Stroke Syndrome Flashcards
First Stroke Neurologist
Correlated brain lesions with clinical findings
Charles Foix
Neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 hrs that are presumed to be of non-traumatic vascular origin
Stroke
2nd most common cause of death (next to heart disease)
Viewed as a pandemic
Stroke
Prevalence of stroke in the PH
0.9-1.1%
Has the highest stroke DALY, mortality rate
China
Highest percentage of global DALYs for neurological disorder
Cerebrovascular disease - Stroke
(followed by Alzheimers and dementia)
Stroke accounts for how much percent in CVD deaths?
30%
Gender with more strokes
Slightly more females have stroke than males
(Women who live longer have a higher chance of developing stroke)
Direct medical cost
Hospitalization, rehabilitation,
nursing home (very few in PH), home health care services (growing business sector in PH)
Indirect medical cost
Home medications, appliances, transportation,
domestic aid, rehabilitation aid, loss of production (work) due to the stroke
T/F: Stroke is a vascular disease of the heart
False: Stroke is a vascular diseases of the BRAIN
Prevalence of stroke: _ in 6 people will have a stroke
1
Rapidly developing clinical signs of FOCAL (at times GLOBAL) disturbance of brain function
Lasting more that 24 hours or leading to death
No apparent cause other than of vascular origin
Stroke (WHO definition)
Abrupt onset of a neurologic deficit is attributable to
Focal vascular cause
Is an acute neurologic event having foundation in pathology of the blood vessels supplying the brain
Stroke (WHO definition)
T/F: Vessel pathology is both acquired or congenital
True: Vessel pathology can be congenital or acquired, but mostly acquired
T/F: Strokes are ischemic or hemorrhagic
True
Non-modifiable risk factors (6)
Age, gender, hereditary factors, race, prior stroke, existing heart disease
Elderly at greater risk
Age
T/F: Males more susceptible
True: Gender (NMRF)
Family history indicates greater risk
Hereditary factors
T/F: Non-white groups at lesser risk for stroke
False: The darker your color is, the higher the risk (Africans, African-Americans, African-Europeans; Non-caucasians)
Modifiable Risk Factors (2)
Lifestyle and Pharmacotherapy
Factors under lifestyle (5)
Smoking, low physical exercise, morbid obesity, excess alcohol consumption, diet (high salt and fat)
Factors under pharmacotherapy (5)
Hypertension, arterial disease, heart disease or failure, risk of thrombotic or embolic phenomena, certain blood disorders (cholesterol, DM)
Risk factors identified to increase chances for stroke among Filipinos (9)
● Hypertension
● Diabetes
● Atrial fibrillation
● Stress
● Smoking
● Habitual snoring - higher risk for stroke
● Myocardial infarction
● Frequent alcohol
● Rheumatic heart disease
Types of Stroke
Ischemic and hemorrhagic
Types under ischemic (4)
Thrombotic, embolic, lacunar, venous
Types under hemorrhagic (5)
subdural, epidural, subarachnoid, intraparenchymal, hemorrhagic transformation
Causes occlusions or diminished blood flow
Ischemic
Most of the time d/t trauma but can also be d/t
anti-coagulation
Subdural
d/t trauma but most are seen secondary to ruptured aneurysms
Epidural
d/t uncontrolled HTN
Intraparenchymal
Causes of stroke (4)
Thrombotic occlusion of arteries or veins
Embolic disease from the great vessels or heart
Occlusion of the small penetrating vessels
Hypoperfusion
Occurs in the venous sinuses
(superior/inferior sagittal sinus, sigmoid sinuses)
Venous infarction
T/F: Most strokes are arterial
True: ischemic stroke
Dislodged to the system and goes to the circle of Willis & the brain circulation
Embolism
Lack of oxygenation (e.g. when you snore a lot -
may lead to sleep apnea & reduction of oxygenation)
