CVA Flashcards
TIA
Transient ischemic attack
Temporary interruption of blood supply to brain
Symptoms last for a few mins to hours but do not last longer than 24
No residual deficits
Precursor to susceptibility for CI or MI
HTN and CVA
-Reducing diastolic by 5-6mm Hg can reduce risk by up to 40%
Homocysteine
High plasma levels w/ low folate and B6 associated w/ increase risk of heart disease which may increase stroke risk
Cigarette smoking
Increase risk by 50%
Associated w/ number per day
Alcohol
Direct dose rln w/ stroke
3+/day increase risk by 45%
Causes of CVA
Cerebral infarction 70%(thrombus or embolus occlusion)
Hemorrhage’s 20%(subarachnoid, subdural, intracerebral)
Thrombus usually form
Branching or curves in arteries
A-fib
Believed to cause thrombus formation
Embolic infarction
(Thrombus, tissue, fat, air, bacteria or foreign bodies)
Results are more damaging as no time for collateral circulation to develop
Heart is most common source of embolic material (atherothrombic disease)
Artery to artery embolism
from atherothrombic lesion in carotid or verterobasilar
Formation of a thromboemboli begins
Distal vessels of the artery
Micro vascular occlusion that progressively increase in number and continue to impair blood flow
Astroglial swelling
Earliest cell changes noted w/ single artery occlusion
Functioning is impaired when
Blood flow falls below 20mL/100mg
Neuronal death occurs when
The brain relieves less than 8-10mL/100mg/min
Complete cerebral circulatory arrest results in
irreversible cellular damage with a core area
of focal infarction
Cells that have 80-100% ischemia will die in a few min b/c they cant produce ATP ->activation of Ca -> chain rxn to cell death
Area surrounding the core
Ischemic penumbra - receives collateral circulation but is not able to sustain fx
Secondary response to ischemic CVA
Decreased perfusion relative to O2 requirements
Areas of altered metabolism distant from site
Decline in O2 metabolism of unaffected side from acute to subacute (delay of corpus callosum fiber degeneration)
Glutamate and secondary damage
Normal: glutamate is an excitatory NT
released into the EC space and is quickly reabsorbed
• If the cells that normally uptake compromised, excess glutamate depolarizes the post synaptic cells
• excess glutamate allows the influx of Ca++ ions
into the cells which begins the process of cell death
• Catabolic enzymes are activated by the release of the Ca++ ions
and damage the cells that support the neurons (glial cells)
The hypoxia triggers
Neurotoxin release —> cell death
Middle cerebral artery syndrome
-Supplies most of the lateral cortex and also frontal, temporal, and parietal lobes
- Contralateral hemiplegia and hemianesthesia (sensory loss) with greater involvement of the face and upper extremity than the lower extremity because of the somatotopic
organization of the cortex
Middle cerebral artery syndrome
– If the dominant hemisphere (~left) is involved, global aphasia (Broca’s and Wernicke’s aphasia) (loss of fluency, ability to name objects, comprehend auditory information, and repeat language)
– If the non-dominant hemisphere (~right) is involved,
deficits in spatial awareness/attention will be present /(Contralateral body and space >ipsilateral body and space)
– Homonomous hemianopsia if involvement of optic
radiations
Anterior cerebral artery syndrome
Uncommon and often a result of an embolus
– Supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobe)
– Results in contralateral hemiparesis and sensory loss with
greater involvement of the lower extremity than the
upper extremity and face because of the somatotopic
organization of the cortex
Collateral flow can compensate for the occlusion so
dysfunction can be minimal
– Primitive reflexes may be present (frontal release signs)
– Abulia (loss of desire to perform tasks or a delay in verbal and motor response if there is significant involvement of the frontal lobe (role in cognitive functioning and initiative)
Internal carotid artery syndrome
Supplies the MCA and the ACA
– Severity depends on the etiology, thrombus, or embolus of decreased blood flow
– If collateral circulation is present, the condition may be asymptomatic
– If collateral circulation is not present, extensive involvement resembling MCA and ACA manifestations may be present with possibility of coma and death
Posterior cerebral artery suplies
arises from terminal branches of the basilar artery and supplies the inferior and medial temporal lobes
– Also supplies the medial occipital cortex and most of the medial parietal cortex
– Also supplies a small portion of midbrain and most of the thalamus
Posterior cerebral artery occlusion-thalamic branches
Occlusion of the thalamic branches produces contralateral sensory loss
– Can also produce thalamic syndrome, which includes abnormal sensations of pain, temperature, touch and proprioception
– The pain can often be incapacitating (intractable and searing!)
