Neuro Flashcards
epidural hematoma
a collection of blood in the space between the skull and dura mater. normally a result of trauma to the parietal lobe which disrupts the middle meningeal artery appears as a lens on CT scan, which follows the curve of the skull and protrudes into brain tissue as a convex mass
obstructive hydrocephalus
CSF flow restriction within or from ventricular system. May be a result of obstruction of arachnoid villi during a subarachnoid hemorrhage
choroid plexus
A highly vascular portion of the lining of the ventricles that secretes cerebrospinal fluid. normal production 20ml/hr (500ml/day)
What part of the brain is associated with coordination, balance, and muscle tone
cerebellum
What is the inner protective layer of the brain
pia mater
What cranial nerve innervates the muscles of the tongue
XII Hypoglossal
What is the cranial nerve that carries sensory and motor signals from face and mouth
V Trigeminal
What is the cranial nerve that controls muscles in the neck and shoulder
XI spinal accessory nerve
cranial nerve that controls smiling and taste
VII facial nerve
Wernicke’s area
controls language reception - a brain area involved in language comprehension and expression; usually in the left temporal lobe
temporal lobe function
auditory stumli recognition, memory and speech
olfactory nerve function (I)
sensory, smell
basilar artery
Asingle midline artery, formed by the fusion of the vertebral arteries, that supplies blood to the brainstem and to the posterior cerebral arteries.
anterior cerebral artery
supplies frontal lobe and superior medial portion of the parietal lobe circulation
glossopharyngeal nerve (IX)
supplies motor function to the pharynx and sensory function to the posterior 3rd of the tongue
Optic Nerve (II)
transmits visual information from the retina to the brain
superior sagittal sinus
A venous sinus located in the midline just dorsal to the corpus callosum, between the two cerebral hemispheres.
The majority of strokes are caused by occlusion of the what vessel
middle cerebral artery
Vestibulocochlear nerve VIII
hearing and equilibrium
Visual processing takes place in
occipital lobe
most common location for cerebral aneurysm
anterior portion of circle of willis
lacunar stroke
Occlusion of single, deep perforating artery causing ischemic lesions Rare
Inclusion criteria for tPA
Clinical Diagnosis of ischemic stroke causing neurologic deficit; Onset of symptoms less than 4 ½ hours before beginning treatment, Age over 18 years
exclusion criteria for tPA
SAH, Within 3 months: Head trauma, stroke or MI, GI bleed, major surgery, arterial puncture, BP over 185/110, INR over 1.7/anticoagulant, hypoglycemia under 50, Seizure, multilobar infarct
Blood pressure goal prior to tPA
lowered slowly to <185/110
blood pressure goal after tPA
<180/ 105 for at least 24hrs
What is tPA and what does it do?
TPA is tissue-type plasminogen activator. This cleaves plasminogen to make plasmin. Plasmin cleaves fibrin, breaking-up blood clots. (crab-linked clot).
