Neurology Flashcards
Frontal lobe function
Planning and execution of movement
speech
smell
problem solving
Parietal lobe function
Sensory input - touch
pressure
Body orientation
Temporal lobe function
Understanding language
Behavior
Hearing
Memory
facial recognition
Occipital lobe function
Vision
Color perception
Cerebellum function
Balance
Coordination of voluntary movement
Fine muscle control
Brain stem function
Breathing
Temperature
Digestion
Alertness/sleep
Swallowing
Hippocampus function
Memory
Amygdala function
Emotions
Thalamus function
Relay signals from lower brain to cortex
Basal ganglia function
Sorting, evaluating and executing motor functions, filtering out unwanted movement
parts of basal ganglia
caudate nucleus
putamen
globus pallidus
subthalamic nucleus
substantia nigra.
grey matter content
neuronal cell bodies
white matter content
neuronal axons forming tracts
what does the sympathetic nervous system do to the eye?
Causes pupillary dilation - Mydriasis by the pupillary dilator muscle
Innervation of the pupillary dilator muscle
Postganglionic sympathetic fibers project from the superior cervical ganglion. Fiber travel with the ophthalmic artery, forming a number of long ciliary nerves that supply the dilator pupillae muscle
what does parasympathetic nervous system do to the eye
Cause pupillary constriction by sphincter pupillae muscle - Miosis
innervation of pupillary sphincter muscle
Receives parasympathetic innervation via the short ciliary nerves. Fibers originate from the Edinger-Westphal nucleus of cranial nerve III.
Pupillary accommodation
Contraction of ciliary muscle: near vision
Relaxation of ciliary muscle: fare vision
innervation og cilliary muscle
These parasympathetic fibers arise from cranial nerve V, also known as the nasociliary nerve of the trigeminal.
Areas of lesion causing effect on pupil
Hypothalamus controls - PSNS - constriction
Paravertebral SNS - dilation
Neck - fibers run with ICA
Trauma to orbit
name of pupillary constriction and dilation
dilation: Mydriasis
constriction: miosis
name of unequal size of pupils
Anisocoria
part of pupil is missing name
coloboma
describe the light pupil reflex
- light in right eye
- AP in pretectal nuclei
- signal from pretectal to EW nuclei - AP
- EW generate AP through the CN III
- Oculomotors nerve causes miosis
causes of mydriasis
CN 3 lesion
Adie’s pupil
Migraine
Drugs
seen in complete CN 3 lesion
mydriasis
ptosis
impaired eye movement
loss pupil reflex
drugs causing mydriases
Anticholinergics
TCA
NSAIDS
oral contraceptives
Antihistamins
causes of miosis
Horners syndrom
Argyll Robertson pupil
Drugs
content of facial nerve?
Motor fibers
Taste fibers - visceral afferent
Parasympathetic - visceral efferent
path of facial nerve motor nerve
from lateral brain
cerebellopontine angle
internal auditory meatus
facial canal
exit through stylomastoid foramen
path of parasympathetic fibers of facial nerve
With facial nerve into internal auditory meatus
what part og tongue is innervated by the facial nerve?
anterior 2/3
what is bells palsy
acute paralysis of the face related to a inflammation or swelling. usually unilateral.
etiology of bells palsy
viral infections: HSV VZV + others
what is bells phenomenon
attempt to close eyes and show teeth one eye can’t close and eyeball roles back
treat bells palsy
protect eye when sleeping + eyedrops
high dose prednisolone 10 days
antiviral therapy if known virus
Ramsay hunt syndrom
herpes zoster infection affecting the geniculate ganglion sudden severe pain, eruption of vesicle in external ear
deafness may be an outcome if CN VIII involvement
hemifacial spasm
- unilateral clonic spasms from orbicularis occuli then to rest of face
- contractions are irregular and increases with emotional stress and fatigue
- cause: vascular comprssion like tumor
vertigo dizziness
Room is spinning due to loss of orientation of body in space
causes of Central vertigo
■ Tumor (astrocytoma)
■ Cerebrovascular disorders
● Stroke
● Vertebrobasilar insufficiency
● TIA
■ Migrainous vertigo
■ Drugs/toxins
■ Multiple sclerosis (demyelination)
■ Inflammation (meningitis, cerebellar abscess)
■ Trauma
etiology of peripheral vertigo (85%)
■ Idiopathic
■ Menière’s
■ BPPV (benign paroxysmal positional vertigo)
■ Trauma
■ Drugs: streptomycin, quinine, salicylates
■ Labyrinthitis
■ Vestibular neuronitis
■ Cerebellopontine angle tumors
● Acoustic neuroma
● Meningioma
non-vertigo dizziness
Psychogenic (diagnosis of exclusion)
■ Depression
■ Anxiety etc
Vascular
■ Orthostatic hypotension
■ Arrhythmia
■ CHF
■ Aortic stenosis
■ Vagovagal episodes
Ocular
■ Decreased visual acuity
nystagmus in central vs peripheral nystagmus
central: Bidirectional horizontal or vertical
Peripheral: Unidirectional horizontal or rotatory
6 things you compare central vs peripheral
imbalance
nausea vomiting
auditory symp
neurological sympt
compensation
nystagmus
Ménière disease is a
Ménière disease is a disorder caused by build of fluid in the chambers in the inner ear. It causes symptoms such as vertigo, nausea, vomiting, loss of hearing, ringing in the ears, headache, loss of balance, and sweating.
to differentiate vertigo from dizziness
vertigo: WORLD IS SPINNING
dizziness: unsteady or lightheaded
Plegia vs paresis
plegi: complete loss
paresis: loss of power
Different pareses/plegias
Hemiplegia/hemiparesis: unilateral weakness of the limbs
Monoplegia/monoparesis: weakness of one limb,
Paraplegia/paraparesis: weakness of both lower limbs,
Diplegia/diparesis: weakness of both upper limbs,
Quadriplegia/tetraplegia or quadriparesis/tetraparesis: weakness of all four limbs,
Lesion of the corona radiata and the internal capsule causes
contralateral severe spastic hemiparesis with involvement of the lower part of the face and the tongue
Isolated lesion of the corticospinal tract in the cerebral peduncle and lesion of the pyramid in the medulla cause
flaccid weakness, however the joint lesion of all descending tracts leads to spastic hemiparesis.
