoneal
foot inversiontibial
root bicepsC5
root brachioradialisC6
root tricepsC7
root finger flexorC8/T1
patellar reflexL4
hip adductorL3
ankle jerkS1

UMN versus LMN

Question Answer
anterior horn cell and projection axonLMN
wasting and fasticulationsLMN
weakness of the upper and lower faceLMN (Bells Palsy)
weakness of the lower face, but not the upper faceUMN
spasticitiy, hyperactive reflexes and Babinski signsUMN


Question Answer
major pathologic features of ADbrain atrophy, senile plaques, and NFTS associated with a substantial loss of neurons in the cerebral cortex and gliosis
criteria for diagnosis of vascular dementiaprescence of dementia and two or more of the following focal neurologic signs, abrupt onset, brain imaging studies
clinical manifestation of dementia with lewy bodiessever problems with visual memory, marked fluctuations of alertness, prominent visual hallucinations, delusions, extrapyramidal symptoms and sensitivity to neurolpetics (marked worsening with drugs like haloperidol)
where are lewy bodes found in dementia with lewy bodiescortical neurons
clinical manifestations of progressive supranuclear palsyfailure of vertical gaze, dysarthria, dysphagia, extrapyramidal rigidity, gait ataxia and dementia
pathology of PSPatrophy of dorsal midbrain, globus pallidus and STN
diagnosis of Hunington's more than 40 CAG repeats in the HD gene on chromosome 4
pathology of Hunington'ssevere destruction of the caudate and putamen (GABA-ergic neurons) and loss of neurons in the cerebral cortex (later 3)
in which dementia are personality changes common early in diseaseFTD

Differential Diagnosis of Dementia

Question Answer
early insidious, short-term memory lossAD
stepwise decline and cerebral infarctionvascular dementia
early personality changes and frontotemporal atrophy on neuroimagingFTD
visual hallucinations and spontaneous parksinoismLBD
ataxia, urinary incontinence, dilated ventricles on neuroimagingNPH
rapidly progressive and myoclonus and seizures


Question Answer
essentialbilateral action tremor of the hands. relieved with alcohol
Parkinson'sresting tremor that decreases with voluntary movement
cerebellarincreases as the hand reaches its target
physiologic tremorlow amplitude not visible under normal conditions
genetics of essential treatmentautosomal dominant
treatment for intention/cerebellarnot medication, but scan and then maybe surgery
treatment for essential tremorpropanolol and primidone


Question Answer
what is the clinical presentation of Duchenneprogressive weakness, Gower manuever, calf pseudohypertrophy
what is the clinical presentation of Beckermilder weakness compared to Duchenne
what is the clinical presentation of myotonic dystrophyfacial weakness, hand grip, myotonia, dysphagia
age of onset for duchenne2-3
age of onset for becker5-15
age of onset for myotonic12-30
prognosis Duchennewheelchair dependent by adolescence. Deach by age 20-30
prognosis Beckerdeath by age 40-50 from HF
prognosis myotonicdeath from respiratory or HF depending on age of onset