mechanical thrombectomy
Catheter and other devices to go in and pull clot out of artery Can be performed up to 6hrs after onset –Earlier therapy improves outcomes Requires advanced stroke center –used in conjunction with tPA in eligible patients (large vessel occlusion)
complications of tPA
Hemorrhage (Dc tPA, CT, cryo) Angioedema (tx of allergic rx) Reperfusion syndrome
most common type of stroke
ischemic (87%)
thromotic stroke
blockage in diseased cerebral artery
embolic stroke
Fragments that break from a thrombus formed outside the brain
INR/PT
international normalized ratio (prothrombin time) -effectivness of Warfrin
hemorrhagic stroke
ICH or SAH
most common cause of a SAH
Trauma; the second most common is berry aneurysm
Hunt and Hess Scale
- used in aSAH (aneurysmal SAH) - classifies SAH severity for surgical risk 1- asymptomatic, minimal headache, slight nuchal rigidity 2- moderate to severe headache, nuchal rigidity, no neuro des or other cranial nerve palsy 3- drowsiness, confusion, mild focal defs 4- stupor, moderate to severe hemiparesis, possible early decerebrate rigidity 5- deep coma, decerebrate rigidity, moribund appearance
Fisher scale
-used to estimate risk of cerebral vasospasm after SAH 1- no subarachnoid blood detected 2- a diffuse depsoit or thin layer with all vertical layer of blood (inter hemispheric fissure, insular cistern, ambient cistern) < 1mm thick 3- localized clot and/or vertical layer of blood >= 1mm thick 4-Diffuse or no subarachnoid blood, but with intracerecral or intraventricular clots
SAH interventions
surgical clip or coiling within 24-48hrs
complications of SAH
- hydrocephalus 20% (normally caused by CSF outflow obstruction by a clot in the ventricular system - rebleed (1st 7 days after aSAH) - vasospasm 20-40% of SAH pts - hyponatremia (<135mmol/L)
ICH
10-15% of strokes (65% brain stem, 57% lobular, 51% deep hemorrhage, 42% cerebellar)
blood pressure goal for ICH related to an epi/SAH(anurysmal)/int capsule/isxhemic CVA w tranformation
systolic < 140, MAP<110
ICH score
GCS Score: 3-4 (2) 5-12 (1) ICH Volume: >30 mL (1) < 30ml (0) IVH (Intraventricular Blood): Present (1) No (0) ICH Location: Infratentorial (1) no (0) Age: ≥80 years (1) <80 (0) 30-Day Mortalities for Total ICH Scores 0 = 0% 1 = 13% 2 = 26% 3 = 72% 4 = 97% 5 = 100% 6 = estimated to be 100%; no patients in the study fell into this category
ICP monitoring
Normal value: 5-10 mmHg Recommend initiating treatment if ICP > 20 mmHG, GCS < 8, evidence of herniation
passive ICP management
analgesia, HOB elevation, sedation, glucose management, tempurature management, seizure management
CN 1
olfactory nerve- smell
CN 2
optic nerve- visual acuity
CN 3
oculomotor- pupil constriction
CN 4
trochlear- down and in eye movement
CN 5
trigeminal- facial sensation
CN 6
abducens- eye adbuction horizontal/lateral
CN 7
facial- facial expression
CN 8
vestibulocochlear- hearing/balance
CN 9
glossopharyngeal- shallow
CN 10
vagus- cough/gag
CN 11
accessory- shoulder shrug
CN 12
hypoglossal- tongue out
what cranial nerve are included in the eye movement
CN 3,4,6
brainstem assessment for unconscious pts
CN 2 + 3- light reflex CN 5 + 7- corneal reflex CN 9 + 10- cough/gag
monro-kellie doctrine
the cranial cavity is a closed rigid box, therefore a change in volume must be compensated for
components of the intracranial compartment
80% parenchyma 10% vascular 10% CSF
zone 1 of the intracranial pressure volume curve
ICP < 15mmHg and compensatory mechanisms are able to compensate for changes
zone 2 of the intracranial pressure volume curve
intracranial volume expands and compensation becomes exhausted marked by a sharp increase in ICP
zone 3 of the intracranial pressure volume curve
Intracranial volume continues to increase until it plateaus, indicating herniation
hypercapnia effect on CBF
vasodilation increasing CBF of 2mg/100g/min for every 1mmHg PaCO2
con of hypocapnea used to manage ICP
-cerebral ischemia, particularly with brain injury -vasoconstriction lasts for 18-24hrs. Due to loss of cerebral interstitial bicarb, normalization of cerebral interstitial pH occurs and mitigates the vasoconstrictive effects of hyperventilation -rebound vasodilation can occur leading to lethal spikes in ICP -hypoxia results from cerebral vasodilation when PaO2 falls below 55mmHg
how does temperature effect CBF
-hypothermia slows metabolism - every 1 degree change over normal temp= 5-7% increase in CBF
CBF=
CPP/CVR
CPP=
MAP-ICP
Cushings Triad
bradycardia, HTN, wide PP occurs in response to brain stem ischemia
abducens nerve palsy
compression of CN 6 at base of the skull
fixed dilated pupil(s)
increased ICP in supratenorial compartmennt. compression of oculomotor nerve causing unilateral pupil dilation and contalatral hemiparesis
where is an EVD levelled to
foreman of mono (level of the trigus of the jaw)
major causes of increase ICP
-Intracranial mass lesions (eg, tumor, hematoma) -Cerebral edema (such as in acute hypoxic-ischemic encephalopathy, large cerebral infarction, severe traumatic brain injury) -Increased CSF production (eg, choroid plexus papilloma) -Decreased CSF absorption (eg, arachnoid granulation adhesions after bacterial meningitis) -Obstructive hydrocephalus -Obstruction of venous outflow (eg, venous sinus thrombosis, jugular vein compression, neck surgery) -Idiopathic ICH (pseudotumor cerebri)
how does the optic nerve sheath diameter reflect ICP?