Unilateral lesion of the base of the pons causes
contralateral hemiplegia/paresis, often sparing the face
Bilateral lesion of the base of the pons causes
quadriparesis/plegia.
Unilateral lesion of the cervical spinal cord at the level of C1-4 segments causes
ipsilateral spastic hemiparesis.
Bilateral lesion of the cervical spinal cord at the level of C1-4 segments causes
spastic quadriparesis
Lesion of the cervical spinal cord at the level of C5-Th1 segments causes
spastic weakness of the lower limbs and flaccid weakness of the upper limbs
Lesion of the thoracic spinal cord causes
spastic paraparesis
Lesion of the lumbosacral spinal cord causes
flaccid paraparesis.
Lesion of spinal motoneurons and anterior roots causes
flaccid weakness of segmental
distribution (in the corresponding myotomes)
Polyneuropathy typically causes
distal symmetrical flaccid weakness of the limbs, first on the lower limbs.
most important symptom of UMNL and LMNL
UMNL: BABINSKY - positive pyramidal sign
LMNL: visible fasciculation’s
lateral corticospinal tract is for
distal limbs and fine manipulation
anterior/ventral corticospinal tract is for
trunk and upper leg muscles (posture locomotor)
UPNL paralysis:
LMNL paralysis:
UPNL paralysis: spasmic
LMNL paralysis: flaccid
spasmicity vs rigidity
Spasticity: resistance in one direction. Velocity-dependent.
Rigidity: resistance in all directions. Not velocity-dependent
fasciculation vs fibrillations
○ Fasciculations: Visible twitching of motor unit of muscle due to spontaneous firing of
action potentials from damaged nerve
○ Fibrillations: Non-visible twitching of individual muscle fibers when nerve is even more
damaged - only seen on electromyogram
main cause of UMNL
stroke
demyelination
ALS
man cause of LMNL
polio
west nail virus
spinomuscular athropy
cauda eq. syndrom
DM neuropathy
botulism
ALS
what are the two fibers innervated in a muscle
Intrafusal Gamma fibers: reflex
Extrafusal alpha fibers contraction
where does the corticospinal tract deccusate
in the pyramids (brainstem)
what is the cerebrobulbar tract?
goes from cortext to pons/medulla and innervate CN
destination of corticobulbar tract
CN 5
CN 7
Nucleus ambiguous: CN 9, 10, 11
CN 12
why is there athropy in UMNL
loss of usage
loss of Ach release causing no AP or protein synthesis,
80% muscle loss
pathophysiology of fasciculations?
no Ach causes increase in R formation and increased mechanical sensitivity - tapping causes activation of reseptorc opening Na channels and AP
why is there spasmic paralysis in UMNL
because of less inhibitory signals from medullary reticulospinal tract causing hyperflexia and hypertonia
which side is the speech senter on?
LEFT hemisphere is dominant in most people
what is aphasia
Aphasia is a speech disorder with an inability to comprehend and/or formulate language. It is caused by
lesions of cortical speech centers and their connections
Broca’s and Werncks aphasia is?
Broca: Expressive
Wernicks: receptive
Areas in Brocas
BA 44
BA 45
areas in wernicks
WA 22
WA 39
WA 40
BA aphasia present?
know what do say but cant say it
NON FLUENT
skjønner men finner ikke ord
WA aphasia present?
difficulty understanding and finding right words, mix up words
snakker om helt rare ting
causes of aphasi
stroke
trauma
brain mass
neurodegenerativ disorders
encephalitis
conduction aphasia
understands and speaks but cant repeat
what supplies speech area?
middle cerebral artery
which artery infarct causes wernicks aphasia?
BRANCH OF MIDDLE CEREBRAL ARTERY: posterior temporal artery
etiology of conduction aphasia
Lesion of the arcuate fasciculus. Characterized by normal speech, but impaired repetition. Patient is aware and frustrated by this.
alexia without agraphia
Lesion in left occipital lobe usually due to infarct of the posterior cerebral artery.
The visual information cannot reach the language areas, and the patient is unable to read, but are able to
write (pure word blindness)
how can you find out which side language senter is on?
dominant hand: right hand - left area
left hand: mix of both 70% left 15% right 15% bilateral
what connect BA and WE
arcuate nucleus
The anatomical basis of arousal is the
Ascending reticular activating system (ARAS),
composed of the pontomesencephalic reticular formation, monoaminergic networks of the diencephalon and the intralaminar and medial nuclei of the thalamus
Disorder of arousal
● Somnolence - Mildest form. Awakens with
verbal stimuli, but is asleep without stimuli.
● Stupor - Patient may open eyes to painful stimuli, verbal is not enough. Slow and inappropriate reaction to stimuli.
● Coma - Cannot be awakened. Abnormal posture (decorticate or decerebrate).
i. Coma I - Preserved brainstem reflexes
ii. Coma II - Lost brainstem reflexes
disorders of awakefullness
Persistent vegetativ state
akinetic mutism
confusion
delirium
locked in syndrom
define persistant vegetativ state
Awake but not awareness of their surroundings.
Rostral brainstem remains intact → Thermoregulation (hypothalamus), sleep-wake cycle, endocrine system, cardiorespiratory and other visceral functions are intact
when is a vegetativ state permanent?