Hypoperfusion
Causes of Hemorrhage (2)
Can be breakage of the blood vessel d/t hypertension or aneurysm
Trauma penetrating injury → leads to fragile vessels from infarction
Clinical findings: Acute Onset of focal deficit (most common) (5)
○ Weakness (most common)
○ Sensory loss
○ Ataxia
○ Speech deficit
○ Visual loss
Arises from the heart, aorta, or the carotid or vertebral arteries
Embolic disease
Can be from valvular disease, akinetic myocardium with thrombus formation, or from the venous system via a right-to-left shunt from septal defect
Cardiac emboli
pts w/ mitral stenosis, traumatic heart disease, endocarditis
Valvular disease
Heart muscle is not pumping anymore (dilated cardiomyopathy)
Akinetic myocardium
Foramen ovale does not close at
the age of 1; atrioseptal defect or atrioseptal aneurysm
Septal defects
Occlusion of the vessel by propagation of thrombus
Atherosclerosis and lipid/fat deposits are
already present → clots and forms over time
Thrombotic disease
T/F: The occlusion over time, and the extent of the symptoms depend not only on the size and location of the vessel, but on collateral flow
True: Thrombotic infarct
T/F: These collateral have more time to expand if the occlusion occurs over time
True: Collateral circulation is a very important
determinant of how bad the stroke will be
Much less common than arterial infarction
Appear in the sinuses
Poses more risk to pregnant, hypercoagulable
Patients present any combination of focal weakness, headache, cognitive di fficulty, and seizures
Venous infarct
T/F: Seizures are common in arterial infarcts except in embolic strokes
False: Seizures are not common in arterial infarcts except in embolic strokes
Usually due to rupture of an intracranial aneurysm
There is acute onset of headache and sometimes neurologic deficit
Subarachnoid hemorrhage
Very prominent symptom of subarachnoid hemorrhage
headache
Due to hypertension, although amyloid angiopathy and trauma
Intraparenchymal hemorrhage
Main cause of intraparenchymal hemorrhage
Hypertension (poorly controlled BP)
Another important cause of
intraparenchymal bleeding d/t a large infarct that bleeds into the infarct
Hemorrhagic infarction
Presentation of intraparenchymal hemorrhage
Weakness, and may have
seizures and decreased level of consciousness
d/t trauma wherein the middle meningeal artery is ruptured
Epidural
d/t trauma wherein venous channels will tear and venous blood accumulate in the brain
Subdural
Epidural or Subdural: Takes a longer time to present itself w/ neurological deficits
Subdural
Temporary interruption of focal brain circulation, which results in neurologic deficit
Transient ischemic attack
Most common cause of TIA
Embolic disease from the heart or cerebral arteries
T/F: The embolus can then break up and go downstream, resulting in return of flow to the region
True
T/F: After the Sx occur, they will NOT recover immediately and these are dangerous signs that the pt is at risk of developing a more severe type of neurologic disease or stroke if risk factors are not addressed
False: They will recover immediately but these are dangerous signs
How long does a temporary neurologic deficit last (TIA)
<24 hours (definition); commonly <1 hour for 15 mins
Most common deficits for TIA are:
○ Hemiparesis
○ Hemisensory loss
○ Aphasia
○ Confusion
○ Hemianopia
○ Ataxia
○ Vertigo
○ Monocular blindness
T/F: The onset of the deficit is abrupt, which helps di fferentiation from the neurologic deficit of migraine, and which has a progressive onset and migration of symptoms
True
T/F: Migraine can present with hemiplegia & has classical symptoms
True
Prognosis of TIA
Gradual recovery
T/F: Usual routine labs are normal for TIA patients
True
