First aid neuro - lesions/strokes/hemorrhage Flashcards
Amygdala lesion
Kluver-Bucy Syndrome
- hyperorality
- hypersexuality
- disinhibited behavior
assoc. HSV-1
Frontal lobe lesion
-disinhibition and deficits in concentration, orientation and judgement; may have reemergence of primitive reflexes
Right parietal-temporal cortex lesion
- non dominant hemisphere normally
- spatial neglect syndrome (agnosia of contralateral side of the world)
Left parietal-temporal cortex lesion
-dominant hemisphere normally
Gerstmann syndrome: agraphia acaculia finger agnosia left right disorientation
Reticular activating system (midbrain)
Reduced levels of arousal and wakefullness - coma
Mammillary bodies lesion (bilateral)
Wernicke-Korsakoff syndrome:
- confusion
- opthalmoplegia, nystagmus
- ataxia
- memory loss
- anterograde and retrograde amnesia
- confabulation
- personality changes
assoc. with thiamine B1 defiency excessive ETOH use, can be precipitatwd by giving glucose without B1
Cerebral hemisphere lesion
- intention tremor, limb ataxia, and loss of balance
- damage to the cerebellum results in ipsilateral deficits; fall toward side of lesion
- hemispheres are lateraly located and afted lateral limbs
Cerebral vermis lesion
Truncal ataxia, dysarthia
STN lesion
contralateral hemibalismus
Bilateral hipocampus lesion
anterograde amnesia
PPRF lesion
eyes look away from the lesion
Front eye field lesion
Eyes look toward lesion
Central pontine myelenosis
-osmotic demyelination syndrome
massive axonal demyelnation in pontine white matter tracts secondary to osmotic forces and edema. Commonyl iatrogenicm caused by overly rapid correction of hyponatremia
can cause:
-acute paralysis, dysarthia, dysphagia, diplopia, loss of consciousness
“locked in syndrome”
Dysphagia
Difficulty with swallowing is the sensation that food is stuck in the throat
Dysarthia
motor inability to speak
aphasia
higher order inability to speak (language deficit)
Broca Aphasia
- nonfluent aphasia with intact comprehension
- broca area inferior frontal gyrus of frontal love
Wernicke aphasia
Fluet aphasia with impaired comprehension and repetition.
-superiror temporal gyrus of temporal love
Global aphasia
nonfluet aphasia and impaired comprehesions, both broca and wernicke areas affected
Conduction aphasia
- poor repetition but fluent speech
- intact comprehension
- can be caused by damage to left superior temporal love and or left supramarginal gyrus
Transcortical motor aphasia
-nonfluent aphasia with good comprehension and repetition
Transcortical sensory aphasia
poor comprehension with fluent speech and repetition
mixed transcortical -
nonfluent speech, poor comprehesion but good repetition
Medial medullary syndrome artery?
ASA
Lateral medullary syndrome (wallenberg) artery?
PICA
Lateral pontine syndrome artery?
AICA
Middle cerebral artery MCA stroke
lesion:
motor cortex: upper limb and face
-contralateral paralysis upper limb and face
Sensory cortex:upper limb and face
contralateral loss of sensation- upper and lower limbs and face
Temporal lobe wernickes
frontal lobe: broca
aphasia if dominant or hemineglect if lesions affects nondominant side
Anterior cerebral artery ACA stroke
Lesion
motor cortex- lower limb
-contralateral paralysis of lower limb
sensory cortex: lower limb
contralateral loss of sensation in lower limb
Lenticulostriate artery stroke
Lesion: striatum and internal capsule
symptoms: hemiparesis/hemipegia
common location of lacunar infacrts secondary to HTN
Anterior spinal artery ASA stroke
areas affected:
- lateral corticospinal tract
- medial leminiscus
- caudal medulla - hypoglossal nerve
- contralateral hemiparesis-upper and lower limbs
- decreased contralateral proprioception (ML)
- ipsilateral hypoglossal dysfunction (lick your wounds)
Medial medullary syndrome - cause by infarct of paramedian branches of ASA and venrtebral arteries
PICA stroke
area affected:
lateral medulla-vesitbular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguous, sympathetic fibers, inferior cerebellar peduncle
Vomiting, vertigo, nystagmus; decreased pain and temperature sensation from ipsilateral face and contralateral body, dysphagia, hoarseness, decreased GAG reflex, ipsilateral horner syndrome; ataxia, dysmetria
LATERAL MEDULLARY SYNDROME
-nucleus ambiguous effects are specific to PICA lesions
AICA
areas affected:
lateral pons,-cranial nerve nuclei; vestibular nuclei, facial nucleus, spinal trigeminal nucleus, chclear nuclei, sympatheitc fibers
middle and infereior cerebral peduncles –> ataxia and dysmetra
vomiting, vertigo, nystagmus, paralysis of face, decreased lacrimination, salivation, decreased taste from 2/3 anterior tongue, decreased corneal reflex (facial nerve), Decreased pain and temperature on face, ipsilateral decreased in hearing and ipsilateral horner syndrome
Lateral Pontine syndrome
Facial nucleus effets are specific to what lesions?