PCA occluded at its origin
contralateral hemiplegia results from infarction of the cerebral peduncle in the midbrain (LCST in middle 1/3)
– Homonomous hemianopsia
– Cortical blindness (if PVC is involved)
– Cognitive dysfunction (memory loss) if hippocampus is involved
– Neglect can occur if significant portion of right parietal lobe is involved (non-dominant hemisphere (~right)-spatial attention/awareness)
Lucunar syndromes
Small vessel infarcts (aka lucanar infarcts because they resemble small lakes/cavities) occur in deep structures of the brain
– Small infarcts at the end of the arteries commonly found in the basal ganglia, internal capsule, and pons
Characteristic of ischemic cysts surrounded by astrocytotic gliosis (scarring of the support structures of the brain)
– Strongly associated with HTN and DM
– Signs are consistent with the neuroanatomic sites that are involved
Types of lucanar stroke
Pure motor lacunar stroke
– Posterior limb of the internal capsule, or anterior pons
Pure sensory lacunar stroke
– VPL of thalamus
Dysarthria-clumsy hand syndrome
– Base of pons, or genu of internal capsule
– Medial motor fibers controlling muscles for the face and the hand are primarily involved
– Syndrome characterized by difficulty with motor aspects of speech (dysarthria) and contralateral weakness (~clumsiness) of the hand
Diagnosing ischemic CVA
- hx of neurological event - timing, pattern of onset, course
- carotid artery and vertebral artery studies are performed using Doppler ultrasound to identify plaque accumulation
- neuroimaging
Timing of embolic vs thrombosis
Embolic occur rapidly w/ no warning
Progressive suggest thrombosis
MRI
Allows ID w/in 2-6 hours
CT scan
Most convenient and readily available
- confirm the dx and assist w/ thx (after 6-12 hours)
- bleeding into the brain can be seen along w/ displacement of brain structures
PET scan
Detection of stroke earlier and w/ higher sensitivity
Eval the areas not immediately affected by infarct showing hypo metabolism and decreased blood flow
Treatment of ischemic CVA
Acute tx: managing the stroke, preventing further embolic strokes
Blood flow and perfusion around the damaged area is the primary concern
Blood pressure should be normalized without compromising circulation
Edema control
Small amounts can create pressure on brain stem/cerebellum —> respiratory arrest (most common cause of death)
TPA
tissue plasminogen activator (TPA)
In emergent state, used to form plasmin which actively digests fibrin strands and is effective in dissolving the thrombus or blood clot responsible for the event
This will potentially save the penumbral neuronal tissue
Mechanical Embolus Removal
device goes into a straight wire that turns in to
a cork screw when it comes out of the guide catheter that is screwed into the clot
A balloon is pumped proximal to the clot to prevent antegrade flow
Then the clot is pulled out
Anticoagulation therapy
Once pt is stable (control BP over 140/90)
Tx of ischemic CVA
Lipid Lowering Agents – Statin drugs
Surgical Intervention – Carotid endarterectomy
Neuro protection– Drugs that are aimed at decreasing the amount of cell death
Nerve Growth – Stem cells
Control of secondary symptoms
Hemorrhage - single most modifiable risk factor
HTN
Chronic — fibrinoid necrosis in penetrating and subcortical ateryies —> weakening of walls —> formation of aneurysmal outpouching or microaneurysms
Hemorrhage risk factors
Excessive alcohol use Long term anticoagulant therapy NSAIDS Liver disease Obesity Etc
Intercerebral hemorrhagic syndromes
Putamen Thalamus Cerebellum Caudate Internal capsule Pons Lobes
Intracerebral hemorrhage
Rupture in a blood vessel - most deadly of stroke subtypes
Due to abnormality of vessel structure/ changes brought about by HTN