Abrupt onset of deficit, with recovery usually lasting less than an hour
Imaging shows no abnormality or signs of previous strokes
Diagnosis of TIA
Differential diagnosis of TIA
Migrane and seizure
Focal weakness or sensory loss can occur as a part of this, either during the aura or during the this → in hemiplegic ____
Migraine
T/F: Focal seizures usually are recurrent whereas TIAs are single, although they can occur
True
General features of infarction: Symptoms (2)
Acute onset of neurologic deficit suggests infraction
Persistence of neurologic deficits
Difference between TIA and infarction
TIA: transient occurrence of Sx w/ immediate
resolution
Infarcts: persistence of neurologic deficits
Signs of infarction (8)
○Hemiparesis
○ Hemisensory loss
○ Hemianopia
○ Gait/Lim Ataxia
○ Aphasia
○ Neglect
○ Ocular Motor Abnormality
○ Doubling of vision
Commonly affected vessels in ischemic stroke (4)
MCA
ACA
Posterior circulation
Vertebrobasilar artery
Contralateral hemiparesis and hemisensory loss, aff ecting arms more than legs
With left hemisphere infarct: aphasia
With right hemisphere infarct: neglect and
constructional di fficulty
Contralateral hemianopia is common although not invariable
Occlusion can occur in its entirety (main stem) or partially → can occlude the penetrating arteries
MCA
Patterns of occlusion: Entire MCA
Contralateral gaze palsy, hemiplegia, hemisensory loss, spatial neglect, hemianopia
Global aphasia (if on left or dominant side)
May lead to coma secondary to edema
Patterns of occlusion: Deep branch
Contralateral hemiplegia, hemisensory loss
Transcortical motor and/or sensory aphasia (if on left or dominant side)
Patterns of occlusion: Parasylvian branch
Contralateral weakness and sensory loss of face and hand
Conduction aphasia, apraxia, and Gerstmann syndrome (if on left side)
Constructional dyspraxia (if on right side)
Patterns of occlusion: Superior branch
Contralateral hemiplegia, hemisensory loss, gaze palsy, spatial neglect
Broca’s aphasia (if on left or
dominant side)
Patterns of occlusion: Inferior branch
Contralateral hemianopia or upper quadrant
anopsia
Wernicke’s aphasia (if on left side)
Constructional dyspraxia (if on right side)
Contralateral hemiparesis mainly a ffecting the leg
If the arm is a ffected, the proximal arm is most
prominent.
Bilateral infarction may produce bilateral leg
weakness, which can be mistaken for myelopathy or spinal cord diseases
Frontal lobe signs can develop with bilateral
infarction - apathy, disinhibition (changes in mood)
ACA
If the entire ACA is a ffected, they can develop: (5)
○ Incontinence
○ Contralateral hemiplegia
○ Abulia
○ Transcortical motor aphasia or motor & sensory aphasia
○ Left limb dyspraxia
If the distal part of the ACA is a ffected, they can
develop: (4)
○ Contralateral weakness of the leg, hip, foot and shoulder
○ Sensory loss of the foot
○ Transcortical motor aphasia or motor and
sensory aphasia
○ Left limb dyspraxia
Contralateral hemiplegia
Ipsilateral oculomotor deficits
Contralateral hemisensory deficits
Contralateral homonymous hemianopsia
Contralateral hemianopia, which may spare the
macula
Confusion with memory loss can occur acutely
PCA
Right homonymous hemianopia
Extension to the splenium of the corpus callosum can cause alexia without agraphia
Larger infarcts, including the thalamus and internal capsule, may cause aphasia, right hemisensory loss, and right hemiparesis
Left PCA
Vertigo and ataxia are common - dizziness & imbalance
Ataxia can be of gait and/or limbs – artery supplies the cerebellum
Ocular abnormalities can include
○ Diplopia
○ Nystagmus
○ Anisocoria - pupillary changes
Dysarthria and dysphagia with medullary involvement
Hemiparesis or quadriparesis with corticospinal tract involvement at any level.