> 30 days
decorticated position
stiff with bent arms, clenched fists, and legs held out straight. Sign of severe damage in the brain
decerebrated position
all limbs are stiff en extended. Results from a rostral brain stem lesion and leads to extension of all four limbs and opisthotonos (spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus)
causes of vegetativ state
Extensive functional or structural impairment of
cerebral cortex
- global cerebral ischemia
- hypoglycemia
- renal/hepatic failure
- post-convulsive state
- Wernicke’s encephalopathy
- final stages of cortical dementias)
○ Extensive white matter damage
○ Bilateral damage to the thalamus
define akinetic mutism
- Awake, but mute and does not move.
causes of akinetic mutism
Caused by bilateral interruption of connections between the supplementary motor
area, cingular region and midline nuclei of the thalamus
are you paralised in akinetic mutism
NO, because of withdrawal reflex to pain, suckling reflex, and grasp reflex
etiology of akinetic mutism
○ Jet bleeding
○ Bilateral ischemia in the anterior cerebral artery
○ Subfalcial herniation
○ Occlusive hydrocephalus
○ Butterfly tumors growing across the corpus callosum
○ Tumors of third ventricle
define delirium
Cannot focus, change or fix attention.
Disoriented and incoherent thinking.
Evolves over 24h.
Inversion of sleep wake cycle. sweating, tachycardia unstable BP
what do you have to have to be counscious`
awareness
arousal
alertness
memory
function of ascending reticuloactivating system (ARAS)
reflexes
sensory information
respiration
HR/BP
sleep cycle
consciousness
posture
composition of ARAS system?
medial column
lateral column
medial column
composed of A LOT of nuclei
4 things to look for first in an unconscious patient
looks like sleeping?
spontaneous movement?
respons to voice/stimuli?
respiration stable?
how do you examine a uncounscious patient?
- observe
- stabile ABC
- GCS
- signs of external rauma
- eye position and reflexes
- limb position and reflexes
- deep tendom reflex
GCS values
< 3 high rate of death
< 8 coma –> intubate
15 is normal
deep tendon reflexes?
There are five primary deep tendon reflexes: biceps, brachioradialis, triceps, patellar, and ankle.
brain stem reflexes
Pupillary Light Reflex.
Corneal Reflex
Oculo-vestibular Reflex
Pain Stimulus.
Gag Reflex.
Cough Reflex.
findings in an unconscious patient and their cause?
1. Pupillary constriction (light reactions are preserved!)
2. Pupillary dilation (NO pupillary light reactions)
3. Fixed, moderately dilated pupils
4. Skew deviation (eyes diverge in vertical direction, one down, the other up)
5. Persistent upward deviation
6. Persistent downward deviation
- Bilateral → hypothalamus and diencephalon damage. Unilateral: Horner’s
- tectum lesions
- lesion below tectum
- caudal part of brainstem and meso-diencephalon damage
- global cerebral ischemia
- hepatic coma
what are the two vestibular reflexes
- move head side to side, pupils should move in opposite direction.
- cold/warm water stimulus COWS
what type of unconsciousness is normally related to metabolic origin?
persistent vegetativ state also called unresponsive awakefullness syndrom
metabolic causes of unconsciousness
● Deficiency of essential substrates (glucose, oxygen, vitamin B12)
● Exogenous toxins (eg. drugs, heavy metals, solvents)
● Endogenous toxins/systemic metabolic diseases (eg. uremia, hepatic encephalopathy, electrolyte
imbalances, thyroid storm
how can you diff between structural defect or coma due to hypoglycemia?
pupillary relex normally intact f hypoglycemia
what glucose level causes coma?
< 0.6 mmol/L
what is seen in hyperglycemia
hyperosmolar effect can cause coma. Can cause involuntary movements, seizures and hemiparesis
symptomes in ketoacidosis
Symptoms: dehydration (due to osmotic diuresis), fatigue, weakness, headache, abdominal pain,
Kussmal breathing, confusion, coma
when is consciousness lost if pO2 drops
< 40 mmHg
pupils in hypoxia?
large and reactive
what happens in renal/uremic encephalopathy`
false neurotransmitters in brain like Octopamine. EEG shows slow waves
symptoms hepatic encephalopathy
pupils small-reactive
Asterixis, myoclonus, dysarthria, ataxia, hyperreflexia, hemiparesis
define
Myoclonus
Dysarthria
ataxia
Myoclonus: uncontrolled jerking
Dysarthria: speech muscle weakness
ataxia: loss of limb muscle control
glucose level in hyperosmolar hyperglycemia`
VERY VERY high - monitor cant read > 600 mg/d
treatment og HHS
0.9% sline then 0.45%
change to dextrose when glucose is 250 mg/d
give regular insulin IV OBS K+ must be > 3.3
what electrolyte disturbance causes coma
Hyper Na / Hypo Na
Hyper Cl /hypo Cl
Hyper Mg
Hypo K+ / Hyper K+
drug intoxication causing coma
overdose in suicidal intent og sleeping pills and sedativs
areas most sensitiv to hypoxia
basal ganglia and cortex
neurological states causing resp failure
The CNS → Raised ICP - hernia
The PNS → Myasthenia, Guillan-Barré syndrom
3 causes of an neurological emergency
- stroke
- seizure
- unconsciousness
what are the 3 main components of intracranial volume?
CSF
brain tissue
Blood
if one increase the other must decrease
CSF volume
approximately 125 mL to 150 mL
normal intracranial pressure
7–15 mm Hg
monroe Kellie principle
cerebral bloodflow is the ratio of CAP and CVP (AP/VP) = cerebral perfusion pressure
IC pressure = CVP
so increase in ICP always increase CVP thus decrease perfusion pe
what are the two principle ways of decreasing ICP
by decreasing CSF (physiological)
by decreasing blood (not physiological)
how can we decrease BF to brain?
Hyperventilation dec. CO2 and causes capillary restriction and decreased CVP
Barbiturate narcosis decreases metabolism need
Hypothermia decreases metabolism need
causes of increased ICP
- Space-occupying lesions (eg. tumor, abscess, hemorrhage) - treat with surgery
- CSF disorders (occlusive hydrocephalus) - treat with CSF drainage
- Cerebral edema (vasogenic, cytotoxic, interstitial)
clinical presentation of increased ICP
● Progressive headache (one of leading complaints)
● Vomiting
● Papilloedema + blurred vision
● Always global cerebral dysfunction due to global cerebral ischemia
treatment of high ICP
● Treat underlying etiology
● Osmodiuretics (mannitol, glycerol)
● Loop diuretics decrease CSF production
● ICU:
○ Controlled hyperventilation
○ Barbiturate narcosis
● Decompressive craniectomy
how can you pres CSF our if head yourself?
valsava manuver
what are the 4 brain herniations?