Weakening of vessels
When the hemorrhage occurs it spreads along the path of least resistance which is usually along the fiber tracts of the white matter
Edema forms in the parenchyma
Neurologic symptoms occur gradually as there is expansion of the hematoma
Intracranial hemorrhages
Most common
Spontaneous bleeding into surrounding brain tissue —> form a space occupying lesion
Incidence of ICH
Increases dramatically over 65 years of age
More frequent in men
intracerebral and HA
Present in 30-40% of cases associated w/ large superficial hemorrhage’s
Leaves cavity
Putamen
50%-80% occur in the putamen
Contralateral sensorimotor deficit resulting from its proximity to the internal capsule
Oculomotor deficits common with pupillary abnormalities, visual field loss, and conjugate gaze deviation
Wernicke’s (receptive) aphasia with posterior putamen lesions
Abulia (lost motivation) and motor impersistence may be seen with anterior putamen lesions
Thalamus
Sensory loss or dysthesias, possibly some motor deficits
Oculomotor dysfunction including gaze palsies, often with downward eye deviations and convergence spasm, or constriction meiosis
With dominant hemisphere involvement (~left), aphasia, disorientation, and memory disturbances can be seen
Cerebellum
Ataxia is the hallmark sign
Nausea, vomiting, dizziness, nystagmus, vertigo
Brainstem signs such as facial paresis can be seen
Should be monitored carefully for compression in the region of the 4th ventricle which may cause life threatening changes
Pons
Brainstem hemorrhages commonly arise in the middle pons
Coma, quadriplegia, unreactive pupils
Caudate
Rupture into the ventricles
Headache, vomiting, LOC
Mimics subarachnoid hemorrhage
Internal capsule may be involved causing sensorimotor (sensory and motor) involvement
Internal capsule
Presents as pure motor, pure sensory, or sensorimotor stroke with ataxia
Lobar
Centered in the immediate subcortical white matter
Symptoms are lobe specific
Subarachnoid hemorrhage
Can occur suddenly with a searing pain
Sometimes the headache will begin with exertion
Can be spontaneous, often seen in individuals who have normal BP
Occurs from bleeding into the subarachnoid space between the arachnoid and the pia which are continuous with the brain
Subarachnoid hemorrhage can result from
Trauma, neoplasm, infections
Aneurysms and vascular abnormalities
Types of subarachnoid hemorrhage
- Barry aneurysm
- venous malformations
- AVM
- cavernous malformation
Barry aneurysm
Congenital abnormal dimension at bifurcation where the medial layer of vessel is weakest
90% SAH due to this
Venous malformations
Veins, thickened and hyalinzed w/ minimal elastic tissue or smooth muscles
HA or focal neuro deficit
AVM
Less than 3 cm in diameter more likely to bleed because pressure is higher
Seizures, HA, progressive focal neuro deficit
May have cognitive decline
Cavernous malformations
Dilated endothelial lined fibrous tissue where no elastin is present in vessel walls
S/s depend on location - thrombus and scarring surround it
SAH clinical manifestations
HA Nausea and vomiting Syncope Neck pain Coma Confusion Lethargy Seizures
SAH dx
Up to 38% misdx —> viral meningitis, migraine/HA
CT
SAH manage
Manage aneurysm
Evacuation of large hematoma and causative aneurysm
Manage vasospasm
SAH prognosis
If hematoma is <3 cm - prognosis good
Mortality rate in >75 yr old - high
Few are able to live independently
SAH are mostly often result of
tearing of the bridging veins between the brain surface and the dural sinus
Results in accumulation of blood in the dural space– If the volume is great enough—> space occupying lesion —> herniation of the cortex into adjoining spaces
SAH dx tool or choice
non contrast enhanced CT
When the hematoma is dense, MRI may be useful
