Exam II Flashcards
Ischemic stroke
Thrombotic or embolic occlusion of an artery stopping blood flow to a cerebral area
Hemorrhagic stroke
Bleeding from an blood vessel due to leakage/rupture
TIA (transient ischemic attack)
Temporary occlusion of cerebral vessel which gets resolved within 24 hours, warning sign of stroke coming in near future)
Early warning signs of stroke
BE FAST
Balance difficulties, eyesight changes, face weakness, arm weakness, speech difficulties, time (call 911)
ABCD prediction scale (chances of TIA progressing to stroke)
Age > 60
BP: >140/>90
Clinical Presentation:
-Unilateral weakness
-speech impairment without weakness
Diabetes
Duration of TIA
->60 minutes, 10-59 minutes
Risk of stroke at 2 days
Ischemic stroke pathogenesis
Occlusion of major arteries
-either directly by thrombus formation
-or by embolus
Vascular causes:
-Atherosclerosis
-Artery-to-artery embolism
Cardiogenic causes
-A-fib
-MI
-Valve diseases
CBF impairments following Ischemia
Normal average CBF is 50 ml/100 g/min
Average cerebral perfusion pressure (CPP) is about 60mmHg
If CBF falls below 20 mL/100 g/min, neuronal functioning is impaired. If it falls below 8-10 mL/100 g/min, tissue death occurs
Middle cerebral artery distribution
Biggest distribution - supplies dorso-lateral regions of frontal/parietal lobes, temporal lobe, basal ganglia nuclei and internal capsule
Anterior cerebral artery distribution
Supplies medial regions of frontal and parietal lobes and anterior region of frontal lobe
Posterior cerebral artery distribution
Supplies all occipital lobe, inferior regions of temporal lobe (hippocampus), midbrain (cerebral peduncles) and thalamus
Vertebrobasilar system
(from 2 vertebral arteries providing collateral circulation) – supplies brainstem and cerebellum
SCA (superior cerebellar artery) distribution
cerebellar cortex, cerebellar nuclei, superior cerebellar peduncle, and a small portion of midbrain
AICA (anterior inferior communicating artery) distribution
supplies CN nuclei V/VII/VIII, vestibular and hearing organs (via labyrinthine artery) – helps with differential diagnosis
PICA (posterior inferior communicating artery) distribution
arises from vertebral arteries, supplies dorsolateral medulla, posterior portion of the cerebellar hemispheres and the central nuclei of the cerebellum, CN nuclei V/IX/X
Prefrontal functional area
ACA & MCA
Judgement, foresight, problem solving, behavior, social appropriateness
Lesion – poor judgement, apathy, poor motivation, flat affect, social inappropriateness, perseveration
Due to connections between Dorsolateral Prefrontal cortex to Basal Ganglia - may have difficulty with dual tasking and motor planning.
Premotor functional area
MCA
Motor planning area (externally guided movements) – reaching, grasping
Lesion – ideomotor apraxia (motor planning problem) – inability to perform a task in response to a verbal command or imitate gestures.
Patient knows what they want to do but cannot plan the motor plan needed to complete a task
problems with bimanual tasks
Supplementary Motor functional area
ACA
Motor planning area (internally guided movements)
Lesion – ideomotor apraxia
Primary Motor functional area
ACA & MCA
Execution of voluntary skilled movements on opposite side
lateral cortex – UE, upper trunk and face
medial cortex – LE, lower trunk
Lesion – lack of voluntary skilled movement
Primary Sensory functional area
ACA & MCA
Detection and localization of sensation from the opposite side of the body and face
lateral cortex – UE, upper trunk and face
medial cortex – LE, lower trunk
Lesion – loss of sensation
impaired balance
Sensory Association functional area
Sensory processing and sensory perception (making sense of the senses)
Lesion (in parietal lobe areas)
ideational apraxia
failure to perceive/conceptualize a sensory environment due to impaired cross-modal processing, so unable to understand the purpose of tools/objects because of loss of higher-level perception (use a toothbrush to comb one’s hair)
Frontal Eye Fields functional area
MCA
Controls voluntary saccadic eye movements and smooth pursuits
Lesion – eyes deviate towards the lesion (look away from paralysis)
Wernicke’s area
MCA and PCA (dominant hemisphere – usually left)
Language comprehension
Lesion – patient cannot comprehend speech. Patient can speak fluently, but output makes no sense, fluent/receptive aphasia
Broca’s area
MCA (dominant hemisphere – usually left)
Expressive language (speak, write, sign etc.)