changes in diameter with CSF pressure changes as there is a layer of subarachnoid space between the nerve and its sheath, which expands due to raised intracranial pressure. EVD, SAH and hydrocephalus will cause falsley elevatd ICP
what does the neuro exam consist of
1 cranial nerves 2 motor/reflex/sensory 3 cerebellar 4 cognitive
what are the 5 parts of the CNS
cerebrum, diencephalon (thalamus and hypothalamus), brainstem, cerebellum and spinal cord
function of the cerebrum
-comprised of the cerebral hemispheres -processes higher-order functions -supplies neuronal connections to nervous system outlets to voluntary/involuntary muscles and diencephalon -receives sensory input from peripheral nervous system
what separates the left and right cerebral hemispheres
falx cerebri
what separates the posterior hemispheres from the intratentorial compartment
tentorium
what is contained in the intratentorial compartment
cerebellum and brainstem
thalamus
- part of the diencephalon - serves as a relay centre for sensory input from the body to the sensory cortex of the parietal lobe -regulates function of the basal ganglia, hypothalamus and cerebellum
hypothalamus
- derived from the ANS, regulates wakefulness/satiety/hormones/thermoregulation -site of ADH production which is stored in the posterior pituitary
brainstem
-midbrain, pons and medulla located between cerebrum and continues with the spinal cord - relays sensory of motor functions between cerebral cortex and spinal cord - houses 10 of the 12 CN - houses the RAS system -houses respiratory centre in the medulla
purpose of intracranial pressure monitoring
detect catastrophic intracranial patho
- prevent secondary injury
- monitor for cerebral edema
ICP > 20-25mmHg- adverse outcomes
what therapy influences the parenchyma
sedation (propofol, midazolam, ketamine) ( managing flow-metabolic coupling)
tempurature control (every degree decreased = 10% decrease in metabolism and blood volume) aim for 36-37.5
osmotherapy ( no difference between mannitol to hypertonic in lowering ICP)
mannitol dose
hernaition 1 gram /kg
non- herniation 0.25- 5gram/kg
maximum sodium level where administering hypertonic saline could be detrimental
150
what treatment influences CSF
what treatment influence valsular volume
venous return (tube ties, collars, HOB at 30(5-10mmHg reduction), PEEP), PaCO2)
-TBI is a contraidication for permissive hypercapnea
MAP goal for epidural hematoma
MAP goal of subdural or DAI
best pressor to use in setting of brain injury
in the settin of cardiac arrest, when does the majority of brain damage occur
Mip’s post arrest mamngemnt goals
map 80, normal co2, temp 35-36, hemoglobin 90, PaO2 100
what in CN 4 responsible for
what does unilateral pupil constriction indicate
what do you consider prior to hypertonic saline
sodium
what does doll’s eyes examine
CN 8
if eyes stay midline-good
if eyes follow head turning-not good
meningitis
hallmarks of meningitis
fever, headache, nucal rigidity (if pt has 2 or more, consider it)
best rule out test manipulate neck side to side if headache doesnt get worse, unlikely meningitis
reason to do LP prior to CT
safe to LP(L3-5, 20-30ml removed) or not, LP can cause herniation
age>55, immunocomprimed,
ABX for viral meningitis
ampicilin , Vancomycin ,acyc
GBS
acute demylinating disease
exposure to a infection = antibodies, antibodies cross react with mylin in peripheral nerves
presentaion: acute peripheral hand ascending upwards (attacks long mylin first), sensation is largly spared