- Cingular/subfalcial
- central
- transtentorial
- transforaminal/tonsillar
what happens in Cingular/subfalcial herniation
Cingular gyrus in pressed under the falx.
May compress circumferential branches of anterior
cerebral artery (pericallosal, collosomarginal) if mass
effect is considerable.
what happens in central hernia
Compression of diencephalon.
Severity is proportional to lateral or axial shift of diencephalon.
what happens in transtentorial hernia
Compression of mesencephalon in tentorial incisure -
damaged blood supply of mesencephalon and secondary
intraparenchymal bleedings.
which artery bleeds in
epidural
subdural
subarachnoid
- MCA
- bridging veins
- intracranial aneurism rupture
what to asses on a intracranial injury
○ Period of loss of consciousness: relates to severity of diffuse brain damage
○ Period of post-traumatic amnesia: reflects severity of damage
○ Period of retrograde amnesia
○ Cause and circumstances of the injury: e.g. epilepsy
○ Presence of headache and vomiting: if they persists, IC hematoma must be considered
imaging in IC hematoma suspicion
stat CT !!
symptomes indicating specific locations of basal skull fractures
○ Anterior fossa fracture: CSF rhinorrhea (contains glucose), bilateral periorbital
hematoma, subconjunctival hemorrhage
○ Petrous fracture: bleeding from external auditory meatus or CSF otorrhea,
bruising over the mastoid (Battle’s sign)
management of intracranial hematoma
Extradural: horseshoe craniotomy flap w/ complete evacuation of the hematoma
Subdural/intracerebral: questionmark flap over temporal and/or frontal areas w/
subdural/intracerebral evacuation of hematoma and necrotic brain
IC bleeding pattern on imaging
Epidural is lens shaped
subdural cresent shaped
types of spinal cord injury
Acute transverse
Brown-Sequard syndrom
Anterior cord
Central cord
Conus medullaris
Spinal cord concussion
Cauda equina syndrom
most vulnerabel spots for spinal cord injury
border between rigid and flexible regions (craniocervical, cervicothoracal, thoracolumbar zones)
outcome of acute transvers spinal cord injury
quadriplegia
anesthesia
loss of all function below injury site
Brown-Sequard syndrom
Rare, mainly due to trauma (e.g. gunshot,
stabwound)
Ipsilateral proprioceptive sensory loss
(proprioceptive tract) and weakness
(corticospinal tract) with contralateral loss of
pain and temperature (spinothalamic tract)
central spinal cord syndrom presentation
Lateral CS stract: cervical+thoracic
White commissure: pain, T, crude touch
anterior grey horn LMNL
posterior spinal cord lesion
Dorsal column: gracilis, cuneate: proprioception, vibration, disc. touch
anterior spinal cord lesion
anterior 2/3 are involved
autonomic fibers: incontinence
Corticospinal tract: UMNL
Anterior grey horn LMNL
spinothalamic tract: pain, temp, crude touch
only preserved is the dorsal column
conus medullaris syndrom
Sensory loss (numbness) in the perianal region and inner thighs (saddle anesthesia) and loss of bladder control (retention with overflow incontinence) without leg weakness or diminished stretch reflexes
Cauda equina syndrome
Radicular pain in several dermatomes, flaccid paralysis of lower limbs with loss of deep tendon reflexes and overflow incontinence
jefferson vertebrate fracture
fracture of both arches of C1
stiff neck, pain when moving, no neuro signs
Dens vertebrate fracture
C2 fracture
Neck pain radiating to occipital region (worse with neck movements), typically the patient
will hold their head
type A C B vertebrate fractures
A: compression = shortening
B: distraction = lengthening
C: Torsonal = rotation
symptoms of impaired circulation of ICA
○ Deterioration of consciousness
○ Homonymous hemianopia of the c/l side
○ Contralat hemiplegia
○ Contralat hemisensory disturbance
○ Gaze palsy to opposite side, eyes deviated to the side of lesion
● A partial Horner’s sy. may develop (SY fibers on the ICA wall)
● Occlusion of the dominant hemisphere → global aphasia
Occlusion of anterior cerebral artery
supplies medial part of hemisphere: lower limb
primary motor cortex: weakness c/l
somatosensory cortex: sensory loss C/l
occlusion of middle cerebral artery
supply lateral part of hemisphere: upper limb
sensory and motor loss + Broca’s area
occlusion of posterior cerebral artery
Occipital lobe: vision
homonymous hemianopia
what does insula do
decision-making
supplied by the vertebrate arteries
medulla and inferior surface of cerebellum
supplied by the basilar artery
brain stem from medulla and up and gives off PICA and AICA
what is supplied by the vertebrobasilar system
brainstem, medulla, pons, cerebellum, occipital lobe, midbrain, thalamus
symptoms of vertebrobasilar insufficiency
○ Drop attacks (weakness of quads→ fall to the ground)
○ Diplopia
○ Dysarthria
○ Dizziness
○ Vertigo
○ Dysphagia
resolves within 24h
cause of vertebrobasilar insufficiency
VBI is usually caused by
atherosclerosis, hypertension,
diabetes, smoking, dyslipidemias.