Lesion – inability to express one’s self through language (but comprehension is intact), nonfluent/expressive aphasia
Primary Visual functional area
PCA
Perceives visual information coming from the retina
Lesion – cortical blindness, loss of vision in contralateral ½ of the visual field, but patient may not feel the loss (visual agnosia)
Visual Association area
PCA
Makes sense of vision – recognizes faces, objects
Internal Capsule functional area
MCA (Lenticulostriate arteries)
Sensory
contralateral loss of pain, temperature, touch and proprioception from entire extremities and face
Motor
contralateral weakness of all muscles of the body
Midbrain functional area
Basillar artery, PCA, SCA
Sensory
Spinal Lemniscus (Pain and temp), Medial Lemnicus (touch and proprio)
Motor
Cranial nerve nuclei III, IV, MLF (causes internuclear ophthalmoplegia), corticobulbar tract, corticospinal tract
MCA syndrome (63% of ischemic strokes)
Clinical presentation:
-Contralateral weakness (UE and face)
-Contralateral sensory impairment (UE and face)
-Aphasia (L/dominant hemisphere) – expressive, receptive, global
-Neglect (R/nondominant hemisphere)
ACA Syndrome (6-7% of ischemic strokes)
Clinical presentation:
Sensory impairment in contralateral LE
Weakness in contralateral LE
Altered mental status
aphasia
Abulia (a lack of drive/will power)
Posterior Cerebral Artery Syndrome (12-13% of ischemic strokes)
-Contralateral homonymous hemianopsia
-Contralateral limb weakness
-Thalamic pain syndrome (abnormal sensations of temperature/proprioception/touch, tingling, paresthesia, intractable pain, allodynia)
Visual agnosia, anomia
Lacunar Syndrome (5-8%)
-Small infarcts at the end of deep penetrating arteries, often affecting white matter. Areas affected are basal ganglia, internal capsule, brainstem, and thalamus.
Lacunar Syndrome clinical manifestations
Clinical Presentation (depends on area affected):
-Pure contralateral weakness (posterior limb of internal capsule)
-Pure contralateral sensory loss (posterolateral thalamus or posterior limb of internal capsule)
-Parkinsonism (basal ganglia)
large majority are asymptomatic
VertebroBasilar Artery Syndrome clinical manifestations
Headache, D/N/V, diplopia, nystagmus, dysarthria, dysphagia
ipsilateral ataxia, dysmetria, and hemiparesis
Bilateral effects if trunk of basilar artery is occluded.
Locked in syndrome due to stroke in basilar artery
Superior Cerebellar Artery Syndrome clinical presentation
Headache, D/N/V, Nystagmus, diplopia, dysarthria, ipsilateral ataxia, ipsilateral horners syndrome
Contralateral loss of touch/pain/temp in extremities, torso, and face, if any
Contralateral mild hemiparesis, if any
Anterior Inferior Cerebellar Artery Syndrome (AICA/lateral pontine syndrome) clinical manifestations
-D/N/V, nystagmus, diplopia, dysarthria, dysmetria
-Ipsilateral deafness
-ipsilateral ataxia
-ipsilateral horners syndrome
Ipsilateral loss of touch/pain/temp and weakness in face
Contralateral loss of pain/temp and weakness in limbs, if any
Posterior Inferior Cerebellar Artery (PICA) clinical manifestations
Results in Lateral medullary syndrome or Wallenberg Syndrome
D/N/V, nystagmus, dysarthria, ipsilateral ataxia, ipsilateral horners syndrome, dysphagia, hoarseness of voice
Ipsilateral loss of touch/pain/temp on face (CN V nucleus)
Contralateral loss of pain/temp on body, if any
Spinal artery and vertebral arteries
Results in Medial medullary syndrome
Supplies: medial medulla
Clinical presentation:
-contralateral paresis of U&LE
-Contralateral loss of touch and proprioception
-Ipsilateral tongue deviation (hypoglossal nucleus)
NIH stroke scale
Not used for diagnosing nature or location of stroke, but to assess severity of stroke
0 - no stroke
0-4 - minor stroke
5-15 - moderate stroke
16-20 - moderate to severe stroke
21-42 - severe stroke
≥ 16 forecasts a high probability of death or severe debility
≤ 6 forecasts good recovery
MRI/PET imaging for stroke
Helps with localizing stroke – lobe, structures that are damaged
Severity/area of damage
Detects the area of ischemic penumbra
Determine who would be ‘good candidate’ for continued use of thrombolytic drugs
Hemorrhagic stroke
Bleeding from an arterial source
Types
Intracerebral hemorrhage
Subarachnoid Hemorrhage
Subdural Hemorrhage
Epidural Hematoma
Intracerebral hemorrhage (ICH)
Bleeding into brain parenchyma, most deadly, Incidence low among young people, increases dramatically after 65 years of age
Risk factors – chronic HTN, alcohol abuse, substance abuse, chronic thrombolytic therapy, smoking, eclampsia during pregnancy
pathogenesis of ICH
Dysfunction in cerebral microvasculature secondary to chronic HTN. Weakening of arterial walls and more prone to aneurysms rupture/leakage.
