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47 Cards in this Set

  • Front
  • Back
What is the effect of cerebral lesion on Motor Function (UMN)
-distribution of weakness
-DTRs (biceps, triceps, etc)
-superficial reflexes (abdomina, cremasteric)
-pathologic reflexes (Babinski, Hoffman)
-primitive reflexes
(Moro, grasp, snouting)
distribution- corticospinal (hemiparesis, quadri-, para-, mono-, faciobrachial)
DTRs increased
superficial reflexes dec
pathologic reflexes present
-primitive reflexes are apparently just for fun
how do cererbal lesion effects on UMN's vary by time since injury
DTRs are increased unless very acute
when muscules is stretched there is sudden loss of resistance near end of range of motion
partial paralysis of face, arm, leg on one side
paralysis of identical parts bilaterally
inability to perform purposeful movements, but not accompanied by a loss of sensory function or paralysis
four tests used to evaluate cortical sensory integration
double simultaneous stimulation
2point discrimination

**deficits indicate parietal lesion
five cutaneous sensory modalities
light touch
inability to recognize objects by use of the senses
the inability to determine the shape of an object by touching or feeling it
hemisensory loss
hemispheric lesion
crossed sensory loss to pain and temp
lateral medullary lesion
acute onset
alteration of consciousness
hyperactivity/autonomic disturbances/hallucinations
tremor, asterixis, multifocal myoclonus
insidious onset
impaired memory plus other intellectual compromise (language) or executive fxn
how do you treat sub-dural induced dementia?
drainage or excision of membranes
weird wet and wobbly
dementia with argyll-robertson pupil
demented patient
memory decreased over months
marked personality change
HIV dementia
three things to do with comatose paitent
support vitals, lines, and spines
intubate if GCS <10
1 amp (25g) dextrose
100mg thiamine IM
1 amp naloxone if narcotics expected

labs (glc, CBC, ABG, UA, serum and urine tox screen)
two lesions that can produce coma
Ascending Reticular Activating System
raphe nucleus (serotonin) /
locus ceruleus epi) /
six causes of coma
head trauma
status epilepticus
drug overdose
6- Motor- on command, localizes pain, withdrawals to pain, flexes, extends, nothing
5- on command, confused, inappropriate, incomprehensible, nothing
4- on command, to verbal, to pain, nothing
requirements for brain death
cause must be known and irreversible, all things that can be corrected must be, T>32C
1. coma- no cerebral response to noxious stimuli in any extremity
2. no brainstem reflexes- no pupillary reflex, oculocephalic, oculovestibular, corneal, jaw, grimace, gag, cough
3. apnea
no doll's eyes =
low brainstem lesion
cold calorics:
brainstem intact-
MLF injured-
low brainstem injured-
-cold contracts towards water, go up if bilat
-only eye on side of cold water contracts, go up if bilat
not brain dead but will never have acceptable satisfactory recovery to any extent
vegetative state

when is it bad?
1/3 systolic + 2/3 diastolic – ICP (have to divide ICP by 13.5 to get mmHg)

uncal herniation effects on
-vital signs
aka lateral transtentorial
-impaired consciousness
-if unilateral- contralateral hemiparesis; if large (Kernohan's notch)- decorticate-> decerebrate posturing
-ipsilateral CNIII palsy
-abnl RR
-small, midposition, minimally reactive pupils
how does uncal herniation occur
temporal lobe and uncus shifts medially into tentorial notch --> compression of CN III and adjacent midbrain --> rostrocaudal deterioration
treat cerebral edema
control the CPP
-systemic BP
-ICP (carbonic anhydrase, DMSO)
lasix, etc
idiopathic intracerebral hypertension
pseudotumor cerebri
-young obses female with menstrual irregularities, headache, papilledema (may lead to vision loss), tinnitus
-weight control, control ICP (acetazolamide, corticosteroids, consider VP shunt)
communicating vs non-communicating obstructive hydrocephalus
obstructive- implies blocked flow (as in the fourth ventricle with Dandy-Walker)- as opposed to over production
communicating- communication exists between the ventricles and subarachnoid space
non-communicating- CSF flow is obstructed within the ventricular system or in its outlets to the arachnoid space
clinical findings of obstructive hydrocephalus
am headaches, blurred or double vision, drowsiness, spasticity -> trouble walking, obesity, precocious or delayed puberty, N/V; head enlargement, separation of sutures, tense fontanelles, setting sun sign

in adults add dementia picture, incontinence if severe; papilledema, unilat or bilat CN VI palsy
mcc obstructive hydrocephalus in child? in adult?
mass lesions, stenosis of Sylvian aqueduct, Dandy-Walker, interventricular hemorrhage, Arnold-Chiari;

SAH (obstructive but communicating), head injury, idiopathic, tumors, NPH, walking-adams syndrome
commom complications of CSF shunt?
mechanical failure (under or over drainage, blockage, component failure)
subdural collections
shunt nephritis
CT for NPH?
distinguishes this from hydrocephalus ex vacuo
-ventricular enlargement out or proportion to sulcal atrophy
-transependymal flow of CSF
-jet sign of third ventricle
-rounded frontal horns
-thin corpus callosum
panic attacks?
syncope- LOC from cerebral hypoperfusion
hyperventilation- choking, SOB, palpitations, parasthesias, hot flashes, shaking
panic attack- add fear of dying
hypoglycemia- you and I both know this one
pseudoseizure- bizarre movements, thrash and writhe, lash out agaisnt assistance, recall ictal state
epilepsy- recurrent real seizures
partial vs generalized epilepsy
partial begin in a focal area
generalized begin in both hemisphers
staring spells with 3Hz spike and wave discharges
absence epilepsy
tx- ethosuximide or valproate
child with GTC seizure <5 minutes, negative work-up
febrile seizure
1week to 14mo old with spasms,
multifocal sharp waves and spikes on chaotic background
west syndrome (infantile spasms)
normal intelligence 9yo
sensorimotor phenomenon on face/mouth upon awakening
centrotemporal sharp waves
rolandic seizures
3x more common than absence
mcc epilepsy
children- birth injury, metabolic, malformations,febrile
15-30- idiopathic, trauma, drug or alcohol withdrawal, neoplasm
30-50- neoplasm, alcohol or drugs, vascular, trauma
50-75- vascular dz, neoplasm, trauma, degenerative dz
neurologic deficit that follows a seizure, lasts up to 24 hrs, may be hemiparesis/hemianopia/aphasia
Todd's paralysis
aka postictal paralysis

may indicate seizure focus like a tumor
when to treat epilepsy?
Strong fam hx, EEG showing epileptic abnl, sz associated neuro deficit, sz associated with MRI or CT abnl, in adults consider type of work, family and driving status
womenly issues when treating epilepsy
AEDs may decrease OCPs
beware neural tube defects
pregnancy may alter drug levels
elderly issues for treating epilepsy
slowed metabolism of drugs means risk of toxicity and overdose