how to treat VBI
Treatment often includes lifestyle changes and treatment of underlying conditions. Patients can
also get started on antiplatelet or anticoagulation. Angioplasty is a possibility
posterior cerebral artery stroke
- Contralateral hemianopia or quadrantanopia
- Midbrain findings: ipsilateral CN III and IV palsy/pupillary changes, contralateral
hemiparesis/hemiplegia (Weber’s syndrome) - Posterior cortical infarction in dominant hemisphere: problems in naming colors and
objects
basilar artery stroke
locked in syndrom
- bilateral loss of corticospinal tract - complete paralysis
- Preserved vertical eyemovement + blinking
- patient is conscious alert and aware
AICA stroke
lateral pontine syndrome
- I/L CN VII palsy
- I/L vestibular nuclei damage: vertigo and nystagmus
- I/L Ataxia: poor coordination
- C/L loss og pain and temp (ST tract)
anterior spinal artery stroke
Causes medial medullary infarct
○ Contralateral hemiparesis (facial sparing), contralateral impaired proprioception and
vibration, ipsilateral tongue weakness
PICA stroke
loss of coordination, balance and muscle tone
CN X - dysphagia and loss of gag reflex
horners syndrom
what is horners syndrom
ptosis
miosis
anhydrosis
occurrence of ischemic vs hemorrhagic stroke?
ischemic 85%
hemorrhagic 15%
what is a ischemic stroke tat resolves within 24h called?
TIA
to causes of ischemic stroke?
endothelial; clotting
embolism/thrombosis
first imaging in a ischemic attach
stat CT no contrast to rule our SAH or ICH
if no SAH or ICH and you cant see lesion on CT you…
take a CT angio and look for filling defect
MRI on a ischemic stroke you do
DWI and a ADC and compare them
DWI show bright hyperintens
ADC show dark hypointens
treatment of ischemic stroke
- last known well < 4.5h ago give TPA
- if last known well is more then 4.5-6h ago evaluate:
- no SAH/ICD
- no DM or previous stroke
- > 18 yr
- NIHSS < 25
- infarct is < 1/3 of MCA territory
contraindication of TPA
If the ischemic stroke is affecting >⅓ of the MCA territory - reperfusion can lead to hemorrhagic transformation
○ Mild symptoms/symptoms improving
○ Cerebral trauma or AMI in the last 3 months
○ Surgery the last 2 weeks
○ Present or previous intracranial hemorrhage/SAH
○ BP >185/110 mmHg
○ Peptic ulcer, epilepsy, hypoglycemia, fracture
○ INR>1.7, abnormal APTT, PLT<100.000/mm3
what to do if no tpa treatment in stroke
mechanical thrombectomy
if large vessel occlusion MCA, ICA, Basilar
BP goals in stroke
if tPA < 185
if no tPA < 220
BP medication in stroke
NIcardipin IV
Labetolol IV
Hydralazine
DOAC’s
dabigatran
rivaroxaban
apixaban
most common cause if hemorrhagicc stroke
sustained HT causing rupture
trauma
cerebral amyloid angiopathy (b-amyloid plaque)
coagulopathy
hemorrhagic transformation from a ischemic stroke
malignancy
most common location of a hemorrhagic stroke
pons
cerebellum
basal ganglia
cortex (least common)
what to look for on imaging in hemorrhagic stroke
midline shift
hydrocephalus/IVH
blood pressure goal im hemorrhagic stroke
< 160
reversal of anticoagulants
warfarin - vit K
Heparin - protamin
Dabigatran -Idarecizumab
Apixaban or Rivarozaban- Adrexanet
when to intubate in cerebrovascular disorders
intubation is necessary if bulbar reflexes are absent/patient is in coma
when to mechanical ventilate in cerebrovascular disorders
saturation < 90% or pCO2 > 50 mmHg → mechanical ventilation
give glucose in cerebral ischemia?
Glucose is contraindicated in cerebral ischemia (except in hypoglycemia).
when to give insulin?
Insulin should be given if glucose levels > 15 mmol/L (target: 7,8-10 mmol/L
nucleus related to dysphagia
nucleus ambignous
dose of tPA
0.9 mg/kg (max 90mg), and 10% is given as i.v. bolus followed by 1h infusion of remaining 90%. Check BP and neurologic symptoms every 15 min during infusion.
when is follow up CT indicated in stroke
24h
when should antiplatelet therapy start in stroke
NOT before 24h
define cerebrovascular disorder
Cerebrovascular disorders include all disorders in which an area of the brain is temporarily or
permanently affected by ischemia or hemorrhage, and one or more of the cerebral blood vessels are
involved in the pathological process.
stroke Protocall
- ABCDE (remember glucose)
- Blood samples (Glucose, INR) and blood pressure
- GCS, NIHSS: neurological screening assessment
- ECG (should not delay CT/MRI)
- CT or MRI (should be interpreted within 45 minutes)
○ Hemorrhage: consult neurosurgeon
○ Ischemia: candidate for thrombolysis - Thrombolysis (rtPA) if within therapeutic window
how can imaging tell us if we are still in the therapeutic window?
DWI shows ischemia while FLAIR shows no ischemia
how can imaging show if there is pneumbra?
DWI-PWI mismatch: DWI shows infarct core, while PWI shows hypoperfused tissue,
INR value allowing thrombolysis ?
< 1.7
mandatory to check before thrombolysis
● Hypoglycemia (glucose): can mimic acute stroke
● Coagulopathies (INR): CI of thrombolysis (should be under 1,7 to perform)
● Blood pressure (BP): hypertension increase hemorrhagic risk of thrombolysis
diagnostic considerations in cerebrovascular disease
Presence of clinical signs (WHO)
● Hemorrhagic vs. ischemic (CT, MRI)
● Pathomechanism (thrombotic, embolic, hemodynamic, small vessel disease)
● Duration of signs
● Brain region (hemisphere, cerebellum, brainstem; territorial-borderzone)
● Anterior-Posterior
● Supplying vessel (carotid artery, vertebrobasilar, lacunar, ACA, MCA, PCA)
● Prognostic by signs (Bamford – OCSP)
○ TACI, PACI, POCI, LAC
○ TACI, PACI, POCI, LAC
TACI: total anterior circulatory stroke
PACI: partial anterior circulatory stroke
POCI: posterior circulatory syndrom
LACI: Lacunar syndrom
cranial nerves run in the cavernous sinus what can happen
oculomotor
Opthalmic
maxillary
abducent
can be compressed if infection causing CN palsy
eye innervation muscle
superior, medial and inferior rectus + inferior bliq by CN III
lateral rectus by CN VI
superior oblique by CN IV
2 venous systems of brain
superficial and deep + sinuses
Thrombotic occlusion of the venous system occurs with:
● Infection (especially ear or sinus infection)
● Dehydration
● Pregnancy and puerperium
● Coagulation disorders
● Malignant meningitis
● Miscellaneous disorders (e.g. sarcoid, Behçets)
most frequent place of venous thrombosis in brain
Superior sagittal and lateral sinus thrombosis (85% of cases)
symptoms of cerebral venous thrombosis
○ Impaired CSF drainage results in headache, papilloedema and impaired consciousness.