Mostly in smaller deep penetrating arteries - lenticulostriates, arteries entering thalamus, brainstem
Clinical manifestations of ICH
Similar types of clinical presentation as ischemic stroke
Initial symptoms are related to area where bleed occurs
Additional neurologic symptoms occur gradually representing expansion of hematoma
As bleed enlarges ICP may increase causing headache, vomiting and decreased alertness.
Seizures
Subarachnoid hemorrhage (SAH)
Bleeding into subarachnoid space
Another deadly type – mortality 40-60%
Mostly in older (>70 yr) women
Risk factors – HTN, alcohol abuse, smoking
Etiology of SAH
Berry aneurysms – abnormal local distension occurring at vessel bifurcations
About 90% of SAH are due to berry aneurysms
Clinical manifestations of SAH
Sudden onset with severe ‘thunderclap’ headache – sudden and severe
Sentinel headache/Sentinel bleeds – warn sign of SAH - preceding aneurysm ruptures by days or weeks
At the time of rupture, additional symptoms include N/V, altered mental status (syncope, confusion, coma), lethargy, seizure, neck pain, nuchal rigidity
Focal neurological signs like hemiplegia or hemianopia are absent, unless bleeding into brain parenchyma
Medical management of SAH
Treatment
Immediate neurosurgery to isolate the aneurysm or rupture site, evacuate hematoma to prevent further damage
Prognosis
Mortality is high in elderly
If hematoma is <3cm, prognosis is good
Subdural hemorrhage
Result of tearing of bridging veins, mostly occur in elderly after falls, If blood accumulates, compression of brain tissue, can result in herniation of cortex into adjoining spaces
Epidural hemorrhage
Result of tearing of meningeal arteries that run in between the dura
Can be torn secondary to trauma
Medical emergency, need immediate evacuation to prevent compression of brainstem structures, which may cause death.
Mild TBI
majority kind, also called concussions, symptoms generally self-limiting and temporary, less severe end of TBI, but still can involve complex pathophysiology
Moderate to severe TBI
Loss of consciousness from several minutes to hours, persistent headache, vomiting or nausea, convulsions or seizures
Open TBI
Penetrating lesions – fractures, gunshots (velocity and not the size of projectile often determine extent of damage)
Meninges are breached
Can cause damage to brain parenchyma, vascular damage (formation/disruption of aneurysms)
Closed TBI
No skull fracture or penetrating injury, but brain experiences forceful contact on the inner side of hard bony skull, can occur without head hitting hard surface (whiplash), can cause diffuse injuries. Symptoms worse if there is rotational component
Can lead to coup-contre-coup type injuries
Increased Intracranial pressure (ICP)
Most critical secondary injury mechanism, needs to be monitored and controlled, can be due from mass effects from hematoma, cerebral edema, hydrocephalus, increased CBF due to other metabolic reasons, CSF outflow blockage
Consequences of increased ICP are…
triggers a vicious cycle vascular dysregulation,
Normally, brain can maintain constant average CBF by automatically regulating CPP (cerebral perfusion pressure) over a range of mean arterial pressure, MAP (50-150mmHg), using cerebral auto-regulatory mechanisms.
CPP = MAP - ICP, auto regulation is disrupted
Postraumatic aneurysms
Delayed vascular change, due to weakening of cerebral arteries overs days to years (average 3 weeks). can develop in internal carotid artery inside the cavernous sinus. Due to proximity of internal carotid artery to CNs II, III, IV, V, VI.
Vasogenic edema
due to fluid leaking from disrupted BBB along endothelial linings
Cytotoxic edema
due to disruption of NA/K ion pumps leading to water entry and retention
Osmotic edema
due to osmolar property changes between extra and intra cellular fluids, causing water entry.
Compressive damage
Increased ICP due to mass bleeding and edema can compress brain tissue. Compression causes midline shift, brain tissue tries to push into openings or spaces, as herniations.
Transtentorial herniation of uncus
shifts the brainstem, pushes against the contralateral tentorium
Headache
Most common complaint after TBI, Migraine headaches w/ w/o may develop hours or weeks after
In moderate and severe TBI, if headache appears later and person deteriorates neurologically after being lucid initially after injury, then suspect increased ICP from hematoma, need to monitor and treat urgently
Concussion (mild TBI) clincial manifestations
Short-lived impairment of neurologic functions that resolve spontaneously, typically within 7-10 days
Headache, dizziness, nausea, cognitive problems, fatigue and sleep disturbances/sleeping more than usual.