Epidural hematoma
meningeal arteries run in the periosteal layer
of the dura —> torn during a traumatic skull injury
and bleeding occurs between the periosteum
and the skull —> Damage from compression
medical emergency and the hematoma must be evacuated because of the potential for extensive pooling of the blood
Dx hemorrhagic CVA - CT
specific area can be ID and the amount of blood present
immediately in individuals suspected of having ICH
Dx of hemorrhagic CVA - MRI
multiplanar views and can discriminate subtle changes and rapidly flowing blood
Limited usefulness in the first 24 hours
Prothrombin time, partial thromboplastin time, and platelet count
Performed to rule out a bleeding disorder
In all individuals
Coagulation factor deficits
Detected by eval of liver enzymes
Differential Dx
Ischemic stroke Migraines Tumor Seizures Abscess HTN Encephalopathy
Intracerebral hemorrhage: manage
Reduction of elevated BP w/ rapid acting antihypertensive meds
Control ICP, edema
Vit K can be useful to correct elevated PPT
Supportive care
Cardiac monitoring
Intracerebral hemorrhage - most important predictor of mortality
Hemorrhage size
Individuals with coma or wide spectrum neurological deficits tend to do poorly compared to alert patients with focal neurological involvement
General manifestations of CVA
Hemiplegia:
Motor control deficits Strength deficits Muscle tone changes Sensory changes Perceptual deficits
Emotional (liability or dysregulation syndrome, apathy, euphoria, depression) Balance deficits Speech deficits (wernicke’s and broca’s) Visual field deficits Mental and intellectual impairment
CVA behavior changes - left hemisphere damage
right hemiplegia
presents with difficulties in communication and in processing information in a sequential manner
anxious, cautious, and disorganized
tend to be realistic about their deficits
CVA behavior changes - right hemisphere damage
left hemiplegia
presents with difficulty with spatial perceptual tasks, they are quick and impulsive
They overestimate their abilities and are at a much greater risk for safety
Cannot attend in a crowded environment
Primary complications of CVA
Seizures
Respiratory involvement due to paralysis of the thorax
Trauma from falls
Thrombophlebitis, and vascular changes are aggravated by nactivity
Choking secondary to feeding and swallowing issues
Secondary complications of CVA
Pain
CRPS (Complex Regional Pain Syndrome)
Shoulder - Hand syndrome (Begins with tenderness and swelling of the hand and diffuse aching pain from altered sensitivity in the arm - Pain interferes with movement re-education)
Edema Primarily in the hand and foot
Shoulder subluxation
Management active rehab
Once medical status has stabilized, return to optimal function
Management of Tone/Spasticity
Management of motor control, force production, reaction time, speed of movement, and endurance
Management of sensory deficits
Bed mobility training
Transfer training
Gait training
Balance training
Wheelchair mobility training
Cognitive and Behavioral training
CVA general prognosis
Most recovery occurs in first 6 months
Failure to recover grip before 24 days is correlated with no recovery of arm function at 3 months
No arm movement accompanied with loss of LE motor control is associated with poor outcomes
Vascular disorders of spinal cord
Rare
Infarction can be a result of any of the same conditions as they occur in Brian
Some symptoms appear to be LMN affecting at level of anterior horn cell
(Vascular malformations, transverse myelitis, MS, degenerative disorders)
Necrosis at several levels = sensorimotor loss and pain
Lesion may involve central structures or nerve roots
Clinical manifestation depend on level of SC affected and specific structure affected
