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47 Cards in this Set
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- Back
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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 |
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how do cererbal lesion effects on UMN's vary by time since injury
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DTRs are increased unless very acute
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when muscules is stretched there is sudden loss of resistance near end of range of motion
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spasticity
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partial paralysis of face, arm, leg on one side
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hemiparesis
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paralysis of identical parts bilaterally
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diplegia
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inability to perform purposeful movements, but not accompanied by a loss of sensory function or paralysis
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apraxia
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four tests used to evaluate cortical sensory integration
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stereognosis
double simultaneous stimulation graphesthesia 2point discrimination **deficits indicate parietal lesion |
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five cutaneous sensory modalities
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pain
temperature light touch vibration proprioception |
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inability to recognize objects by use of the senses
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agnosia
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the inability to determine the shape of an object by touching or feeling it
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astereognosis
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hemisensory loss
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hemispheric lesion
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crossed sensory loss to pain and temp
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lateral medullary lesion
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acute onset
alteration of consciousness hyperactivity/autonomic disturbances/hallucinations tremor, asterixis, multifocal myoclonus |
delirium
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insidious onset
impaired memory plus other intellectual compromise (language) or executive fxn |
dementia
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how do you treat sub-dural induced dementia?
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drainage or excision of membranes
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weird wet and wobbly
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NPH
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dementia with argyll-robertson pupil
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neurosyphilis
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demented patient
young memory decreased over months marked personality change |
HIV dementia
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three things to do with comatose paitent
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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) |
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two lesions that can produce coma
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Ascending Reticular Activating System
and raphe nucleus (serotonin) / locus ceruleus epi) / parabrachialis |
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six causes of coma
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anoxia
stroke head trauma metabolic status epilepticus drug overdose |
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GCS
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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 |
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requirements for brain death
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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 |
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no doll's eyes =
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low brainstem lesion
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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 -nothing |
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not brain dead but will never have acceptable satisfactory recovery to any extent
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vegetative state
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CPP=
when is it bad? |
1/3 systolic + 2/3 diastolic – ICP (have to divide ICP by 13.5 to get mmHg)
<50 |
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uncal herniation effects on
-consciousness -hemiparesis -EOM -vital signs -pupils |
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 |
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how does uncal herniation occur
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temporal lobe and uncus shifts medially into tentorial notch --> compression of CN III and adjacent midbrain --> rostrocaudal deterioration
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treat cerebral edema
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control the CPP
-systemic BP -ICP (carbonic anhydrase, DMSO) corticosteroids mannitol lasix, etc |
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idiopathic intracerebral hypertension
aka? tx? |
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) |
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communicating vs non-communicating obstructive hydrocephalus
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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 |
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clinical findings of obstructive hydrocephalus
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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 |
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mcc obstructive hydrocephalus in child? in adult?
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mass lesions, stenosis of Sylvian aqueduct, Dandy-Walker, interventricular hemorrhage, Arnold-Chiari;
SAH (obstructive but communicating), head injury, idiopathic, tumors, NPH, walking-adams syndrome |
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commom complications of CSF shunt?
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mechanical failure (under or over drainage, blockage, component failure)
infection subdural collections pneumocephalus craniosynostosis shunt nephritis |
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CT for NPH?
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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 |
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syncope?
hyperventilation? hypoglycemia? panic attacks? pseudoseizure? epilepsy? |
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 |
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partial vs generalized epilepsy
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partial begin in a focal area
generalized begin in both hemisphers |
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staring spells with 3Hz spike and wave discharges
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absence epilepsy
tx- ethosuximide or valproate |
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child with GTC seizure <5 minutes, negative work-up
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febrile seizure
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1week to 14mo old with spasms,
multifocal sharp waves and spikes on chaotic background hypsarrhythmia MR |
west syndrome (infantile spasms)
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normal intelligence 9yo
sensorimotor phenomenon on face/mouth upon awakening centrotemporal sharp waves |
rolandic seizures
3x more common than absence |
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mcc epilepsy
children? 15-30? 30-50? 50-75? |
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 |
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neurologic deficit that follows a seizure, lasts up to 24 hrs, may be hemiparesis/hemianopia/aphasia
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Todd's paralysis
aka postictal paralysis may indicate seizure focus like a tumor |
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when to treat epilepsy?
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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
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womenly issues when treating epilepsy
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AEDs may decrease OCPs
beware neural tube defects pregnancy may alter drug levels |
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elderly issues for treating epilepsy
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slowed metabolism of drugs means risk of toxicity and overdose
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