○ Venous infarction produces seizures and focal deficits (e.g. hemiplegia).
CT sign of venous thrombosis
‘Empty delta’ sign (following contrast the wall of the sinus enhances but not the central
thrombus on CT)
treatment of cerebral venous thrombosis
Treatment: Correct causative factors (dehydration/infection etc.) + anticoagulation with heparin or alternative
cavernous sinus thrombosis signs
● Commonly results from infection from the jaw
● Painful ophthalmoplegia, proptosis and oedema of periorbital structures are associated with facial numbness and fever.
● The disorder may be bilateral.
● Treatment with antibiotics and if indicated, sinus drainage.
prognosis of intracranial bleedings?
approximately half of patients
die within 30 days
most common site of intracranial bleeding
In hypertensive patients 70% occur in the basal ganglia/thalamic region. In normotensive patients, 37% occur in this area
signs of intracerebral hemorrhage
- Basal ganglia - Hemiparesis, sensory loss, eye deviation
- Thalamus - Sensory loss, later hemiparesis, gaze disturbance
- Lobar - Better prognosis, intraventricular bleeding is rare
- Cerebellar - Nausea, ataxia, dizziness, signs of brainstem compression (30% mortality)
- Pons - Fast progressing hemi- or tetraparesis, disturbed eye movements, decerebration, small
pupils, disturbance of breathing, coma, death (high mortality
pathological effect of intracerebral hemorrhage
● Space-occupying effect → Brain shift
● Continued bleeding → Expanding may continue beyond the first few
hours.
● Within 48 hours: disruption of BBB, vasogenic and cytotoxic edema, neuronal damage and
necrosis
● Resolution in 4-8 weeks → Cystic cavity
complication of intracerebral hemorrhage
● Repeat hemorrhage
● Vasospasms
● Deep vein thrombosis
● Dysphagia (can lead to aspiration pneumonia)
● Elevated ICP → Brain herniation
● Seizures
● Hydrocephalus
● SIADH
caus of SAH
● Aneurysms (75%), perimesencephalic hemorrhage (10%), A-V malformations (5%)
● 20% of investigations fail to reveal the source
signs and symptomes of SAH
Signs and symptoms
● Severe headache w/ instantaneous onset
● Loss of consciousness, coma
● Epileptic seizure
● Nausea, vomiting
● Neck stiffness present in most pts
● Focal signs (e.g. limb weakness, dysphasia)
● Reactive hypertension
● fever
diagnosis of SAH
● Urgent CT: detects 95% of SAH within 24h
● Lumbar puncture: if CT is neg. but history is very suggestive of SAH,
needs to be done >12h after headache onset to allow breakdown of RBCs → a pos. sample is xanthrochromic (yellow due to bilirubin)
● MRI: may be used in pts w/ multiple aneurysms
● CT/MR angiography, digital angiography: more detailed info
treatment of SAH
● Re-examine CNS often (BP, pupils, GCS)
● Maintain cerebral perfusion by keeping well hydrated (aim for SBP<160 mmHg)
● Nimodipine to prevent vasospasms
● Surgery: within 48h, if not a delayed intervention is recommended (after 14 days)
aneurism surgery?
Endovascular coiling vs. surgical clipping, depending on accessibility and size of aneurysm (coiling is preferred)
Balloon remodelling and flow diversion are newer techniques used for anatomically challenging aneurysms
define status epilepticus
A state of continuous seizure lasting ≥ 5 min, or ≥ 2 repetitive, separate seizures with consciousness not fully regained in the interictal period.
what is epilepsy
Epilepsy: a chronic neurologic disorder characterized by a predisposition to seizures
Generalized tonic–clonic seizure
A generalized tonic–clonic seizure, commonly known as a grand mal seizure, produces bilateral, convulsive tonic and clonic muscle contractions.
Focal seizures
are seizures which affect initially only one hemisphere of the brain.
Pediatric absence seizures
(also called petit mal seizures) are characterized by a brief altered state of consciousness and staring episodes. And do not cause your child to fall or have significant shaking movements.
4 stages of a seizure
Prodromal.
Early ictal (the “aura”)
Ictal.
Postictal.
how is the postictal stage after a seizure
Period that begins when a seizure subsides and ends when the patient returns to baseline. It typically lasts between 5 and 30 minutes and is characterized by disorienting symptoms such as confusion, drowsiness, hypertension, headache, nausea, etc
causes of seizure in adults
○ Antiepileptic drug withdrawal
○ Acute cerebral embolization
○ Metabolic disorder
○ Alcohol intoxication
○ Tumor
○ Neuroinfection
causes of seizure in children
fever
infection
what can determine the end of status epilepticus
The termination of status epilepticus must be confirmed by EEG (due to non-convulsive or
electrographic status epilepticus)
why must treatment in status epilepticus happen fast
The risk of a focal status epilepticus turning in to a generalized one is relatively high, therefore
treatment is similar in both forms
treatment in status epilepticus
0-5 min usually self limeting do ABCDE, IV accsess, glucose
5-20 min give midazolam IM 10mg or lorazepam IV 0.1mg/kg
20-40 min Valproic acid IV
40-60 min repeat diazepam
etiology of viral meningitis
○ 80% is caused by enteroviruses (coxsackie, echo, nonparalytic polio).