Factors that may prolong recovery time are LOC for >1minute, significant cognitive problems, younger age, female gender and depression
Signs at different levels of Consciousness/disorders of consciousness
Coma is lowest level of consciousness, rarely lasts for more than 4 weeks
wakeful post-comatose unawareness (PVS)
Minimal conscious state (can track objects visually, inconsistent ability to follow commands, simple communications (yes/no gestures))
Decorticate posturing/rigidity clinical manifestations
sustained posturing of UE in flexion and LE in extension
If situation continue to worsen, Decerebrate posturing/rigidity – sustained posturing of UE/LE and trunk on full extension
Compression of brainstem vital centers can elicit abnormal pulse rate, respiratory rate, BP changes, excessive sweating, salivation.
Decorticate posturing
due to compression of cortical connections to the red nucleus, resulting in disinhibited rubrospinal activity
Decerebrate posturing
due to further compression cortical connections to reticular/vestibular nuclei, resulting in disinhibited reticulospinal/vestibulospinal activity
Cheyne-Stokes breathing
rhythmic pattern of increasing/decreasing rate of breathing, bilateral hemispheric or midbrain lesions
Hyperventilation
‘overbreathing’ where blood CO2 decreases causing respiratory alkalosis – pontine/midbrain lesions
Apneustic breathing
prolonged pause at the end of inspiration – mid- to lower pons lesions
Ataxic breathing
irregular rate and depth of breathing – medullary lesions
Motor deficits associated with TBI
Hemispheric lesions can involve one limb or cause hemiplegia, cerebellar lesions can cause ataxia, basal ganglia lesion can cause tremors/bradykinesia.
Flaccidity can gradually be replaced by spasticity
Movement disorders can occur immediately due to acute trauma, or can develop later (dystonia)
Kernohan’s notch phenomenon
due to transtentorial herniation,
If cerebral peduncles are compressed against contralateral tentorium - false localizing signs, resulting in ipsilateral hemiplegia
CN damage due to TBI
Eye exam can yield valuable info about coma – if completely normal pupillary reaction – suggests lesion is above midbrain
CN II damage in optic canal (most vulnerable area of the nerve) –monocular blindness, and bilateral loss of pupillary reaction
Pain associated with TBI
Headache and neck pain common with whiplash, Neuropathic pain, thalamic pain (allodynia), painful leg and moving toes syndrome, fibromyalgia
Heterotopic Ossification
Abnormal bone growth in periarticular soft tissue (muscles/tendons)
Can be associated with trauma, immobility or spasticity following injury
Onset about 4-12 weeks after injury
First detected as tenderness, swelling, pain with movements, loss of ROM, later can be palpated as mass
Second Impact Syndrome (with successive concussions)
Effect of a second concussion before the brain has a chance to recover fully results in worse clinical presentation, Second injury can cause rapid/severe disruption of cerebral autoregulation, LOC and progressive disability or death if not monitored and treated.
Chronic traumatic encephalopathy (CTE)
Progressive degenerative condition, thought to be caused by multiple repeated concussive blows over a lifetime. Deterioration in cognition and behavior.
evidence of degeneration, deposition of protein Tau
Moderate/Severe TBI in ICU/Acute settings medical management
Goals - Assess LOC, assess severity, changes in severity, locate lesion
Pupillary response and oculomotor signs - valuable in diagnosis depth of LOC and localizing brainstem damage
Sluggish or unreactive pupillary response may indicate severe TBI, or increased severity with increasing ICP with successive exams
Gaze palsies – lesion of oculomotor nerves on one side, tonic downward gaze – compression of thalamus, ocular bobbing – pontine lesion
Mild TBI (Concussion) treatment
most recover fully in 7-10 days, Concussed brain is less responsive to usual neural activation, and if premature cognitive and physical activity is forced before complete recovery, it can be vulnerable to prolonged dysfunction. So need to rest – including cognitive rest, avoid repeat concussion
Coma sign when associated with herniation
compression of the midbrain tegmentum, uncal and central herniation
Pupillary dilation associated with herniation
Compression of ipsilateral third nerve, uncal herniation
Miosis associated with herniation
compression of the midbrain, Central herniation
lateral gaze palsy associated with herniation
stretching of the 6th nerve, central herniation
Hemiparesis associated with herniation
compression of contralateral cerebral peduncle against tentorium, uncal herniation. May occur ipsilateral to hemispheric lesion due to false localizing
Decerebrate posturing associated with herniation
compression of the midbrain, central and uncal herniation
Hypertension. bradycardia associated with herniation
compression of the medulla, central, uncal, and cerebellar (tonsillar)
Abnormal breathing patterns associated with herniation
compression of the pons and medulla. Central, uncal, and cerebellar (tonsillar)
Posterior cerebral artery infarction associated with herniation
vascular compression, uncal herniation
Anterior cerebral artery infarction associated with herniation
vascular compression, Subfalcine (cingulate)