Vertebrobasilar artery
A ffects the proximal part of the PCA
Cranial Nerve III Palsy → weak medial rectus,
dilated pupils
Caused by the involvement of the fascicles of the 3rd nerve within the midbrain
Contralateral hemiparesis
Parasympathetic involvement
Weber’s syndrome
Cranial Nerve III Palsy
Larger involvement
Caused by the involvement of the fascicles of the 3rd nerve within the midbrain, cerebral peduncle, & red nucleus
Contralateral hemiparesis
Contralateral ataxia, tremor, involuntary
movements
○ Ataxia – d/t involvement of the red nucleus
○ Rubral tremor
Benedikt’s syndrome
● A.K.A. Lateral Medullary Syndrome
● Involves the vertebral artery & posterior inferior cerebellar artery
● Presents with:
○ Ipsilateral ataxia, vertigo, nystagmus, nausea
○ Ipsilateral facial numbness
○ Contralateral body hermo-analgesia
○ Ipsilateral Horner’s Syndrome
● Trigeminal nerve is involved
Wallenberg syndrome
● Medial Medullary Syndrome
● Presents with more motor symptoms
● Contralateral hemiparesis
● Contralateral decrease in vibration and position
sense – d/t involvement of the medial lemniscus
● Ipsilateral tongue weakness – d/t involvement of the hypoglossal nucleus
Medial medullary syndrome
● Internal capsule or basal ganglia: contralateral hemiparesis and/or incoordination
● Brainstem: Contralateral hemiparesis, may have ipsilateral appendicular ataxia depending on the location of the lesion, ocular signs are also common
○ Medial rectus palsy, nystagmus
● Pure motor or pure sensory symptoms suggest penetrating vessel occlusion
Penetrating arteries
Focal deficit, often with headache and or seizures, can suggest venous infarction
Occurrence in postpartum women, or in young people generally at lower risk of arterial infarctions, suggests venous infarction
○ Higher venous infarction in stroke-like
presentations of young women
Veins and venous sinuses
Transient blindness in one eye from temporary occlusion by platelet-fibrin or cholesterol emboli (on side of involved artery)
Aka Amaurosis fugax
Territory: ocular manifestations
Occasional headache (usually supraorbital or temporal)
Homonymous (partial) visual field defects
Language defect – involvement of dominant
hemisphere
Contralateral hemiparesis or hemiplegia
with/without sensory deficits
Patients may awaken from sleep unable to move the a ffected side. → a.k.a. wake-up strokes
Territory: cerebral hemisphere manifestations
Steps in emergency management (7)
ABC (airway, breathing, circulation)
Vitals signs
ECG, insert IV line, BP
Initial medical and neurologic assessment
History
Perform detailed neurologic and medical exam
Determine candidacy for immediate stroke intervention
Tests performed in the Emergency Department
(immediate)
○ Blood exams: CMP, CBC, PT, aPTT
○ Imaging: Chest X-ray, Plain cranial CT/MRI
○ Urine: Urinalysis
○ Physiologic: ECG
○ Metabolic parameters should be done in the ER
Patients with signs and symptoms of acute CNS bleed should have the CT performed as soon as possible
If the CT confirmed bleed, then neurosurgery should be emergently consulted
Whether they are good candidates for
evacuation of hemorrhage or not – either
minimal invasive or invasive surgery
The only exception to this would be a patient who would clearly not be a candidate for surgery e.g., patient who are unstable for any procedure or a patient who refuses consideration of any procedure
Considerations of surgery
Performed on selected patients and at institutions where the staff is trained and experienced in the intervention (e.g. USTH)
Specialists at these institutions will determine when these are appropriate
Just because a procedure can be done does not mean that it should always be done
Warning on neurointervention
Stroke warning signs: Main symptoms (5)
Weakness
Trouble speaking
Vision problems
Headache
Dizziness
Stroke warning signs: BEFAST
Balance loss
Eyes: vision loss
Facial weakness
Arm weakness, sensory problem
Speech problem
Time: address immediately if possible
Embolic infarction, most likely
Thrombotic infarction
Abrupt Onset of Focal Deficit
Thrombotic infarction
Lacunar infarction
Awaken with Focal Deficit
Thrombotic infarction
Lacunar infarction
Venous infarction
Intraparenchymal hemorrhage
Rapid but not Abrupt Onset of Focal Deficit
Subarachnoid hemorrhage (SAH)
Intraparenchymal hemorrhage (less likely)
Acute Onset of Severe Headache without deficit
Subdural hemorrhage
Epidural hemorrhage
Headache and Focal Deficit after Injury
Intraparenchymal hemorrhage
Hemorrhagic transformation of ischemic stroke
Subacute Onset of Neurologic deficit
Epidural hemorrhage (this is a classic history)
Coma after head injury, with or without a lucid interval