vital capcitiy ,20ml/kg = intubate (caution due to automonic instability (brady or hypertensive) = prior to intubation prepare atropin and hydralazine
long term tx: IV IG, plasma
myasthenia gravis
autoimmune disease (antibodies) that act against ACH in neuromuscular junction. Pt will have preserved sensation, proximal weakness
indication to intubate: bulbuar dysfunction, vital capacity < 20ml/kg (caution, pt will have hypersecretions)
myasthenia crisis: tipping pt into crisis with meds
TX: steroids, IV IG and plasmapheresis
Contraindication for giving phenytoin
toxicity or injestion of a sodium blocker (TCAs)
refractory status epilecticus treatment
propofol, mizaloam or ketamine IV infusion
other considerations for seizure management
reduce fever (fever reduces seizure threshold), magnesium (2-5g maintian mg > 1)
approach to causes of seizures
DIMS
drugs- non-compliance with AEDs, OD (salicylates,sympathomimetics, isoniazid)
infection- meningitis/encephalitis (especially HSV)
metabolic- NA,Mg,Ca, renal failure/uremia, hypogycelmia, liver failure
structural- neoplasm, TBI, NMD
stroke- ischemic, ICH
other- antibody
when do you administer seizure prophylaxis in TBIs
temporal lobe pathology, penatrating trauma, diagnosed with seizure disorder prior to injury
Asia scale
at what level of spinal injury do you intubate pts
C 5 and above
if bicepts are fuctioning, unlikely to require intubation
at what level do you expect neurogenic shock
T 1 and below is where sympathetic efferent nerves inervate the heart. therefore injurieas above =unopposed vagus cardiac stimuli, and poolin gof blood due to lack of A1 innervation to lower
meds of choice: norepinephrine, epinephrine
MAP goal: 85
what is the treatment goal for an unsecured aneurysm
prevension of rebleed: bleed occurs during systole, that is why systolic goal is less than 140 SYSTOLIC
complications of SAH
hydocephalus
vasospasm
Na (high or low) (low can be DI due to hypothalmus not functioning)
seizures
cardiac (arrythmias, cardiomyopapthy for catecholmine storm )
BP targets for SAH management
BP < 180 if lysed
BP <220 if not
BP <140 is hemorrhagic complication
signs of uncul herniation
unilateral pupil dilation unreactive pupil, contralateral paralysis (motor crosses below midbrain)
tonsilar herniation
cerebellum pahtology (stroke or hem) herniation which compresses the brain stem (DLOC, weakness,central apnea, CN reflexe loss (too late)). This is because the tentorum is above it, stoping it from herniating upwards
meningies extend to what level of the spinal cord
L 1-2
how is a sensory stimuli transmitted to the brain
touch pressure vibration proproseption sensed and enters the dorsal tract where it interacts with interneurons and sends a signal up the dorsal root, to the medulla and transmitted up the opposited side of the brain through the thamli. Motor responses exit through the ventral tract to the effector muscle
lower limbs- lumbar
upper limbs-cervical
aterospinal artery infarct
- infacarct of 2/3 of the spinal cord
- bilateral loss of motor function, pain/temp sensation
- doral column spared= intact vibration/fine touch/proprioception
central cord syndrome
- hyperextension of the neck (backwards), imcomplete cord syndrome
- variable sensory
- weak proximal muscle weakness
- distal muscles are strong
brown sequard syndrome
- hemipalaysis and hemi anesethia
- loss of pain and temp contralateral
- ipsilateral weakness
cauda equina
- tx within 24hrs
- loss of bladder, lower sphicter, lower leg loss of control
bs, central, anterispinal infact, cauda equina, subacute