AICA
Nucleus ambigous effects are specific to what lesions?
PICA
PCA stroke
affect
occipital cortex and visual cortex
contralateral hemianopia with macular sparing
Basilar artery stroke
affect the pons, medulla, lower midbrain, corticospinal and corticobulbur tracts, ocular cranial nerve nuclei, PPRF
-preserved consciousness and blinking, quadriplegia, loss of voluntary facial, mouth and tongue imovements
Locked in syndrome
Acom aneurism
- most common lesion in aneurysm
- can lead to stroke
- saccular (berry) aneurysm can impinge on CN
-lead to visual field defects
Pcom aneurism
-common site of berry aneurysm
-can lead to CNIII palsy
down and out with ptosis and pupil dilation
CNIII palsy
down and out with ptosis and pupil dilation
Berry aneurism risk factors
ADPKD Ehlers danlos marfans advanced age HTN smoking black race
Berry aneurism rupture
- most common site is junction of the AComm and ACA
- rupture leads to subarachnoid hemorrhage (worst headache of life) or hemorrhagic stroke.
- can cause bitemporal hemianopia via compression of optic chasm
Charcot bouchard micoaneurysm
assoc with chronic HTN, affects small vessels (basal ganglia and thalamus)
central post-stroke syndrom
neuropathic pain due to thalamic lesions
-intial sensation of numbness and tingling followed in weeks to months by allodynia (ordinary painless stimuli cayse pain) and dysaesthesia.
occurs in 10% of stroke patients
Epidural hematoma
- rupture of middle menigeal artery (branch of the maxilarry artery)
- often secondary to fracture of temporal bone
- lucid interval
- rapid expansion under systempic arterial pressure can cause atranstentorial herniation –> CN III palsy
CT - Lens (biconvex)
hyperdense blood collection
Can cross the flax, tentorium
the middle mengeal arter is a branch of what artery?
maxillary
Subdural hematoma
- Rupture of bridging veins
- slow venous bleeding (less pressure = hematoma develops over time)
- elderly, alcoholids, blunt trauma, SHAKEN BABY
CT: Crescent shaped hemorrhace that cross suture lines, may also see midline shift. CANNOT cross the falx , tentorium
Subarachnoid hemorrhage
Rupture of an aneurysm (such as berry aneurism)
- Rapid time course
- WORST HEADACHE OF MY LIFE)
- Bloody or yellow (xanthocromic) spinal tap
- 2-3 days afterward risk of vasospasm due to blood breakdown (not visible on CT, treat with nimodipine) and rebleed
Intraparenchymal hemorrhage (HTN)
most commonly caused by sytemic HTN
also seen with:
amyloid angiopathy, vasculitis, and neoplasm
typically occurs in basal ganglia and internal capsule (charcot-bouchard aneurysm of lenticulstirate vessels)
Most vulneralbe areas to ischemia?
after 5 minutes of hypoxia irreversible damage hippocampus>neocortex>cerebellum>watershed areas
stroke imaging
Bright on diffusioon weighted MRI in 3- 30 mins
dark abnormality on noncontrast CT within 12-24 hours
hemorrhage imaging
CT
remember dont use tPA if you suspect a hemorrhage
Stoke histo 12-48 hours
red neurons
Stoke histo 24-72 hours
necrosis and neutrophils
Stoke histo 3-5 days
macrophages
Stoke histo 1-2 weeks
reactive gliosis (astrocytes) + vascular proliferation
Stoke histo > 2 weeks
glial scar
Ventricular system
lateral ventricle –> 3rd ventricle via the right and left interventricular foramina of monro
3rd ventricle to 4th ventricle via cerebral aqueduct of sylvius then 4th to subarachnoid space via foramine of luschka = lateral and foramen of magendie = medial
Communication (non-obstructive)hydrocephalus
-decrease in CSF absorption by arachnoid granulations, which can lead to increased intracranial pressure, pappiladema and herniation
Normal pressure hydrocephalus
a type of communicating
-does not result in increased subarchnoid space volume.
expansion of ventricles distort fibers of the corona radiate and leads to clinical triad of wet wobbly and wacky
urinary incontinence, ataxia and cognitive dysfunction
Hydrocephalus ex vacu
a type of non communicating
- appearence of increase CSF in atrophy (alzheimers, advanced HIV, Pick)
- intracranial pressure normal, triad not seen
Non-communicating hydrocephalus
-caused by structural blockage of CSF circulation within the ventricular system (stenosis of the aqueduct of sylvius)