○ Less commonly caused by VZV, HIV, mumps.
○ Outbreaks are especially common in early spring and late autum
etiology of bacterial meningitis
○ Most common pathogens: pneumococcus pneumoniae, N. meningitidis, Listeria (mostly
in alcoholics or when using systemic immunosuppressants)
○ In childhood Staphylococci are the most common pathogens.
why can pathogens proliferate easy in the brain
The primary immune response in the CNS is weak, as there is no MHC I and II antigens on
neurons or astrocytes; thus they are not able to do phagocytosis
most common rout of infection to meninges in meningitis
Most common route of infection: colonization in nasopharynx → subdural space → subarachnoid
space → meninges and basal cisterns (meningeal signs
Clinical signs and complications of meningitis
● Nuchal rigidity, meningeal signs and altered consciousness
● In case of N. meningitidis infection a petechiae can develop
● Serous or purulent exudate block absorption or circulation of CSF → hydrocephalus, cranial
nerve abnormalities and altered consciousness
● Increased ICP due to vasogenic edema because of increased permeability of BBB
● Exudates in venous sinuses → thrombosis, reactive vasculitis and brain ischemia
● Ventriculitis when infection reaches the sinuses
● Bacterial: no AB treatment can lead to death in less than 24h. Prophylaxis is given to close
contacts
diagnosis of bacterial meningitis
Fluid: cloudy, unclear
Protein: high
Lactate: high
Glucose: low
Cell count: High - leukocyte count > 1000/mm3
↑ Granulocytes (> 80%)
Do ELISA
diagnosis of viral meningitis
Fluid: clear
Protein: norm
Lactate: norm
Glucose: norm
Cell count: Variable cell count (leukocyte 10–500/mm3)
↑ Lymphocytes
Do PCR
meningitis treatment
● Empirical treatment with 3rd generation cephalosporin + amoxicillin + vancomycin i.v. should
be administered before culture results are ready
● Confirmed N. meningitidis: ciprofloxacin given to close contacts
● Viral: symptomatic treatment
define encephalitis
Encephalitis: inflammation of the brain parenchyma
etiology of infectious encephalitis
Arboviruses are the most common
Most common causative agents: HSV-1, VZV, tick-born encephalitis viruses and Enterovirus spp.
In immunocompromised patients: CMV, JC viruses,
isteria, Mycobacterium, Mycoplasma spp
what is limbic encephalitis
Limbic encephalitis: Antibodies against cell surface antigens such as receptors, e.g. anti-NMDA
receptor Ab mediated encephalitis (ovarian teratoma)
define multiple sclerosis
A chronic degenerative disease of the CNS characterized by demyelination and axonal degeneration in the brain and spinal cord, which are caused by an immune-mediated inflammatory processes
type of reaction in MS
Type IV HS reaction - cell mediated
pathophysiology of MS
cross reaction of Ab by T-cells. attacks myelinproteins on nerve cells causing oligodendrocyte destruction and plaques called sclera - hence name multiple sclerosis - result is brain athropy
types of MS
Plot neurological destruction up and time.
Relapsing-remitting (90%)
Secondary progressive
Primary progressive
in the CNS the only nerve with oligodendrocyte myelination
is the optic nerve causing optic neuritis
symptomes on optic nerve because of MS
loss of visual acuity
loss of color vision
afferent pupil difect - marcus gunn pupil - mydriasis
what is seen in MS with eye movement
bilateral internuclear opthalmoplegia
loss of connection between CN 6 and 3
when you look to the side only lateral movement works not medial by CN 3. But if you ask the patient to focus on a pen it works
diagnosis of MS
MRI:
periventricular lesions
brainstem lesions
SC lesions
Cerebellum lesions
CSF: oligoclonal bands = IgG Ab from plasma cells
VEP: decreased AP due to reduced conduction velocity
Serology
treatmeant of MS
- high dose CS OR
- Plasmapheresis
- Supportive: Spasmicity: dandrolone / Antidepressives
- preventive: immunosuppression Natalizumab
define brain edema
an excess of brain water, there’s three types of cerebral edema
a) Vasogenic
b) Cytotoxic
c) Interstitial
define vasogenic edema
● Damage to the BBB → high protein content extracellular edema, spreading in white
matter along the nerve fibers
● Perifocal in tumors, central abscesses, parenchymal hemorrhage, generalized in
meningoencephalitis
● Dx: T2-weighted MRI is most sensitive
● Tx: corticosteroids
define cytotoxic brain edema
● Ion gradient btw the intra- and extracellular space decreases → Na+, Cl-, water moves
into the neurons → damage to voltage-gated Ca++ ch. → Ca++ influx → fluid
accumulates within cells
● Typical in cerebral ischemia in the area of cerebral cortex and basal ganglia, supervened
by vasogenic edema as the capillaries are damaged
● Dx: diffusion-weighted MRI
define interstitial edema
● Develops in occlusive hydrocephalus
● Increased CSF pressure → CSF pressed across ependymal layer of ventricles into the
brain parenchyma
● Dx: hypodense halo surrounding the ventricles on CT, high intensity signal on
T2-weighted MRI
treatment of brain edema
1) Causative treatment
2) Osmodiuretics (mannitol, glycerol)
3) Loop diuretics: decreases CSF production
4) Controlled hyperventilation: reduction of pCO2 by 10 mmHg decreases the ICP by 30% because of cerebral vasoconstriction
5) Barbiturate narcosis w/ EEG or plasma level monitoring
6) If ICP is so high that herniation is unavoidable → decompressive craniectomy
7) If occlusive hydrocephalus → temporary CSF drainage
define wernick-korsakoff syndrom
Wernicke encephalopathy is an acute, reversible condition caused by severe thiamine (vitamin B1) deficiency, often due to chronic heavy alcohol use. Wernicke-Korsakoff syndrome is by definition when symptoms of two different conditions are seen
together; Wernicke´s Encephalopathy (WE) and Korsakoff Syndrome (KS).
site of lesion in wernick-korsakoff syndrom
Lesions are bilateral around 3rd and 4th ventricle and the cerebral aqueduct.
define Korsakoff syndrome
(chronic and only 20 % reversible with treatment): memory symptoms
- Anterograde amnesia (problems learning new information) and short-term memory loss
- Confabulations (make up information to fill memory gaps)
- Disorientation in time and space
etiology of wenicks-korsakoff syndrome
- Chronic alcoholism (most common)
- Malnutrition (starvation, eating disorders, gastric surgery, cancer, prolonged vomiting etc) → decreased absorption of thiamine
diagnosis of wernicks korsakoff syndrom
↓ Serum thiamine levels
↓ Erythrocyte transketolase activity (thiamine dependent)
↑ Serum lactate and pyruvate
Evidence of alcohol-related liver dysfunction
Brain MRI: T2-weighted hyperintense lesions in the mammillary bodies, midbrain tectal plate, dorsomedial nuclei of the thalamus, cerebellum, and around the aqueduct and the third ventricle
treatment of wernick korsakoff
Thiamine replacement iV
treat underlying condition
Define Guillian-Barre
acute immune-mediated polyneuropathy that typically manifests with bilateral ascending flaccid paralysis and sensory involvement.
coars of Gullian barre (GBS)
About two-thirds of GBS patients experience symptoms of an upper respiratory or gastrointestinal tract infection up to 6 weeks prior to onset of GBS.
pathogens related to GBS
Campylobacter jejuni: Campylobacter enteritis is the most common
Cytomegalovirus (CMV)
HIV
Influenza
Zika virus
Epstein-Barr virus
SARS-CoV-2
Mycoplasma pneumoniae
pathophysiology of GBS
Postinfectious autoimmune reaction that generates cross-reactive antibodies (molecular mimicry)
Infection triggers humoral response → formation of autoantibodies against gangliosides
diagnosis of GBS
CSF analysis:
May be normal in the first 1–2 weeks of the disease. Typical: albuminocytologic dissociation (i.e., increased protein levels with normal leukocyte count < 10 cells/mcL in CSF)
Electromyography
Pathological spontaneous activity is a sign of an unfavorable prognosis.
symptomes of GBS
Limb involvement:
Bilateral and ascending from the lower limbs
Progressive flaccid paresis or paralysis
Paresthesia (prikking): stocking‑glove distribution
Hyporeflexia typically begins in the lower limbs.
Back and limb pain (often an early symptom)
Involves nociceptive and neuropathic pain
Autonomic dysfunction
Cardiac arrhythmias, blood pressure fluctuations
Urinary retention and/or intestinal dysfunction
Respiratory muscle involvement may lead to respiratory failure.
Cranial nerve involvement
Facial palsy: due to bilateral facial nerve involvement (most frequently affected cranial nerve in GBS)
treatment of GBS
IVIG or plasmapheresis
define myasthenia gravis (MG)
Autoimmune disease of the neuromuscular junction (NMJ) characterized by muscle weakness that worsens with activity and improves with rest
type of reaction in MG
Type 2 HS reaction - cytotoxic
age distribution of MG
young women 20-30
Old men 60-70
pathophysiology of MG
Responsible for inhibition of signal transduction at the neuromuscular junction (NMJ)
Antibodies target postsynaptic AChRs of normal muscle cells → competitive inhibition of acetylcholine (ACh) → AChR decay through receptor internalization (↓ receptor density at the postsynaptic membrane) and activation of complement (→ muscle cell lysis) → impaired signal transduction at the NMJ → skeletal muscle weakness and fatigue
classification of MG
Ocular myasthenia: only the extraocular and/or eyelid muscles
Generalized myasthenia
All skeletal muscles may be involved.
Especially ocular, bulbar, limb, and respiratory muscles
serotypes of MG
Seropositive MG (80–90% of cases): positive assays for antibodies (in blood) against the acetylcholine receptor (AChR-Ab)
Seronegative MG (10–20% of cases): negative for AChR positive for MuSK Ab
MG symptomes
Eye muscles: diplopia, blurred vision
Bulbar muscles: dysarthria, difficulty chewing and/or swallowing
Proximal muscles: difficulty standing from a chair , climbing stairs, brushing hair
Respiratory muscles: dyspnea, respiratory failure
MG diagnosis
● Clinical picture
● IV edrophonium (Tensilon) test: assess for improvement over 2 min, positive if clear
improvement in weakness
● Electromyography: Repetitive stimulation → decremental response (reduced amplitude)
● Serology: anti-AChR Ab (present in 70-90%), MuSK antibodies (30%)
● Chest CT/XR to screen for thymic hyperplasia
MG treatment
- Cholinesterase inhibitor: first-line agent is pyridostigmine
- Immunosuppressants
Indications: inadequate symptom control with (or intolerance to) pyridostigmine - Thymectomy
diseases of micturition
- Spastic, neurogenic bladder
- Flaccid neurogenic bladder
- Detrusor-sphincter dyssynergia
- Frontal lobe incontinence
Spastic, neurogenic bladder
CNS lesions above sacral spinal cord → Disinhibition and increased sensitivity
(hyperreflexia) of detrusor muscle → Urge incontinence and decreased bladder capacity
Detrusor-sphincter dyssynergia
● Uncoordinated function of detrusor muscle and external sphincter.
● Urge to urinate, but cannot due to sphincter spasm → Retention.
● From CNS lesions above sacral spinal cord. May have together with spastic bladder
Flaccid neurogenic bladder
● Hypotonic bladder wall → Increased capacity.
● From lesion in sacral spinal micturition center (S2-4) or distally (conus, cauda equina,
peripheral nerves).
● Bladder wall is insensitive and paralyzed → Overfilling → Overflow incontinence,
constant urine dripping
Frontal lobe incontinence
● Disorders that affect the frontal lobes can cause detrusor hyperactivity or altered social
behavior regarding micturition
